How is the sequenced genome of a person useful to him in practice, now? Currently it is possible and not so expensive for a person to have his genome. This is useful in general for understanding how life works. But, in practice, how is this useful for the specific person at this point in time?

A human genome sequence can uncover large deletions and insertions in the genome and would give the genotypes of both common and private (rare to very rare) small polymorphisms (e.g. SNPs) and SSRs (simple sequence repeats). From this information, one can learn about some curiosity traits (say, sensing asparagus metabolites in the urine, slow or fast twitch muscles, curly vs not curly hair) and, more importantly, about disease risk. Ancestry and family relationships can also be learned as in, for example, a half-sibling relationship.

As many diseases are polygenic with numerous loci each making small contributions to the variance, it becomes very difficult to fully describe the level of increased or decreased risk. In other words, we don't yet know all the players and so assessing their contribution to risk of disease can't be done with complete confidence. To further compound this problem are both epistasis and gene-environment interactions. Epistasis is a gene-gene (gene-gene-gene, etc) interaction, such that genes A and B separately make no contribution to the phenotype (disease risk), but do so in combination - say in ab/ab individuals. A gene-environment interaction can be described as when an allele associates with increased risk only when an environmental factor (e.g., exercise, fat in the diet, sun exposure, oxygen tension (altitude), etc), passes a certain threshold.

Still, the most powerful predictor of disease risk, onset and progression is family history. A genome sequence approaches that history (half your genome is from your mother and half from your father, of course), but remains fairly uninterpretable in terms of complex traits. You may carry a couple variants posing increased risk for heart disease, but what about the other hundred or so loci that also make small contributions to this affliction? Sure, if we knew exactly what those other hundred were and how much they each contribute and if they interact with each other or the environment. An incomplete picture emerges.

With rare diseases and altered genomes (say in cancer compared to normal) great strides are being made to either identify the small number of defective genes (rare diseases) or the commandeered pathways exploited for uncontrolled growth (cancer). In this regard, much can be learned and will have quicker, but still measurable in years, applications to the clinic.


What effect do oligosaccharides, like those found in legumes, have on the composition of intestinal flora in humans and if so how so? I know that intestinal flora metabolising oligosaccharides, like those found in legumes, is the cause for the well known fact that legumes cause flatulence, but does an oligosaccharide-rich intestine change the composition (i.e. which specific bacteria make it up) of intestinal flora in humans?

The answer to this is fairly complex, and it depends on whether you are talking about short-term or long-term changes to the microbiota.

When talking about short-term changes, the answer is almost certainly a resounding yes. Any ingested nutrient will lead to an increase in the growth rates of bacteria capable of metabolising that nutrient, and will therefore lead to a change in the composition of the intestinal microbiota.

This is, unfortunately, difficult to observe, as most studies of the intestinal microbiota use fecal samples to look at intestinal microbial composition. Since stool represents an average of what happens between two bowel movements, it is difficult to draw inferences about short-term changes in the microbial composition of the bowel. However, there is evidence from Pythons that suggests extensive remodelling of the microbial composition does indeed occur, at least in animals with less regular feeding schedules.

In the case of long-term changes, there is strong evidence that specific oligosaccharides contained in human milk specifically select for certain strains of Bifidobacterium and Lactobacillus. Apart from this very specific set of oligosaccharides however, there is a paucity of studies dealing with the effects of diet on the gut microbiota, and even fewer looking at specific nutrients.

The premise that long-term changes to the gut microbiota can be made with diets is the foundation on which the entire prebiotics industry is built. The most popular prebiotics are fructo-oligosaccharide, inulin, galacto-oligosaccharide and lactulose. These are said to encourage the growth of beneficial strains of Bifidobacterium and Lactobacillus. However, there is currently no consensus on the long-term effects of these oligosaccharides on the microbiota.


Can lactate be created in ketosis? After looking at Cori Cycle (from wikipedia)

I have a question about how the lactate can be produced in ketosis. According to this article:

  in a low-glucose state, where the body senses that dietary glucose might not be coming anytime soon, peripheral insulin resistance is triggered. This prevents the muscles from taking up “precious” glucose that the brain requires. The brain’s sensitivity to insulin is preserved, allowing it to grab what glucose it needs from the paltry – but sufficient – levels available to it.

it seems that the glucose is not even transfered into muscle cells. In spite of this fact, the lactate is still somehow created during hard exercise even in full ketosis when ketones are present in the bloodstream. How is it possible?

First, there are inaccuracies and misconceptions in the article you quote, which also relates to obese people with insulin-resistance (pre type II diabetics) rather than normal people. These are:

I’m not sure what a “low glucose state” is supposed to mean, but the tissues of the organism co-operate to ensure that the blood glucose concentration normally never falls below about 4 mM, with a range of approx. 4–8 mM. Thus, glucose is available in the blood for tissues that can take it up in a particular circumstance. These are not “paltry levels”, as quoted.
The body’s metabolism cannot predict the future. The scientific credentials of anyone who writes “the body senses that dietary glucose might not be coming anytime soon” are hardly to be trusted. (I don't think much of his literary style either.)
In short-term starvation, when the blood glucose concentration falls towards the lower end of its range, insulin resistance is not triggered. Insulin secretion from the pancreas stops (and glucagon secretion starts).
The brain is not sensitive to insulin (i.e. its glucose
transporter(s) is not), whereas the muscle is. This is what allows the brain continued access to glucose.

Some of this is elaborated in my answers to: “What is the purpose of gluconeogenesis?”,  “How do muscle cells synthesize glycogen?” and “During starvation, does the human body do anything to prioritize which organs receive nutrients?”. A section from Berg et al. may also be of interest.

Answer

Lactate can (and must) be generated by non-aerobic muscle metabolism (i.e. in muscle lacking mitochondria) during exercise because anaerobic glycolysis, with conversion of pyruvate to lactate, is the only way the muscle can obtain ATP to power its contraction. The source of this is the glycogen stores laid down in the muscle after a meal, and glucose taken up from the blood.

I don’t know anything about low-carb diets, but I assume they include protein, so that some of the amino acids from this can be converted to glucose by the liver (glucogenic amino acids) as well as those that cannot (the ketogenic ones that can give rise to ketone bodies). Even if the blood glucose is at the lower end of its range, in the non-starved state the muscle can take it up from the blood. (The blood glucose will be restored by the so-called Cori Cycle.) Even in starvation, if the muscle is working there will be a concentration difference between blood and muscle glucose that will allow uptake.

I think that this question is provoked by the feeling that the existence of ketosis means that glucose is not available to cells. This, as I hope I have explained, is a misconception, perhaps arising from confusion with the different situation of ketosis in long-term starvation.

Finally, there are other sources of lactate besides muscle, regardless of diet. One is the erythrocytes which lack mitochondria and therefore can only use anaerobic glycolysis to produce the ATP they need for active cation transport etc.


Is it possible to estimate tree height from stump/breast diameter and species? Kindly pardon my poor knowledge, my area of expertise is not biology.

I am currently working on project where I have access to tree's stump and breast diameter and its species. We are trying to estimate tree's impact on microclimate on its surrounding.

To simulate it, we need approximation on tree height. So is there a database or textbook I can refer which provide information on estimating tree height from these features?

I understand that there would be no absolute value here but rather a distribution.

This is an interesting question for me because my first research internship centered pretty much entirely around this.  It got pretty deep into the weeds as this was a CS, rather than biology, internship and we were mostly analyzing the math behind the allometry (e.g. Log-transformed linear vs. nonlinear regression for fitting the curve, OLS vs. RMA regression, traditional vs. monte carlo methods for comparing curves with different numbers of parameters, etc.) but much of the work we did is applicable here.

So, what you have here is DBH, or Diameter at Breast Height, which, lucky for you, happens to be the most common method for estimating the biomasses of trees.  Here is the way that it works.  Basically, a research team will go out and measure the diameter of a bunch of trees.  Then they will cut down those trees and weigh them.  What they will end up with is a graph with a bunch of points that give you the weight of trees of particular diameters.  Then you fit a curve to this graph and, next time you want to estimate the biomass of a tree, you plug that tree's diameter into the equation for your curve.  There are a bunch of databases containing allometric equations for different tree species.  You just need to find one that contains the trees that you are interested in.  Given that you are working in New York, this might have what you need:

https://www.fs.fed.us/psw/publications/documents/psw_gtr253/psw_gtr_253.pdf

Though you are better off figuring out the species of the trees you are looking at and seeking out allometric equations for those specifically.  There might even be allometric information included with the data you are being provided.  One thing that may be an issue is that correlations between DBH and biomass are much more common than correlations between DBH and height.  Though both exist, you may have more trouble tracking down the latter for specific cases.  Additionally, these numbers are very rough estimates that vary a great deal depending on the techniques used to collect the data, fit the curve, and extract the equation.  In my own research, I found that log-transformed linear regression tended to be more successful over all (oddly enough) but that nonlinear regression was more effective on young forests dominated by stands of small trees.  We also had a rather odd finding that log-transformed linear regression of two lines with a breakpoint tended to be less accurate in both situations but more accurate overall (i.e. it did better on big trees than nonlinear regression and better on small trees than linear regression) but we weren't able to come up with a mechanism to explain why this would be the case so we scrapped the findings.  At any rate, all of this should illustrate that these numbers are very rough estimates that can be heavily influenced by environmental biases and that different research teams may even disagree on the proper allometric equations to use on a given species.  This is why databases are helpful, as they tend to average out a large number of allometric studies rather than relying on a single one, but even these should be taken with something of a grain of salt.

If you are expected to actually come up with these equations yourself, then you need to actually measure the diameter and heights of a bunch of trees, plot them, and fit a curve to them.  But from the sounds of it, you are only expected to estimate tree height based on diameter.  If that is the problem you are being asked to solve, chances are that there are allometric equations available to help solve it, perhaps even ones that were provided to you.


Are there examples of cells with more than one nucleus? I've always wondered why cells have only one nucleus, as having multiple would seemingly prevent mutation. Are there examples of organisms with multiple nucleuses? If not, is there a reason?

Are there examples of cells with more than one nucleus?

