Removing a restriction site and introducing other at its place What would you do if you want to remove an EcoRI restriction site
  and introduce BamHI restriction site at apprx. the same location ?

One of the answers in my textbook was : To construct a DNA fragment with the structure:

5'AATTGGATCC3'
    3'CCTAGGTTAA5'

I understand that this would ligate efficiently to the sticky ends generated by EcoRI cleavage and would introduce a BamHI site but I don't understand how this will remove/not regenerate the EcoRI site.

The recognition site for EcoRI is GAATTC, and the enzyme cuts after the first base. See this picture from NEB:

The overhang is: AATT, which is supplied by your oligo and fits into the overhang. If the next nucleotide whould be a C than the site would be recreated, since its a G its not. The new sequence of the old EcoRI site is GGATTG which is not recognized by EcoRI.

One technical note: To avoid religation of the digested DNA which carries this site, I would treat it with alkaline phosphatase to remove the phosphate end at the 5' end of the DNA.


Do sweat pores change diameter? In Cholinergic Urticaria, some people believe that the itching which is generally more in winters might be because that the diameter of sweat pores is less due to less activity(less sweat production) and in summers the diameter is usually more due to high activity (more sweat production).

Question: Hence the question in general, Do sweat pores change diameter?

Pores don't change size; that is, the diameter of pore does not increase or decrease in hot or cold environments. Your skin, where pores are located, is not muscle but an organ so the pores don't contract or expand.

Pores can become clogged with dirt, oil, and debris (make up). When pores are clogged, you are more inclined to notice which would cause the illusion that the pore is bigger.

  It's important to know that you can't actually "shrink" your pores. They're nothing but small openings in the skin -- because they don't have muscles, they can't open or close. So although you can't physically change the structure of your pores by making them smaller, there are things that you can do to minimize their appearance$^1$.


What does 21q21.1-q21.2 mean? I am reading a journal paper about the association between NCAM2 and autism, and I have come across the following:

We performed microarray analysis and identified a 1.6-Mb deletion of
21q21.1-q21.2, containing the NCAM2 gene but no other functional gene.

I am not sure what the '-q21.2' after '21q21.1' in '21q21.1-q21.2' means. Does it mean that the deletion goes between band 21.1 to 21.2 on the long arm of chromosome 21 (21q)? Any insights are appreciated.

Cytogenetic map notation uses the following form:
A[p/q]BC.D
Where A is the chromosome number, p is the petit / short arm, q is the queue / long arm, B is the band, C is the sub-band, and D is the sub-sub-band.
So, 21q21.1-q21.2 designates a region on the long arm of chromosome 21, band 2, sub-band 1, between sub-sub-bands 1 and 2.
Source:  NCBI Genetics Review (archived version)


What does ophthalmologist see in your eye? I always wondered what ophthalmologists see inside someone's eye and what they're looking for. The whole thing is a mystery to me. Are there any photos of what the eye of a patient looks like from the doctor's point of view?

The name of the instrument is ophthalmoscope. It is used to determine the health status of your retina. Retina is the one of the few places in the body where you can observe the blood vessels directly.

The link also includes a picture of what your eye looks like from doctor's point of view.


Recent and good quality articles on systems biology I'm a biotechnology student and I have to write a sort of non-experimental thesis (30 pages long) within the end of a three years study.

I'm very interested in the "systems biology" field and I'm searching good (innovative) and recent (max 3-4 years old) articles about this subject, but unfortunately I've found my research more difficult than I expected.

I'd like to focus on not immediate/easy articles and possibly containing new and promising approaches.

Does anybody have suggestions?

PS: it all started from Uri Alon's great lessons on YouTube.

This question is extremely vague, and can't have any real answer without you specifying a question or at least focus. Keep in mind, there is no high-road to research, you will have to dig in and start reading papers to gain understanding of your field. If you want help from others, you should at least take time to list the papers that you have already read and why you liked them to give readers a flavor of your interests.

To start you off, consider this Google Scholar query for systems biology since 2009. If you've read specific older papers that you've liked, for example this popular 2002 minu-survey:

Kitano, H. (2002). Systems biology: a brief overview. Science, 295(5560), 1662-1664.

Then you can learn how the field has advanced since by doing a forward search in Scholar (and restricted to 2009+). Hopefully this will provide you will some ideas so that you can ask a more precise question!


Waggle dance in the dark Karl von Frisch discovered waggle dance [1] as communication system when bees talk about feed resources;
Long story short, using a polar coordinate system, bees dance to reveal flowers to sisters.
My question is simple: how can this be possible since bees are in hives, which are dark?
That is, how can a bee sees its sister dancing in a dark hive?

[1] https://en.wikipedia.org/wiki/Waggle_dance

In bees that dance in the dark (not all do, some dance in the light) they don't watch the dance, they participate. The follow the dancer using their antenna and sound to keep track of them.