Yes, they are called Multinucleate cells. There are two types of multinucleated cells

Syncytia
Coenocytes

I highly recommend having a look at this answer for the definitions.

Examples of Syncytia include

Osteoclasts
Skeletal muscle fibers (thanks @kmm)

Examples of Coenocytes include

Codium (Thanks @GerardoFurtado; see picture below)
Blastoderms early in the development of a fruit fly

  Are there examples of organisms with multiple nucleuses?

Side note: The plural of nucleus is nuclei

In many fungi, during sexual reproduction, a fusion of cytoplasm happen early in the mycelium but a fusion of the nucleus happens only very late (just before sporulation). This is a type of Coenocytic mycelium. In these species, non-negligible fractions of their cells are multinucleated.

There are endosymbiotic and endoparasitic eukaryotes in other eukaryotes that would result in a cell containing several nuclei but that would not count I would guess as the nuclei belong to different species.

Picture of Codium. The entire algea is a single multinucleated cell.


In the context of twin studies, what do 'unique environmental factors' and 'shared environmental factors' refer to? I was reading this study on sexual behavior and they refer to both terms without clarification. Does 'unique environmental factors' refer only to the prenatal environment or does it include individual experiences with, say, illness as well? Would friends be considered a 'shared environment factor' or an 'individual environment factor?'

Shared environmental factors are those shared by the twins: uterine/prenatal environment and then the home environment and other environments both twins are raised in or remain in together. Unique environments are any environment not shared by the twins - they generally appear later in age.


Interpretation of faint band for Linear Array HPV Genotyping Test After having used the test for research it would appear as if it is very specific. What is one to make of bands that are there but faint? Or what if there are two bands and one is big and bold and the other is faint? Intuitively, I would believe that the starting concentration of the type represented by the bold band is way higher than the type represented by the faint band. Is my intuition correct? Any insights into what that means? Are both HPV types driving the disease process (eg papillomas) or is it just the bold one? Any data? Any intuitions? Any references?

I received this answer privately and was given permission (in fact asked) to share it without attribution.

The package insert for the Linear Array assay defines any visible band as a positive band, so a faint band counts as a positive.
The difference in band intensity could be related to viral type abundance but really depends on which bands are being compared.  Because this is an end-point assay, it's possible that some virus types amplify with better efficiency than others when found in a mixed infection and it is also likely that overall sensitivity or detection limits may be different for each type.  Additionally the probe for HPV52 is cross-reactive with types 33, 35, 58 and in the presence of any of those additional types, it may increase its intensity.

The driver of the disease process is the virus with the most oncogenic potential (but I assume that is only when we are talking about cancer or dysplasia, perhaps not when referring to recurrent respiratory papillomatosis or genital warts), which does not change in the presence or absence of other viruses (and regardless of the band intensity).  Additionally, it's important to remember that the resulting disease is clonally derived, originating with a single-type infection (ie. each lesion will be linked to only one HPV type).  When multiple viral types are found within an exfoliated sample it signifies multiple different infection sites (and not multiple virus types within single cells).  Not all of these will progress to high-grade disease, but rather, the lesions caused by genotypes with the highest associated risk are the most likely.


What is the space between -10 promoter sites and start sites (+1) Between the transcriptional start site of a gene and the -10 promoter region there is always a space of around 10 nucleotides, what is this space function and purpose?

Do you see the space between operator and promoter.. that is what I am referring to, even without an operator it is usually still there

Also, if I want to insert a specific promoter into a vector backbone, how much space should be between the promoter -10 and +1 transcription start site? Is it always 10 bp?

By "start site", do you refer to the "start codon"?

I think the spacing you are referring to is the 5' UTR.

  The 5′ untranslated region (5′ UTR) (also known as a Leader Sequence or Leader RNA) is the region of an mRNA that is directly upstream from the initiation codon. This region is important for the regulation of translation of a transcript by differing mechanisms in viruses, prokaryotes and eukaryotes

Have a look at the wikipedia article for more information about its roles.

The 5' UTR is typically 3 to 10 nucleotides long in prokaryotes but can be much longer (up to several thousands of nucleotides) in eukaryotes. On which species did you notice this spacing of about 10 nucleotides?


How are limits determined for systotic and diastotic blood pressure? I know that the upper limits for systotic/diastotic blood pressure are 120/80. What is the mathematics behind these numbers? I am curious because I did not find information regarding how the numbers are arrived at. I am not sure if the numbers are based on statistical study or is there a scientific basis for the same.

120/80 are not upper limits on blood pressure - many people have blood pressures far in excess of those numbers. Instead, these are numbers beyond which studies have shown connections to negative health outcomes - heart disease, for example.

There is nothing magical about the numbers 120 or 80 besides their divisibility by 10; a blood pressure of 121/81 is no more risky than 120/80 than 122/82 is over 121/81. Because of this, drawing a hard line isn't possible - it's just a suggestion.

Typically, systolic pressures less than 130-135 aren't given any special consideration beyond normal advice to exercise and eat well, unless there are other conditions/risks. Guidelines from the American Heart Association and the UK's NHS are to consider treatment only for diastolic pressures above 140mmHg. There has been some disagreement about these precise limits, with some recommendations for lower targets, for example here. Some of the disagreement seems to be the types of interventions - the guidelines to treat diastolic hypertension only above 140mmHg are mostly considering medications, whereas the guidelines to treat prehypertension are aiming for improved lifestyle: diet, exercise, etc.


How to run agar gel electrophoresis at home I've looked at various sites explaining how you can easily make your own gel electrophoresis kit at home. But they always test various food dyes on these home made kits instead of actual DNA samples. Extracting DNA from plant matter can also be done easily at home, so why can't you just run this on the homemade kit?

There are a few reasons why this is usually not suggested.

DNA itself is not visible (at least not in the quantities you'd run on your gel). You need a compound (dye) that binds to the DNA to make it visible, and because they bind to DNA most of these compounds are carcinogenic. Even if you use such a dye, many of them only show up under UV light, an additional difficulty. You could also buy a safe dye that works and is visible, but that makes staining also more laborious. Food coloring will be visible all the time, already when running the gel.
The nice CSI gels you see on TV are showing (supposed) PCR products of short tandem repeats, giving you nice bands at different heights on the gel. These bands also have a convenient size for gel electrophoresis. Restriction analysis of plasmids is also something you'd see more often, and also here the pieces are between 100 and 10,000 bp. DNA extracted from plants consists of genomic DNA, huge strands (millions of base pairs) that will not really run on an agarose gel. Getting a selection of discrete-sized DNA fragments is really not so easy in your kitchen, that's why they go for food dyes.


Difference in variance of Cys in protein sequences Suppose I have got two sets of proteins (amino acid sequences). In one set, I find that the variance in the percentage concentration of the Cys is way more (65.34) than the variance of Cys in the other group (0.456). Does it mean anything? Does this have any sort of biological implication?

The concentration has been calculated by dividing the total number of Cys found by the size of the protein sequence.

No, because it's extremely likely your sets are not a representative sample of the true distribution in proteins.

Your bias might be caused by an effect on the functionality of the protein, but it might as well be a bias in which organisms are sequenced or something caused by the alignment or the way you are searching for your sets.


Which is the tissue damaging agent in krokodil (street desomorphine) I've just read about krokodil and saw some quite hideous pictures about what it does to the human body. I guess just desomorphine alone wouldn't have this effect.
Which ingredient(s) causes the damage to the tissue?

Note: Don't click on the links, or even search for information, if you don't have a strong stomach

From what I've read, it's not necessarily 100% known, most likely because it's not easy to study (small, reclusive users who die quickly of a complex concoction) but the line everyone has quoted is:

  "They extract [the drug] and even though they believe that most of the oil and gasoline is gone, there is still remnants of it. You can imagine just injecting a little bit of it into your veins can cause a lot of damage… it eats you from the inside out".

That's from Dr. Frank LoVecchio in Phoenix, Arizona, who saw two cases within a week.  It's not hugely scientific, but it's not wrong.  Krokodil is never pure and highly toxic chemicals are thus injected into the veins.  If you want specifics, then gasoline, hydrochloric acid, phosphorous scraped off matchboxes, paint thinner, iodine, and cleaning oils.  Injecting any one of those should be enough to kill a repeated user.  Those substances rupture blood vessels, and the subsequent leakage creates gangrenous wounds like you see in the pictures.


D/L configuration for amino acids Why would this be "L-cysteine"? This is taken from the answer key for my biochem final.

From what I understand if the -NH3(+) is on the left then the alpha-amino acid is in the L-configuration.

Am I wrong, or is my prof wrong?

We can look at the list of amino acids on wikipedia for a start. And we can look at this L-alanine:

What makes your image confusing is that it's a Fischer Projection, and I hate those because you have to remember what way the stereochemistry goes. In Fischer Projections, vertical lines face away from you, while horizontal lines face towards you. So if we convert the L-alanine I provided to a Fischer Projection, first we have to rotate the alpha carbon to put the methyl side chain in line with the rest of the carbon backbone. Now we look at the alpha carbon with the NH2 and H looking at us to create the Fischer projection. Here, the amine is on the left, not the right. You drew the amine on the right, which would give you the opposite orientation. If your professor had the amine on the right, I think he was wrong.

Additionally, the D vs L nomenclature is confusing. I prefer the S vs R nomenclature because that's what I was taught for molecules in general. Most amino acids fall into the S configuration, but cysteine is an R, because the sulfur atom has higher priority. However, cysteine is still an L, and the amine would still appear on the left in the Fischer Projection. This is why biologists stick to D and L for amino acids.


Why do hot water baths affect only males' fertility? Why not females'? Here is the link where urologists are warning men not to take hot water baths.

Why does it affect only males' fertility? Why not females also?

Well, the answer by @An J has already explained the prima facie of your question which is: sperms need lower temperature for development. But I will be explaining in my answer: Why do the sperms actually need a lower temperature for their development?

This is a debatable subject, but there have been several models or hypothesis about this. I found this literature on it, and it summarises the thing excellently. Hope it helps:

  Throughout the Cenozoic, the fitness benefits of the scrotum in placental mammals presumably outweighed the fitness costs through damage, yet a definitive hypothesis for its evolution remains elusive. Here, I present an hypothesis (Endothermic Pulses Hypothesis) which argues that the evolution of the scrotum was driven by Cenozoic pulses in endothermy, that is, increases in normothermic body temperature...

  The model argues that stabilizing selection maintained an optimum temperature for spermatogenesis and sperm storage throughout the Cenozoic at the lower plesiomorphic levels of body temperature that prevailed in ancestral mammals for at least 163 million years. Evolutionary stasis may have been driven by reduced rates of germ‐cell mutations at lower body temperatures...

  The fitness advantages of an optimum temperature of spermatogenesis outweighed the potential costs of testes externalization and paved the way for the evolution of the scrotum. The scrotum evolved within several hundred thousand years of the K‐Pg extinction, probably associated initially with the evolution of cursoriality, and arguably facilitated mid‐ and late Cenozoic metabolic adaptations to factors such as climate, flight in bats and sociality in primates.

About the function of the scrotum from the article

  The scrotum is a sac‐like thermoregulatory structure that houses the testes at a temperature lower than the core body temperature (Tb; Moore, 1926; Wislocki, 1933; Ruibal, 1957; Setchell, 1998). The cremasteric muscles in the scrotum contract and relax to draw the testes closer to or allow them to dangle further away from the body in order to maintain the testes at an ‘optimal’ temperature for spermatogenesis (sensu Moore, 1926; Tsperm) and sperm storage of 34–35 °C (Setchell, 1998; Gallup et al., 2009; Mawyer et al., 2012). In humans, the scrotal temperature is maintained about 2.7 °C lower than the Tb (Momen et al., 2010). Notwithstanding the relative fitness benefits of a cooled epididymis vs. the cooled testis, four nonmutually exclusive hypotheses currently dominate explanations for the evolution of the scrotum: the Cool Spermatogenesis Hypothesis (Moore, 1926), the Galloping Hypothesis (Frey, 1991), the Mutation Hypothesis (Short, 1997) and the Activation Hypothesis (Gallup et al., 2009).

Cool Spermatogenesis Hypothesis

  ...argued that Tsperm and the maintenance of sperm viability during storage in the epididymis is about 34–35 °C (Moore, 1926; Appell et al., 1977). Scrotal temperatures that approach those of the core Tbcompromise fertility (Moore, 1926; Bedford, 1978b, 2004; Setchell, 1998), particularly if evaporative cooling of the scrotum is impaired (Momen et al., 2010).

The Galloping Hypothesis

  ... (Frey, 1991)proposes a trade‐off between testes vulnerability (fitness cost) and the avoidance of strong intra‐abdominal pressure fluctuations during galloping which impair spermatogenesis in abdominal testes (fitness benefit).

The Mutation Hypothesis

  ... maintains that the testis is a ‘hot spot’ for germ‐cell mutations and that the lower temperatures of the scrotum reduce the rates of mutation on the Y chromosome through mutagenic metabolites (Short, 1997).

The Activation Hypothesis

  ... storage of sperm at a lowered temperature ensures that they undergo ‘thermal shock’ during ejaculation into the higher temperatures of the female, which increases their motility and hence the probability of a successful insemination (Gallup et al., 2009).


How to prepare sample for SDS PAGE? I usually take my protein sample 0.8ml and sample buffer(2X) 0.2ml for my sample preparation in SDS PAGE. Am I using correct proportion? my protein sample concentration is 4.1mg/ml. What is the standard protocol?

Sample preparation for protein gels is not a complex task. Simply mix the appropriate amount of sample buffer with your sample and load it. For a 2x sample buffer use equal amounts of sample and buffer, for 5x sample buffer use 4 parts of sample and 1 part of buffer (for examle 40µl + 10µl). Heat the mixed samples for 5 minutes at 95°C, cool them immediately on ice and load an appropriate amount of it on the gel. How much is possible really depends on the type of gel you use - 20-30µl should usually be possible.

Do not load too much protein, otherwise you will not be able to seperate them appropriately. I usually use between 20-30µg of total protein per well or as little as 50ng for purified proteins (this depends on the antibodies as well).

Have a look on this webpage for some further information.

For sample buffers I usually use the following recipes. I prefer the 5x, because I can load more protein, if the preparation is not very good. I also prefer the use of DTT to Mercaptoethanol, as it is much less smelly. If you have no DTT (or prefer mercaptoethanol) it can be replaced by an equal amount (200mM in the 2x, 500mM in the 5x buffer). If you use DTT, you need to make aliquots of the buffer and store it at -20°C, a working aliquot can be kept at 4°C for two weeks or so.

2x sample buffer:

4% SDS
20% glycerol
100 mM Tris-Cl, pH 6.8
2 mM EDTA (ethylene diamine tetraacetic acid)
200 mM DTT (dithiothreitol)
0.1 % (w/v) bromphenol blue dye

5x sample buffer

10% SDS
50% glycerol
250 mM Tris-Cl, pH 6.8
5 mM EDTA (ethylene diamine tetraacetic acid)
200 mM DTT (dithiothreitol)
0.25 % (w/v) bromphenol blue dye


Is hydroxyproline an amino acid? (Classification question) So I know that hydroxyproline is created from proline via hydroxylation as a post-translational modification. I also know that proline is considered an amino acid. However, once you hydroxylize it, you have made a covalent modification to the original amino acid. Can hydroxyproline be correctly considered an amino acid? Or is it simply an amino acid derivative and NOT an amino acid?

Or, a more general question - how much can you change an amino acid and still call it an amino acid?

The other commenter answered correctly that proline is an imminoacid, not an amminoacid. But in biochemistry it is referred to as amminoacid since it basically works like every other amminoacid in any polypeptyde.

  how much can you change an amino acid and still call it an amino acid?

Have a look at:

Selenocysteine
Ornitine

As you can see there are some weird modifications of amminoacids in biology. Just like proline/hydroxyproline any amminoacid can be very well modified and be used in proteinogenesis or non-proteinogenesis. Every modification of an amminoacid is allowed, and it will still be considered an amminoacid, even if it doesn't make up a protein. The only parts which can't be changed are the COO- and NH3+ groups, obviosuly, since they give the name of the molecule: "ammino" means that it has a NH group and "acid" means it has a COO- group.


Effects of tobacco smoke on plant health We know that tobacco smoking is associated with a wide range of negative health effects in humans, which holds for active smoking, second hand smoking and probably even third hand smoking.

What are the effects of second hand smoke exposure on plants?

For example the german wikipedia page on nitrogen dioxide claims that exposure to nitrogen dioxide leads to reduced yield in apple and pear trees, white birch, barley and salad. It is also stated that first physical signs of alterations can be detected with one time exposure at levels as low as 3 ppb for less than one hour. However I cannot access the source because it is a book.

Bonus: How does cannabis smoke differ from tobacco smoke with respect to plant health?

Results from the peppermint plants study show that all the peppermint plants contain minor amounts of nicotine before treatment, but the experiments revealed that the plants also incorporate nicotine considerably from the soil as well as from tobacco smoke. These findings demonstrate for the first time that the reported occurrence of nicotine indeed may originate from tobacco. The incorporated nicotine was subsequently metabolized by the plants.

Effects:
Apart from the nutritional aspects, the results on nicotine uptake may also affect basic plant biology, because they demonstrate that alkaloids can be transferred from one plant, after its death, to another plant species.

  The plants, said Dirk Selmar, the study’s lead author, appeared, at
  first, to be unchanged. “As far as we have seen, there have been no
  negative effects on the growth,” he wrote in an email. Yet, tests for
  nicotine, conducted at various stages in the plants’ life, found that
  they had “tremendously elevated nicotine levels,” Selmar said.

References:

https://link.springer.com/content/pdf/10.1007%2Fs13593-015-0298-x.pdf
http://www.takepart.com/article/2015/04/15/nicotine-plants-second-hand-smoke
https://www.ehow.com/info_7987584_effect-cigarette-smoke-house-plants.html

some anecdotal answers (to be taken with a grain of salt) on your 2nd bonus question: https://www.rollitup.org/t/is-smoking-weed-around-a-growing-plant-bad.182179/


How do communities relate to food webs? I am a biology student who has just completed drawing a food web for class. As I was making it, I learned that a food web is the sum of all feeding interactions. My teacher associated food webs with communities, but I do not understand what the communities of a food web are.

How are communities related to food webs?

The Details
Ecological communities are groups of multiple (2+) species of either plants, animals and/or other organisms that interact in a unique habitat. More accurately (from Wikipedia and corroborated by Begon et al. (2006)), we can define an ecological community as an:

assemblage or association of populations of two or more different species occupying the same geographical area and in a particular time.

These organisms could be interacting in a number of ways:

As you can see, one or both species can be effected either positively, negatively or neutrally (not at all) in these various types of interspecific interactions.
I should note that a community doesn't have to contain all organisms within a certain habitat.

Sometimes we might limit our discussion of a community to a single guild or single trophic level. Other times we might use the terminology simply to describe two interacting species (either within or between guilds/trophic levels).

Really, "communities" are more conceptual "units" used to describe two or more interacting species. More accurately, it's an interaction between populations of 2+ species. In this way, community ecology is an extension of population ecology.

Food webs (i.e., a system of interlocking and interdependent food chains) are essentially summaries of the feeding relationships within an ecological community (Molles, 2010). In other words, they are focused strictly on trophic interactions. These trophic interactions are primarily concentrated within the (+,-) interactions between species. This means that the interactions that dictate a food web are going to consist mainly of consumption (predation/herbivory).

From University of Michigan (my emphasis):

Food webs are graphical depictions of the interconnections among species based on energy flow. Energy enters this biological web of life at the bottom of the [web], through the photosynthetic fixation of carbon by green plants.
Energy moves from lower to higher trophic (feeding) levels by consumption.

Example
An example of a community that does not qualify as a food web:

A community of plants includes just the plants that are competing in the same space and as a result make up (i.e., are classified as) some sort of vegetation type. These species are competing at the same trophic level and do not consume one another. This is classic ecological competition.

If we examine the trophic interaction between each of these plants with each of their sources of energy, each of their consumers, each of their consumers' consumers, etc. then we are talking about a food web.

Final Thoughts
So the term "community" is used generally to describe interacting species of organisms in a given habitat, while "food webs" describe a more specific aspect of a community -- the trophic interactions of the members of that community.

Of course, it could be the case that all species in a given community are represented in a food web, but this is not necessarily the case.

It could also be the case that not all species represented in a food web be part of the same community...

One could also consider food webs to be broader than a community because they can describe the trophic interactions of species/populations across communities. From this perspective, food webs "lie at the interface of community and ecosystem ecology" (Begon et al. 2006).

Citations:

Begon, M., C.R. Townsend & J.L. Harper. 2006. Ecology: From individuals to ecosystems. Fourth edition. Blackwell Publishing Ltd. Malden, MA. pp 469 - 601.

Molles, M.C. 2010. Ecology: Concepts and Applications. Fifth edition.  McGraw-Hill. New York, NY. p. 544.


What kind of spider is in this pic I took? What kind of spider is this?

It has a weird black and white backpack looking thing. Found a couple of them in Auburn, Alabama. Any help is greatly appreciated.

It's a Spiny Orb Weaver, aka Spiny-backed Orb Weaver. Orb Weavers are a very large genus of spiders; this one is a Gasteracantha cancriformis. The spikes can be black or red; there are many colors as well.


Why did we lose our fourth type of cone cell (in the eye)? Most species of birds, reptiles and fish have four types of cone cells in their retina, thus they have four independent channels for conveying color information. They are:

short-wave (S) cones: sensitive to colors with short wavelengths.
middle-wave (M) cones: sensitive to colors with medium wavelengths.
long-wave (L) cones: sensitive to colors with long wavelengths.
ultraviolet (UV) cones.

This condition is called tetrachromacy. Wikipedia mentions:

It was the normal condition of most mammals in the past; a genetic change made the majority of species of this class eventually lose two of their four cones.

We have only three. My question is, why did we lose our UV cones? I searched a little about this and here's what I found:
Scientists Have Found a Woman Whose Eyes Have a Whole New Type of Colour Receptor

According to estimates, that means she can see an incredible 99 million more colours than the rest of us, and the scientists think she's just one of a number of people with super-vision, which they call "tetrachromats", living amongst us.
They took 25 women who had a fourth type of cone cell, and put them in a dark room. Looking into a light device, three coloured circles of light flashed before these women's eyes.
To a trichromat, they all looked the same, but Jordan hypothesised that a true tetrachromat would be able to tell them apart thanks to the extra subtlety afforded to her by her fourth cone.

Which means some of us still have it. What I don't understand, though, is why this isn't a more common trait? Evolutionarily, is being able to perceive vision using three cones "enough" for humans?

Let's be clear most mammals, including basal primates, had only 2 cone cell types. Primates evolved a new cone cell becasue frugivores have a distinct advantage being able to distinguish reds and yellows. The mammal lineage may have never had a fourth cone cell, if they did it was lost early.

Eutherian mammals lost the third cones cells likely because we spend several hundred million years as small nocturnal animals during the dominance of dinosaurs. in small nocturnal animals, there is a strong competition between having more rods for better low light vision vs having cones for color vision, so a loss of some cone cells may have been neutral or even beneficial. There was some work on bats that seemed to contradict this, but they failed to control for frugivory in the bat lineages they studied; So there is an issue with their results. There is a lot of variation in color vision across vertebrates so it is no surprise a consistent selective pressure could have a lasting effect.

source


Mesophytic Climax community in succession? My textbook says that in all cases of ecological succession (xerarch, hydrarch, etc.), the ultimate climax community, assuming constancy of environment, is a mesic community. Xeric or hydric pioneers are ultimately succeeded by mesic climax communities. Why is this so? In an environment under consideration, if for example water stress prevails (characteristic of xeric environments) shouldn't the final community be xeric and hence better adapted to the environment? Is my book wrong, or is there something I am missing in the understanding of the development of climax communities?

Moreover, I did find it written somewhere that mesic communities do depend on the climate of the place. But then doesn't the fact it is mesic contradict a few climatic conditions wherein ecological succession might occur?

Reference:-
Ecological Succession
Climax Community

The concept of a "climax community" has not been accepted as reality for more than 40-50 years. Frederic Clements was an early botanist examining succession in the first 20 years of the 20th century. It was Clements who developed the concept of the climax: he posited that the habitat and the populations acted upon one another in a reciprocal way until finally a stable state (the climax) was reached.

However, the work of Gleason (e.g, 1926), Tansley, Watt (1957), Whittaker (e.g., 1972), Davis (1969),  etc. have changed the field's understanding of succession and its acceptance of the existence of a stable "climax". Whittaker was first to propose the use of the term "stable state," as it carried less assumptions about the community' inability to be replaced.

It's now clear from work of countless studies and authors (along with my own research), that disturbances play a significant role in plant dynamics and that previously accepted 'stable states' are perhaps only remnants of historical characteristics of the system (see below). As a result, some accepted stable-state communities no longer appear to be the norm in some areas (likely due to both present and past disturbances and fluxes in the system). See Abram's papers for a discussion on hypotheses of this phenomenon in the Eastern deciduous forest of the U.S.

Regardless, even in a system without disturbance (which none exist), the stable-state community would be fully dependent on climate, substrate, community assembly limitations and geographic/environmental/biological filters.


Finding Regulatory Elements: How Have People Been Doing This? First up, I am NOT asking about how to search for and match regulatory elements using a database. I'm asking about how people found what to search for and match in a genome, how they built those databases. My question is,

How did people identify regulatory proteins/nucleotide elements in the first place?

Did they first find the proteins we now call transcription factors and sigma factors, or did they tamper with the genome to find the regulatory parts and then traced them to the proteins?

Is there a book on the history of research gene regulation to recommend?

Also, I tried Googling. Every site recommended one database or the other. I would be grateful too if you could tell me what should I have searched for?

I am more interested in Prokaryotes, but answers on Eukaryotes would also be welcome.

Context: I'm a freshman doing research (yep. the experience is kinda crazy for me) and I'm interested in finding regulatory elements in Mycobacterium smegmatis and its phages.

As it can be seen from (more or less recent) discovery, most of the regulators were discovered through specifically designed experiment to exhibit one particular factor. Several examples include:

The discovery of Sp1, the first eukaryote transcription factor to be discovered (as described in the video linked in the comments)
The discovery of the Lac operon in E. coli.

None of these were intended to be screens for regulatory sequences in general. If you are looking for regulatory sequences of a specific gene, the technique of reporter gene, combined for instance with a random mutagenesis screening can provide you with a mapping of regulatory elements.

The following article might be of interest to perform a screen based on UV-mutagenesis: UV mutagenesis in Escherichia coli K-12: Cell survival and mutation frequency of the chromosomal genes lacZ, rpoB, ompF, and ampA.

If your question is more general: "all the regulatory sequences associated with one gene", then this question is generally unanswered, and can probably be better tackled first using bioinformatics analysis (such as promoter prediction, etc).


What is the maximum electric potential that can occur in the human body? Neurons can generate a voltage, if there is an action potential. Also, membranes where an ion concentration gradient is present, generate some membrane potential.
What I wish to know is, which cellular element in the human body creates the greatest potential differences? And how high can they be so high? Are there also biochemical reactions, where significantly high electric/electrostatic voltages are important? How strong are these?

To the best of my knowledge, the potential difference across the hair cells in the inner ear (cochlea) (Fig. 1) is the highest in the (human) body. It is about 120 mV, mainly due to the exceptionally high positive potential of the scala media as provided by the stria vascularis, referred to as the endocochlear potential. This potential is mainly built up by the high amount of K+ pumped into the scala media by ion pumps located in the marginal cells and basal cells (Salt et al, 1987) in the stria vascularis. Adding the potential difference of -40 mV of the hair cell it yields a total difference of 120 mV (Fig. 2).

References
- Morrill & He, J Otology (2017); 12: 151-64
- Salt et al., Laryngoscope (1987); 97(8 Pt 1): 984-91

Fig. 1. The cochlea. source: Morrill & He (2017)

Fig. 2. The potential difference across the hair cells is 120 mV, due to the endocochlear potential of +80 mV in the scala media. source: University of Minnesota Dulluth


What type of spider is this? What kind of spjder is this? It was found in nova Scotia

The rounded carapace of the cephalothorax, and the relatively slim, banded legs indicate that this is one of the terrestrial Dolomedes fishing spiders.  The 'w' stripes on the abdominal pattern have white markings on the margins, but are not 'underlined' completely across in white, which rules out Dolomedes scriptus, in my experience.  Also (although I think this can be somewhat variable in these particular Dolomedes), this spider does not have the familiar white rim to the cephalothorax and abdomen.  Accordingly, I'll go with a rather light-colored individual of the fairly variable Dolomedes tenebrosus.

The links I enclose allow you to explore images of these spiders for your own interest:

https://bugguide.net/node/view/38828

https://bugguide.net/node/view/2011

Oh, yes - almost forgot.  Although these spiders can give a noticeable bite, the venom is less trouble than the standard Polistes paper wasp sting.  I have been bitten only once despite handling numerous females, and had almost no effects beyond a bit of pain and a small red bump.  Like most spiders, these can control the amount of venom they inject, so mine might have been a 'dry bite', but I've heard nothing about bad effects from bites by this very common spider.  I think it's safe to assume that this is a harmless spider - to us.  They love beetles and other large arthropods.


Competition for mates in sea horses This source here

  ...research has shown that it is STILL the males that compete for
  females.

says that male sea horses compete for mates but this source here

  Females exhibit a competitive behavior that's normally a male-type
  attribute, and males end up being choosy, which is normally a more
  female-type attribute.

.says that female sea horses compete for mates.

Can anyone provide me a trustable source regarding this ? I would also like to know if there are any recent papers exploring why males get pregnant in sea horses.

Second paper is an article in science Daily and have a pretty decent source from Texas A&M University. It's much better than the first as it is un-sourced post on yahoo answers.

Source:
"Male Seahorses Are Nature's Mr. Mom, Researchers Say." ScienceDaily. ScienceDaily, 2 May 2008.

Why male seahorses gets pregnant?

Genetic answer:

May be because only $MHII\beta$ gene present in the male pouch which carries the babies.

Source and more on this topic:

The impact of sex-role reversal on the diversity of the major histocompatibility complex: Insights from the seahorse (Hippocampus abdominalis)


Why to use transgenic mice in ALS models? In ALS mice model with mutant SOD1 - there are use of transgenic mice, with insert of human mutant SOD1.

Why is that? Why not to mutate directly mice SOD1 ?

In transgenic mice, after few generations these human gene thrown out and not present any more.. Why thrown out? Is the second question.

Looking for an answer for a while. Thanks a lot.

The use of a mouse with the replacement of one of its genes with a human version is to better mimic the human disease phenotype, or to prove something about the biology of the human phenotype with research that can't be conducted in humans.

Genes and their corresponding proteins or RNA usually differ somewhat between mouse and humans. If you wanted to study whether a certain SNP in a gene (found in humans) was the reason for part of your phenotype, you may want to use transgenic mice to test hypotheses with different exacerbations (treatments).  One way to do this is to create a mouse with the human gene replacing the mouse gene, and another mouse with the human gene containing the trait-linked SNP.

If you tried to do this with the mouse gene, you couldn't be sure that the same SNP would have the same functional consequences.  If you didn't remove the endogenous gene from the mouse before replacing it with the human version, you would never be sure if observed experimental phenotypes weren't confounded by both copies of the gene and their corresponding gene products being active in the same animal.

In your example, with SOD1 and ALS, creating a humanized mouse with human SOD1 allows researchers to more fully study the same protein product made in humans, while giving the mouse treatments that would be unethical in humans.

Your understanding in your last part is incorrect. Mice don't lose genes after a few generations.


How do cells figure out the big-picture shape? I'm wondering what makes cells to divide (and stop) in such a way that they make our hands the shape that our hands are...

Hands are complicated and the genetic machinery behind their shape doubly so.

It's easier to figure out worm segments first, and then work up from there. An egg has head/tail information encoded in it even before fertilization: see here

You can imagine the first or second cell division would give a 'head' cell with higher concentration of head polarity transcription factors. These transcription factors switch on other regulatory genes, and the complexity works upwards from there. For more information about how worms and other segmented animals work out what goes where see Hox genes. The sad truth is that most of how this is done is unknown or not well understood.


Does breathing air containing 3% carbon dioxide gives you a headache? As far as I know, breathing air containing relatively high levels of CO2 may get you a headache.

I also know that CO2 level in the fruit bodies of peppers can reach levels as high as 3% at certain stages in development (Blasiak, 2006). So clearly it is possible in a natural setting to achieve these high level of CO2, at least in a micro-environment like around the locules of pepper seeds developing in its fruit.

So I was wondering, if we would have to breath air containing 3% CO2, would get a headache if we breath it in?

http://en.wikipedia.org/wiki/Carbon_dioxide#Toxicity

"In concentrations up to 1% (10,000 ppm), it will make some people feel drowsy.[83] Concentrations of 7% to 10% may cause suffocation, even in the presence of sufficient oxygen, manifesting as dizziness, headache, visual and hearing dysfunction, and unconsciousness within a few minutes to an hour.
...
Occupational CO2 exposure limits have been set in the United States at 0.5% (5000 ppm) for an 8-hour period.[90] At this level of CO2, International Space Station crew experienced headaches, lethargy, mental slowness, emotional irritation, and sleep disruption."
So according to this, yes you could breathe it, and yes, you would get a headache."


Measuring transgenic gene expression with a microplate reader I have been working on genetically engineering an E. coli strain to autotrophically oxidize arsenite into arsenate for bioremediation of arsenic contamination in groundwater. For my research, I have been finding ways to quantitatively measure how much arsenite the bacteria oxidizes over time.
After researching ways to quantitatively measure arsenite being oxidized, I have concluded to use the method of Johnson and Pilson (https://www.sciencedirect.com/science/article/pii/S0003267072800059?via%3Dihub).

The arsenate that is formed from arsenite oxidation forms a molybdenum-blue complex with phosphate in the water. As the concentration of arsenate increases, the absorbance value of the water should increase proportionally.

Here was my plan: First, after growing my transgenic bacteria on an amp-plate, I would pipette out various concentrations of cells and arsenite in wells of a 96-well spot plate. I currently plan to use the Fisher Scientific Multiskan FC microplate photometer. I planned on incubating the cells while shaking at 37 C. The main problem I have come across is that my experiment would not be controlled. Over time, the growth of cells will change the absorbance value, not just the molybdenum-blue complex. I need to isolate the variable of just arsenite oxidation.

I have thought of a few possible solutions, but I feel as if I may be missing something crucial. When learning about microplate readers, I know that researchers can use them to measure gene expression. How do these researchers eliminate the variable of cell growth effects on absorbance values?

For one, I have thought of finding a way to filter the cells to one side of the well where they will not affect the absorbance values. Would it be possible for me to cut out a dialysis bag to where it is dipping into the well? In that case, the cells could be suspended in the well, oxidizing arsenite (if my hypothesis is correct).

Anyway, I really want to find a simple method for quantitatively measuring arsenite concentrations over time using a microplate reader without having cell growth affecting absorbance values.

Spectophotometry

Does the photometer allow using different wavelengths of light? Perhaps using a spectrophotometer might give you a control and your desired value, i.e. blue light may be absorbed by your sample, but red might not? The absorbance spectrum of the molybdenum-blue complex is very specific and you could use this to your advantage using spectral photometry.

Photometry + correcting for absorbance due to cell growth

Another approach is to quantify over time how your bacteria affect absorbance as a function of time and then subtract this from your experimental values.  For example, in a wellplate, place the following adjacently: use a (i) well without cells, and only arsenite in solution, (ii) cells without arsenite, and (iii) cells with arsenite. This should allow you to quantify quite accurately how much the arsenite, the cells, and how much both affect absorbance.

Of course as you say there may be an interaction between the cells and the arsenite slowing or speeding up cell growth, so that would be a pickle to disentangle. You could try, perhaps in the wellplates (this would be best!), to find out what effect arsenite has on growth and correct your final data this way.

Periodically sampling the solution; removing bacteria from the measurement

Another idea would be to culture your cells in arsenite, and take samples to obtain time-points. For each sample, you filter using small syringe filters (these are cheap and are typically used for sterilizing solutions, i.e. getting rid of bacteria but keeping the solution, given their pore size of ~.1 microns) and then perform photometry for the molybdenum-blue complex. This is typical practice in microbiology.

PCR? An idea.

Last but not least, it's good to remember this is an indirect readout of transgenic gene expression. Similarly, you could use quantitative PCR to quantify the expression of any transgenes - here, you use housekeeping genes as controls for cell number, and the mRNA expression of your transgene as the readout. You would be reading out the expression of mRNA, but I personally don't think it would be more 'indirect' than measuring arsenate concentrations in solution, especially when there are confounding factors and awkwardness in getting a clean measurement. The PCR approach would be quite accurate and likely more reliable.

These are just some initial thoughts - perhaps you could add a comment or we could chat about this if you think it could spark up some concrete ideas!


Is there a GPS super tiny for passerine birds? I wonder if there is a really tiny GPS device that can be mounted on passerine birds (or circa 10 grams birds) without affecting their flight. This web site shows information for bat’s GPS. But it also only last for 24 hours. I wonder if there is some lightweight and long battery life about 2–5 grams. I found this also, but haven’t found if it contains a long battery life.

Is there a study on GPS tracking small birds?

The technology is not there (yet) for deployments on 10 gram birds. The limits for GPS technology are around the 50 g range, for birds. Also bear in mind that the smallest loggers are generally not capable of transmitting, so you would need to recapture the animals to retrieve your data.

As your question implies, there is a strong trade-off between device weight and battery life. There are GPS devices weighing as little as 1 g, but their lifespan is very limited (10 fixes for the 1 g device; 50 for a 1.1 g device).

As a side note: your question implies that small passerines can carry 20 - 50 % of their body mass in tracker without their flight being affected. The ethics boards I am familiar with generally limit trackers to ~ 5 % of the mass of the animal.


Do primates other than humans have a consistent sleep schedule? I'm doing some sleep research and would like to compare a human sleep pattern as recorded by a wrist-based actigraph with a "natural" sleep pattern, such as from apes. In an experiment like that, a human wears an activity monitor on a non-dominant arm over multiple days. The monitor analyzes activity pattern and can detect when the user is asleep versus active.

Can someone suggest a research article or a website that did a sleep study of primates (monkeys/apes) either in captivity or natural habitat over multiple days?

I'm particularly interested in how consistent their bedtimes are - do primates go to sleep in the evening whenever they feel like, or do they stick to a more consistent sleep schedule?

This is only a partial answer, but a reasonable starting point.

In a blog-article "The Evolution of Primate Sleep", the author identified 3 main patterns - the third pattern seems most relevant to your question.

What he found was that there are 2 divisions of sleep patterns - several primates, such as some species of lemurs are nocturnally active, whereas apes, gorillas etc tend not to be active at night.  Seemingly adapting to the diurnal cycle.  In the article "Mammalian Sleep Dynamics: How Diverse Features Arise from a Common Physiological Framework " (Phillips et al.), primates uniquely undergo monophasic sleep.


Well to well variation in thermal cycler fluorescence? We have an old BioRad ICycler Thermal Cycler with MyIQ single color fluorescent detector. While it's meant for RT-PCR, we've been using it for melt curves and binding assays for different types of RNA using thiazole orange as the intercalating fluorophore. However, when we tried to get serious about this assay and do things in triplicate we noticed that the well to well variation was terrible, making statistical significance difficult to get.

After reading through the manual I tried to get "persistent well factors" for the instrument to correct for this variation. However, the instrument's protocol for this requires heating to 95⁰C, so intercalating fluorophores won't work, the RNA melts and fluorescence is lost, so I tried with fluorescein. This didn't solve the variation.

So I tried to make my own well factors by making 10mL of Poly(rA) Poly(rU) RNA solution with thiazole orange and filling 96 PCR tubes with 100µL each and measuring fluorescence. Then I calculate the average fluorescence and divided the average by the value for each well to determine a factor, F, for each well. Then I tried to normalize subsequent experiments by multiplying each well's fluorescence by its F to get a corrected value. However, while this reduces the variation a little, it's still pretty bad.

Do you have any suggestions to reduce the well to well variation in these experiments or otherwise correct the data?

I have no prior experience with RT-PCR instruments, everything I know about it comes from playing around with the instrument. I don't know if I'm missing something really basic.

Step by step protocol

Prepared 1xSSC buffer, 150mM NaCl, 15mM Sodium Citrate, pH 7.5
Weighed 5mg Thiazole Orange, dissolved in 1mL Methanol
Diluted Thiazole Orange 1000 fold in 1xSSC
Took 71.4µL (100µg) Poly(rU) Poly(rA) solution, 1.4µg/uL
Diluted RNA with 8.93mL 1xSSC
Added 100µL diluted Thiazole Orange to diluted RNA, final volume 10mL
Set up 96 PCR tubes, used 8 channel pipette and trough to transfer
100µL RNA solution to each
Placed PCR tubes in all 96 positions of thermal cycler
Ran melt curve protocol, start at 25⁰C, increase 1⁰C every cycle,
60 cycles, so final temp is 85⁰C. Each cycle is 10 seconds.
Measure fluorescence every cycle.
Repeated melt curve 3 times, total of 4 curves.
Put data from each curve into spreadsheet. 96 data points at each temperature.
Averaged fluorescence across the whole plate at each temperature.
Used this average, standard deviation, maximum, and minimum
values to make the plots below.
Calculated correction factors for each well at each temperature by
dividing the whole plate average fluorescence by each well's
fluorescence for melt curves 2, 3, and 4. Averaged correction factors from each curve.
Calculated corrected fluorescence for curves 1, 2, 3, and 4 by
multiplying the averaged correction factor for each well by the
observed fluorescence for that well.
Replotted the corrected values to show reduced variation.

Data is shown below. I repeated the melt curve 4 times because the first melt usually has a lower intensity than subsequent melts. Y axis is fluorescence, X axis is temperature in celsius, and I plotted the average fluorescence at each temperature with the standard deviation along with the minimum and maximum to show how far outside the standard deviation some wells are falling. I calculated the correction factors for melt curves 2, 3, and 4 and averaged them. When I used these averaged factors on melt curves 2, 3, and 4 it did a good job at eliminating variation. When I applied the correction factors to melt curve 1, it reduced the variation, but not by much.

There can be several reasons for variability and since you said that the machine has not been serviced for a long time, I guess that should be one main source of errors. Multichannel pipettes can also sometimes cause problems (based on personal experience) and it is mostly because the tips don't fit properly in all channels.

Try varying some parameter (for e.g. concentration of RNA) and see the effect on melting temperature; if the inter-replicate variability is not high enough to make the inter-sample difference insignificant then you can continue with your experiment. Take more number of replicates to minimize variance.

If the variability is very high then I guess you would need to get your machine repaired or use more sensitive equipments designed specifically for these kind of studies.


If our skin is burned by the sun what causes the red color of the skin? Mostly it is not a good sign we are burned because too much UV light has damaged our skin and increases skincancers.

But the red color we get after a few ours, what is the exact cause of it and why is it red? Is that our blood we see or other changes in skincells or our immunesystem reacting?

And why does it takes a while before it gets red?

Sunburn causes damages in the skin which further triggers an immune reaction.
This immune reaction causes a dilation of the capillaries in the skin to allow a higher transport rate towards the inflammation site. This dilation and the higher blood flow in the area causes the "redness" of inflamed tissues. See the image for illustration (from here):

The delay in the appearance (for more severe cases also the swelling) is caused by the time it takes for the body to react and to develop an immune response. For further information you can look here and here.


meaning of "usually greater than 200 base pairs" From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

  Homologous recombination. All cellular organisms have molecular functions dedicated to recognizing and recombining DNA molecules that have extensive sequence similarity at the region of cross-over, usually greater than 200 base pairs. The principle molecule involved in homologous recombination belongs to the family of RecA/Rad51 DNA binding enzymes that catalyse post-replicative strand exchange during meiotic/mitotic recombination or repair of DNA double-strand breaks. These enzymes show some sequence preferences (Raja et al., 2006) and require minimally efficient processing segments of 20–30 base pairs to initiate strand exchange (Majewski and Cohan, 1999).

I'm not sure of the meaning of "greater than 200 base pairs". Does that relate to "sequence similarity"? Is similarity somehow measured in base pairs?

Or does that relate to "the region of cross-over"? Is the meaning "the region of cross-over is usually greater than 200 base pairs"?

No, similarity is not measured in base pairs. They are talking of regions of cross-over being marked by at least 200bp of highly similar sequence between the two strands involved in exchange.


Adult Bugs in Low Humidity House Heated With Wood? I have a home heated with wood. The humidity is currently around 30% but I'm guessing these bugs have reproduced when the humidity was higher. They really have a hard time when I see them in the basement.

I do have some wood that was a little punky. They seem to come out as soon as I start a fire in the stove, probably due to the heat?

Approx 3cm long

Located in the eastern townships of Quebec, Canada. Any suggestion on what this is and how to treat them?

The pictures are not entirely clear, but I’m relatively certain that it is a wood wasp of the genus Xiphydria (family Xiphydriidae). Traits that point to this is e.g. 2 pair of wings (i.e. a wasp and not a fly), narrow slender antenna, elongated body, the shape of the head sitting on a relatively long “neck”, often with light/white markings on the top and or the back of the head (which can be seen on picture 2) and often white markings along the side of the abdomen (which your insect has) The second picture also shows the relatively robust ovipositor (used to inject eggs into wood).

They also lay eggs into dead wood (usually deciduous wood) and are not uncommon to find in houses, hatched from fire wood.

The species is very hard to determine though, but X. mellipes could be one bet. This species also seem to be found in Canada, see zoology.ubc.ca/entomology. It is also similar to Xiphydria camelus which is common here in Sweden, but I’m sure if it is also found in Canada.

(Xiphydria mellipes from wikimedia commons

Pictures of some species can be seen at bugguide.net).

These insects are not dangerous to find inside, and they only attack dead wood in standing or fallen trees, not construction wood. They are not uncommon to find indoors (along with longhorn beetles and other wood insects) if you bring in mixed fire wood, especially if the wood wasn’t processed and dried quickly after felling. An interesting feature of these insects is that many (all?) inoculate the wood with particular fungi spores, and the fungi later function as the food for the larvae.


We know archea and eukarya are more closely related but endosymbiotic theory says eukarya have evolved from prokaryotes, justify the statements? I am confused if eukaryotes have evolved from prokaryotes then how are they more closely related to archea?

Actually endosymbiotic theory (we should write "Endosymbiotic theory of origin of eukaryotic organelles") suggests a theory about only the eukaryotic organelles (mainly Plastid-family and Mitochondrion).

I'll divide my answer into 3 parts:

# Theory of archaeal origin of the eukaryotic host.
* 1. How Archaea (Archaebacteria) and Eukaryotes shared a closest common ancestor
# Endosymbiotic theory of origin of Eukaryotic cell organelle.
* 2. How mitochondria originated?
* 3. How plastid was originated?

Please keep in mind, in origin and evolution of eukaryotes, origin of the host cell (and the nuclear genome) is a different event; and origin of eukaryotic organelles mitochondria and plastid is another different event.

Theory of archaeal origin of eukaryotic host

1. How Archaebacteria (archaea) and precursor of eukaryotes evolved from their nearest common ancestor.

It has been established (First by Carl Woese, mainly based on her prolonged researches on  rRNA sequences) (PDF) (REFERENCE-1 *) that Eukaryotic "host cell" (with the nuclear genome) shares the closest common ancestor with Archaebacteria, not the eubacteria.

Further reading: Relationships of Eukaryotes and archaea

Fig-1: Here the horizontal axis is the time axis.
(The small black balls here indicating many other possible extinct lineages (hypothetical, just todemonstrate how evolution works) )

On other hand, After the group bacteria (eubacteria) developed (better to say the precursor of bacteria further diversified, bacterial groups like proteobacteria and cyanobacteria developed. For bacterial phylogeny, see Wikipedia (image)

Endosymbiotic theory:

Now endosymbiotic theory tells that the origin of some eukaryotic organelles (at least Mitochondria and Plastid) were different and distant taxa from the eukaryotic cessls, and they came from outside and entered into the cell and formed symbiotic relation; and the endosymbionts gradually lost their free-living ability, were gradually became part of host cell. The peculiarity of this "Endosymbiosis" phenomenomenon in evolution is that; not only the "parent" taxa; but another "distant taxa" merge from side of the lineage. The concept is not only confusing but it was so shocking that when H. Margulis first proposed this hypothesis, the idea was rejected. Later on, genome-based research proven that the origin of mitochondria (and as we will see, plastids); were originated from mutualistic- symbiosis.

2. How mitochondria evolved in eukaryotes?

It has been suggested, the "precursor" of eukaryotes (which was descendant of closest-common ancestor with archaebacteria), the host cell, engulfed some aerobic eubacteria (perhaps allied to proteobacteria) those aerobic eubacteria gave rise to mitochondria. These derived protists were unable to photosynthesise. This endosymbiosis is very much similar to previous one.

Fig 2a: origin of the organelle mitochondria.

So our evolutionary tree now look like

Fig 2b: Origin of mitochondria in eukaryotes, placed in evolutionary tree.
The white balls here represent living and contemporary groups.
(Just like previous picture the extinct groups are hypothetical and representitive; but the relative positionsof clades for proteobacteria and cyanonbacteria is actual, and taken from from Prescott's microbiology **)

(A common example of intracellular endosymbiosis will help us to understand the theory-  we can still see such intracellular symbiosis in rhizobial bacteria colonising plant root/tissue; where we get both intracellular stage and culturable extracellular phase)

3. How Plastids evolved then?

From this group of protists, a certain group again engulfed a sort of eubacteria (allied to cyanobacteria). The cyanobacteria gave rise to plastids  , and photosynthetic protists.

There are disputes about whether plastid and mitochondra evolved simultaneously or at an interval. According to T. Cavalier smith they originated simultaneously, but according to other newer sources like this  and  this   , mitochondria appeared first.

Fig.3.a. one lineage eukaryote that already formed mitochondria, forming another association with a photosynthetic eubacteria.

It is not clear to me whether all eukaryotes (protists and their derivative higher plants, fungi and animals) had a plastid containing ancestor; or at least some non-photosynthetic protists came before origin of chloroplast (However just to mention, some of photosynthetic protists again evolved progeny with lacked  photosynthetic ability due to retrogressive evolution (degradation) of plastid, such as Helicosporidium sp. etc )

So our final evolutionary tree looks like

Fig.3b. Chloroplast originated similar way from eubacteria (bacteria)

REFERENCES:

BOOKS

* 1. : Molecular Biology, Author: R. F. Weaver, ED-5; Publisher: McGraw-Hill.

: Cell Biology: Concepts and Experiments. Author: Gerald Karp, ED6, Publisher: Wiley.

** 3. : Prescott, Harley, Klein's Microbiology; Edited by Willey, Sherwood, Wolverton, Ed7, MackGraw-Hill.

Papers and Reviews

Bacterial evolution, Author : Woese; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC373105/ ; PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC373105/pdf/microrev00049-0051.pdf
Endosymbiotic theories for eukaryote origin. Authors: Martin, Garg, Zimroski; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4571569/ , Pdf: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4571569/pdf/rstb20140330.pdf


From STRUCTURE to FSTAT format From numerical simulations I output a file that is input to STRUCTURE (Hubisz et al. 2009). I now realize that I would need to process my data with FSTAT (Goudet 1995). Both are text files.

Is there an extant algorithm that would reformat a file that is input to STRUCTURE into a .fstat format?

PGDSpider will do the trick.

PGDSpider is able to parse 31 and to write 35 different file formats including STRUCTURE and .fstat.


In our 23 chromosome pairs, do the 2 members of the pair have distinct or virtually identical sequences? I understand that we have 46 DNA molecules in the nucleus of our cells, arranged in 23 pairs: 22 autosomal and 1 sex chromosome pairs.
I have read in different sources that the pairs contain nearly identical members, excluding any mutations. I have also read that the pairs contain 1 member we inherited from our mothers and 1 we inherited from our fathers, which are different due to inheritance.
This seems contradictory, given that genealogical companies match up on the differences on these chromosomes.
My understanding was that meiosis creates sperm and egg cells that each carry 23 chromosomes - they are haploids. During the first steps of meiosis that creates the reproductive cells we have a combining of the parent's chromosome pair from their parents to create 4 daughter cells, each independently viable, where the recombination of the chromosome pair has occurred at somewhat predictable spots (for you perhaps :-) ) and that these spots can be related to genes. It is this step that give us our genetic variation between siblings for example. A new person's DNA is partially formed from any one of these highly varied daughter cell possibilities.
Fertilization combines the reproductive cells to produce the 46 chromosome zygote with is again diploid.
I think this understanding supports the second interpretation that our chromosome pairs are not 2 nearly identical DNA molecules but are distinct.
Have I got this right? Is there a missing process or a misunderstanding in my interpretation?

Homologous chromosomes (those that are paired up), excluding the sex pair are almost identical in size, shape and genes (members as you called them) present in them.
Genes determine traits and each homologous chromosome controls the same traits. The level of identity of a gene inside a population varies between genes. There are very conserved ones that do not change even between humans and yeast and others that vary alot event inside a species. This changes can be small in sequence length, a simple base (letter) swap or one deletion, and have a huge effect on the traits. This is how chimps and humans are very different but share 98.6% of their genome and humans are very similar and share 99.9% of their genome.
In summary, on the bigger scale homologous chromosomes are very similar (size, shape, traits inside), on the smaller scale homologous chromosomes have small changes that affect greatly.
EDIT: elaborating on when recombination occurs.
The zygote do not recombine the chromosomes it gets from it's parents. Each parent chromosomes recombine in the first step of meiosis. We do not expect them to be identifcal on the gene level (or the SNPs level). Each chromosome represent each paren't genetic material.
Lets look at parents A chromosomes
parent a Paternal: a-b-c-d-e                       parent b Paternal: a-B-c-D-e
parent a Maternal: a-B-C-D-e                   parent b Maternal: a-b-C-D-e
possible recombination  (a)                       possible recombination (b)
(a-I) a-B-C-d-e                                         (b-I) a-B-C-D-e
(a-II) a-b-c-D-e                                         (b-II) a-b-c-D-e
Now the child can be any of the 4 possible combinations (and obviously all other not shown). Let's say (a-I) and (b-II). This chromosomes do not recombine until they get to the meiosis stage.


Can I kill bacteria with distilled water? Given that bacteria are hypertonic (contain more salts) compared to distilled water, and that they rely on ion concentration differences across the plasma membrane to survive, can I kill a bacterial solution by adding an excessive amount of distilled water to make them explode? If I add distilled water on a surface, are the bacteria on it going to die?

Indeed, bacteria are susceptible to osmotic stress from being in pure water. They are also susceptible to starvation in such an environment.

However, wild bacteria tend to have many mechanisms that protect against this and allow them to survive in spite of being exposed to water. Note, also, that freshwater can serve as a habitat for many species of bacteria: Consider ponds, streams, lakes, etc.

Thus bacteria which you encounter in everyday life will likely have been those that survived osmotic stress in the first place. And drying, and mild disinfectants, and sunlight, and temperature variation... So it is unlikely that water alone will kill them.

Here is a recent article on this topic: http://jgp.rupress.org/content/early/2015/04/07/jgp.201411296.short

And here's one about how osmotic stress affects susceptibility to other antibacterial effects: https://www.sciencedirect.com/science/article/pii/S0740002014001890


How and why did bats and dolphins develop echolocation? By how and why, I mean, what factors pushed them to develop echolocation and how did the intermediate stage (before a full-fledged echolocation system was developed) look like?

There are many conditions in which echolocation has evolved, and bats, dolphins, and even some birds (oilbirds) have evolved the ability to echolocate with different anatomical structures. Echolocation is a great example of convergent evolution, where a very similar feature is developed through very different stages in different taxa. Stephen Rossiter (from Queen Mary University of London) has uncovered that both bats and dolphins have similar mutations in a unique protein called "prestin", that increases hearing sensitivity. This could be a key step in developing the ability to echolocate.

Before a fully fledged echolocation system developed, fossil odontocetes seem to have developed high frequency hearing and sound production structures (for more details see research by Travis Park, Erich M. G. Fitzgerald, Alistair R. Evans http://rsbl.royalsocietypublishing.org/content/12/4/20160060 DOI: 10.1098/rsbl.2016.0060).

Instead of anatomical limitations (eyes on the side of the head) driving the development of echolocation, it seems to have evolved because it gives predators a competitive edge over visually oriented predators.


How to conduct PSI-BLAST for a given protein sequence against bacterial protein database only? I have a list of 100+ proteins and I need to conduct psi-blast for each one of them against "bacterial proteins" only.

I went to NCBI's protein blast tool, but couldn't figure out how to select/limit the targeted database.

Here are the 2 configs I tried:

Database: pdb, Organism: bacteria (taxid:2)
Database: landmark, Organism: bacteria (taxid:2)

Can anyone tell me if either of the approaches is correct? If not, please point the right way.

Edit 1 - add more details

All of my data is from "Supplementary Table 10" of paper "Comparative genomics of the neglected human malaria parasite Plasmodium vivax".

About 5% of all my protein sequences are ISS predicted. Remaining sequences are IEA predicted

Your approach is correct but it is worth considering which database will work best for you. Questions to consider are;

Does the database provide a large search space for the organism(s) you're interested in?
Do its IDs work well for searching other databases?
How does the host database handle identifiers over time?

For protein sequences I would use;

Database; UniProtKB/Swiss-Prot(swissprot)
Organism bacteria (taxid:2) (or a subset)

The reasons for this are that I am comfortable with how Uniprot handles their ID's, they provide a large search space with includes clear delineation between reliable (reviewed) and other (unreviewed) sequences, and finally UniprotKB IDs map well to genes. The latter can be problematic. I also know that I won't have trouble searching PDB with UniprotKB IDs.
Despite using and liking the Protein data bank (PDB) I wouldn't use them for this kind of search as they are a structural database which reduces your search space. PDB has 8292 structures for E.coli compared to 23 017 reviewed and 1,335,860 unreviewed sequences in Uniprot. If you are only interested in structures then the PDB is an ideal fit.
I haven't used landmark.


Which poison makes seastars inedible to possible predators? In the new citizen science project (see: Sea Floor Explorer), numbers of seastars, scallops, crustaceans and other animals are counted. Already one can see a heavy bias in favor of seastars, both the fat and brittle kind.

I would be interested in why this creature is so succesful, especially if it is poisonous to e.g., crustaceans, and what poisons exactly are responsible.

Asterosaponins are the class of compounds - they have a cholesterol like organic core.

Apparently, these saponins make pore-forming complexes with Δ5-sterols of cell membranes, and so are deadly to all usual kind of life, including bacteria and fungi. Quote:

  Starfish and sea cucumber cell membranes are resistant to their own
  saponines due to the presence of Δ7- and
  Δ9,11-sterols, sulfated Δ5-sterols, and
  β-xylosides of sterols instead of the free Δ5-sterols.


Red flowering climber ID Here's another climber from the same garden in Araku Valley

So what is this climber?
Does it have any economical uses?

It's an Ipomea also known as a Morning Glory. There are 600 species of Ipomea including the sweet potato. There are many colors of mixed Ipomea, your one is probably a fairly random hybrid. It is perhaps most similar to Ipomoea Rubriflora and Ipomea Coccinea:


Can I force evolution in a group of cells by removing all the smaller cells? I actually have algae growing in water in a container. I was thinking if it was possible to filter the water so that all the small cells will be filtered out and only the bigger ones will remain to reproduce cells that tend to be bigger.
Is that possible?
What type of filter should I use?

Short answer

Yes that would work in the condition that the trait you select for (size) is heritable.

Long answer

The kind of selection you would apply is called truncated selection because you fix a limit in size (depends on your filter) under which individuals do not survive and above which individuals survive and reproduce equally.

The response to selection ($R$) is given by the breeder's equation:

$R = h_N S$

, where $S$ is the selection you apply. In your case, $S$ is the difference between the mean size of the parent generations and the mean size of those you allow to reproduce in the parent generations. $h_N$ is the heritability (more info in additional info).

So, if you measure the mean size of your cells, filter them, measure their size again (or infer their size based on previous measurement and the size of you filter) and calculate the difference between the two measurements you get $S$. Then you let your filtered individuals to reproduce and you measure the size of their offspring which is $R$. By dividing $R$ by $S$ you get the heritability $h_N$. If you do not observe any difference in size between your two generations it means that the heritability is 0 ($\space h_N = 0\space$). Of course, you'll need a population that is composed of enough cells in order to have a good estimate.

Additional info

To be a bit more accurate $h_N$ is the heritability in the narrow sense. It represents the part of variance in the population that has to be accounted to additive genetic variance. The word additive genetic variance might seem obscure. In other words

$$h_N = \frac{V_{Ga}}{V_{P}} = \frac{V_{Ga}}{V_{G}+V_{E}} =  \frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}}$$

, where $V_{GA}$ is the additive genetic variance, $V_{GD}$ is the dominance genetic variance, $V_E$ is the variance due to environmental variance and $V_P$ is the total variance (phenotypic variance)

Hope that helps. Do not hesitate to ask further question if something is unclear or if I missed one of your point.

Edit

Filter

The filter you need should allow you to discriminate the cells based on their size. Therefore, it should be relatively accurate. It is common to classify the phytoplankton based on their size, see this. You should try different filters and see what filter allows a good discrimination.

EDIT

I assumed your cells were all of the same species. Is it the case? If you just sampled them from a lake and let them grow in a container then you very probably have various species. Therefore, you would select (based on their size) for species with your filter rather than selecting individuals within a species (based on their size again). It is kind of the same process anyway and the breeder's equation still holds.


Testing CO₂ for cell culture I'm am refurbishing some old CO2 incubators. I would like to test the precision of the CO2 sensor. There is a sample port on this incubator.

What sorts of  methods are commonly used to measure CO2 in these incubators?

Strangely, the manufacturer of the incubator makes no recommendations.

I need to be able to report the measurement as a percentage.

Found this:

http://www.mybacharach.com/fyrite-gas-analyzers.htm

Probably what I need


What is the purpose of co-translational transport? During intracellular proteins synthesis, all proteins are made by free ribosomes in the cytoplasm and some, but not all ribosomes (those which make membrane or secretory proteins) move to the endoplasmic reticulum (ER) and attach to it during translation (called co-translational transport).
Why are proteins that will be exported to the outer of cell are not made in the ER directly?
What is the function of ER in intracellular protein synthesis?
What is the purpose of co-translational transport?

Why are proteins that will be exported to the outer of cell are not made in the ER directly? What is the function of ER in intracellular protein synthesis? What is the purpose of co-translational transport?
This is a eukaryotic cell that we are talking about.Once the mRNA is synthesized , it has to move out from the nucleus to the cytoplasm.During its exit, SRP (Signal Recognition Particle) recognizes specific signal sequences in the mRNA and forms a complex with that mRNA.then SRP complex targets ER membrane proteins for cotranslational-transport.
If the secretory proteins are not moved into the ER , disulfide bonds would not be formed from cysteine residues . Because the necessary Enzymes required for this process are found only and only in the ER (namely PDI and ERO1).
Plus, these secretory proteins often have to be glycosylated to perform their action correctly.The Enzymes are located in the ER.
Moreover I believe that these secretory proteins will aggregate and degraded later if they are not transported into the ER.
I do not know WHY this process exists this way. That is Evolution and it is just about adaptation to the environment and not necessarily based on pure logical reasons.
Further readings : Molecular Cell Biology Lodish et al 8th ed at sections 13-1
and 13-3.
In addition see : Protein translocation across biological membranes , Targeting proteins to membranes: structure of the signal recognition particle   Post-translational translocation  Regarding to Ero1 and DPI
Formation and transfer of disulphide bonds in living cells


Do cows chew in a preferential chirality? One of the enduring myths in molecular physics, when talking about chirality as pertains the existence of enantiomers and the differences between them, is that the way cows chew is also chiral, i.e. the up-and-down and the around-in-a-plane movements combine in such a way that you can distinguish a cow chewing from its mirror image. This is mentioned in e.g. Wikipedia, among other resources.

A recent question in the Physics site asked for the source of this factoid, which turns out to be

  Movements of the Lower Jaw of Cattle during Mastication. P. Jordan and R. de L. Kronig. Nature 120, 809 (1927),

and this is a rather unsatisfactory source: they report on a survey that finds that 55% of cows chew in a 'right-circular' fashion and 45% chew left-circularly, but they then go on to disavow any statistical significance in the result:

  The number of observations was, however, scarcely sufficient to make sure if the deviation [in the ratio of the two kinds] from unity is real.

Given that this isn't a physics question, I thought I'd bounce it over to the mammalian behaviourologists out there: have there been further studies about which way cows chew? I imagine that they're out there, but I wasn't able to find them.

This study deals with the chewing direction of cows. It splits the chewing into three phases, the first jaw movement, the middle ones and the last one. It finds out that the first one is always in the opposite direction of the middle ones, that generally the middle ones are usually in the same direction and that seemimgly cows change chewing direction from one middle jaw movement period to another.


Can you name this plant that likes shade on Asturias? This was located in the Turón valley on Mieres, Asturias, Spain. Usually, I find this plant in shadowy, not too illuminated spots, although I'm not sure if that's important or simply coincidence. This picture is from yesterday 16th February 2019. The plant is lower than knee high, so let's say a maximum of 30cm tall maybe.

You have found a helleborus, possibly helleborus viridis.
https://en.m.wikipedia.org/wiki/Helleborus_viridis


How much heme is in cooked pork and beef; why is cooked pork ("the other white meat") not red? The new video See how Impossible Pork will make you forget about pig meat includes a very short discussion of

the addition of heme to the product to make it taste like beef
the deep red color of a heme solution
that pork is not nearly as red as beef, (after cooking it's essentially off-white)

Does pork (pig/swine muscle tissue) have substantially less heme content than beef (steer/bovine muscle tissue)? If heme is contributing to the flavor of cooked meats (rather than raw) such as pork and beef, why do they no longer have a red color after cooking?

Yes.
Pork has substantially less heme than beef (Cross et al. 2013).

As to why the red colour is lost, it is due to the Maillard reaction, by which the iron in the myglobin is oxidized from Fe(II) to Fe(III).  This results in a colour change in the meat (Tamanna & Mahmood 2015).

Sources:

Cross AJ, Harnly JM, Ferrucci LM, Risch A, Mayne ST, Sinha R. 2013. Developing a heme iron database for meats according to meat type, cooking method and doneness level. Food Nutr Sci 3(7): 905–913.

Tamanna N, Mahmood N. 2015. Food Processing and Maillard Reaction Products: Effect on Human Health and Nutrition. International journal of food science 2015: 526762. doi:10.1155/2015/526762


Evolution after the development of sexual reproduction My understanding of evolution is that genetic mutation occurs in individual members of a species, and they become a new species.

Isn't a definition of species a group of genetically similar organisms that are pretty much exclusive in breeding ability?

Wouldn't there have to be a male and female with the same genetic divergence at the same time to make a new species?  What is the popularly accepted mechanism for the splitting into a new species in organisms that require sexual reproduction?

My understanding of evolution is that genetic mutation occurs in individual members of a species, and they become a new species.

  Isn't a definition of species a group of genetically similar organisms that are pretty much exclusive in breeding ability?

Well, no.

You are correct in that the origin for any new species lies in mutations which occur in individuals and are then passed down through DNA.

You are misunderstanding that simply because a mutation exists in an individual that they become a new species. Take Lactase Persistence as a widely studied example in humans. The majority of the world is lactose intolerant after they stop drinking their mother's milk, but a single point mutation results in the ability to consume dairy products into adulthood. It does not make people who are lactose tolerant a new species, but it does open up a potential new nutrient source, which benefits the people who have it and thus it was passed down successfully over other variations.

In addition to that example, the definition of "Species" is NOT exactly defined. There are many variations, including (but not limited to):

1) A group of organisms that cannot interbreed in the wild.
2) A group of organisms with significantly different phenotypes (appearances).
3) A group of organisms with sufficient* genetic divergence.

*There is absolutely no scientific consensus on how much genetic divergence is necessary to create a new species. We share >95% of our genetics with Chimpanzees, so it's not much - it could be as little as a few key genes out of the entire genome.

So where you define the boundaries of species is up for grabs to some extent, but the most common is what you delineated - when a member of one group cannot interbreed with another group.

  Wouldn't there have to be a male and female with the same genetic divergence at the same time to make a new species?  What is the popularly accepted mechanism for the splitting into a new species in organisms that require sexual reproduction?

Nope. Assuming everything necessary for the gametes to produce fertile offspring is present (aka - the chromosomes aren't significantly altered and the gametes are compatible) then a new species emerges through successive generations.

One mother or father gives their mutation to their children, which pass it on to their children, which pass it on to their children, etc. If the mutation is significantly advantageous it will allow the children with the mutation to better survive in the environment, and over time it could become the dominant phenotype that could lead to the creation of a new species as further mutations build in the new group - further differing the generations of the mother/father from the original group the mother/father were born into. Good examples are the HAR - Human Accelerated Regions which are sets of genes that are pretty much the same throughout all other vertebrates, but startlingly different in humans. The HAR did not create humans, but it's thought the mutations contributed greatly to our intelligence - which allowed other mutations to be taken advantage of (like the humble opposable thumb) as our lifestyle changed due to the increased intelligence.

Not all mutations need to be advantageous, though. There's lots of fuzzy areas. If a mutation isn't beneficial, but also isn't that detrimental, it can also stick around in a population. These mutations might not lead to the creation of new species, but can certainly contribute to genetic divergence.