Beehives are often dark, so instead of watching the scout dance, the recruit bees follow the dancer using their antenna and the sounds produced during the dance to determine the directions to the food source.

https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/waggle-dance#:~:text=The%20dance%20conveys%20information%20about,directions%20to%20the%20food%20source.


too low extention time for Taq polymerase PCR I am currently working on my masters degree and have recieved the following question:

  "you want to amplify by PCR a gene 1kb long. The Taq Polymerase you have in the lab is able to synthesize 1kb/minute. You make a mistake in programming the PCR machine and set the extension time to 30 seconds instead of 1 minute. what will happen? what do you expect to see on a gel?"

The answer I came up with was that there would be insufficient time for complete replication of the target and therefore only incomplete copies would be made. These strands would show up in a band below 1 kb because the are shorter.
This answer however, was incorrect. I browsed the web but could not find any clear answers on what would happen. anyone knows what happens?

To get amplification of a DNA fragment you need primers to anneal first so that you can extend from. The extension time is designed so that DNA is synthesized from one priming site to the other. Therefore if you have a lower extension time you will make a product that is missing the other priming site. This means that all new template strands can be amplified from one end only and you get linear amplification, not exponential. Therefore there will be too little DNA to visualize on a gel.


How to interpret McDonald-Kreitman test results? It is easy to get the numbers right and calculate neutrality index. It is easy to memorize "equals", "greater", "lesser", etc. At least on the exams, when certain level of simplicity is assumed. But instead of memorizing I'd prefer to understand. So far I struggle to get past the numbers. Could anyone, please, explain reasoning behind the them? Why certain values means the trait is advantageous or not? An easy to understand example would be helpful as well. Thank you.

A helpful way to phrase it for me is that "If there's a disproportionate fraction of non-synonymous mutations between species relative to what exists within species, it is because non-synonymous mutations are being selected for in the one species but not in the other, thus there's positive selection."

By the way I'm not an expert in this so take the explanation with a grain of salt.


What do the initial cell divisions look like in bird embryogenesis? The germ disc in a bird (a disc because its a chordate) is a mystery to me. The ovum (yolk) is a huge mass of nutrients. It then gets impregnated. Then, what? What does the initial cell divisions look like (they can't be symmetrical since yolk is clearly pushed to one end of the whole thing. )

This is covered well in almost any text that talks of early embryonic development in birds. Basically, the cleavage divisions look roughly symmetrical if you look end-on from the animal pole. But, as mentioned in the question, the process is quite asymmetrical in profile, with the blastoderm being at one end and the huge yolk occupying the other.

The yolk later gets invested by a layer of cells (the splanchnopleure) to form the yolk sac while the blastoderm forms the embryo proper.

You could see this page for more details. (Not just this page, this site in general is an excellent resource for learning embryology.)


Can Leptospirosis be spread through human urine I am wondering if Leptospirosis can be spread via the urine of an infected human individual. All of the sources I have been able to find on the web have stated that the disease is primarily spread through infected animal urine, however, none of them mention human urine.

However, Wikipedia states:

  After 7 to 10 days the microorganism can be found in fresh urine

Which would imply that it could be spread via the urine of an infected individual?

It can be spread from human to human through urine but it is very rare seeing as we are relatively clean creatures (most of the time) and our excrement hardly ever comes into contact with other individuals without first being purified.

Sources:

Leptospirosis
CDC: Leptospirosis infection


Is a set of chromosomes made up of many copies of DNA, or is one complete string of DNA broken up into one set of chromosomes? I know technically the question isn't really accurate but hopefully it gives the essence of what I'm trying to ask.

By the way I was taught in school, I was under the impression that a chromosome was made out of multiple complete copies of DNA. But, what I'm reading online makes it sound like a single complete string of DNA is broken up into sections and those sections are wound into chromosomes (so that one complete set of chromosomes would make up one complete string of DNA).

I'm assuming neither are 100% correct, but could someone explain it in a way that I can understand?

A chromosome is one long molecule of double-stranded DNA.  As a diploid organism, you (almost certainly) have two copies of each autosomal chromosome; one from your father, one from your mother.  You (almost certainly) inherited one copy of the X chromosome from your mother, and you either have a second one from your father, or you inherited a smaller Y chromosome instead.


Extinction of species I barely know anything about biology and realize that this might be a stupid question, but I'll ask anyway! I know that species "transform" into other species through the process of evolution. Many species around today still co-exist with the species in which they evolved from, right? Actually, is it correct to say that all species coexist with some common ancestor?

Anyway, my question is; if the monkeys that we evolved from are still around today, then where are all the in-between species. Are there still early humans, like Neanderthal's or Hominids or what have you still roaming around some where?

If all early forms of humans are gone, is it because the more modern humans had a greater evolutionary advantage? But wouldn't these less modernized humans have those same advantages over the less evolved monkeys?

This is a common misconception about evolution, many skeptics ask something along the lines of "If humans evolved from monkeys, why are there still monkeys?" The answer is that evolution is not a linear process of one species becoming the next species becoming the next. Species branch off much more like a tree. At some point in the past the last common ancestor of humans and monkeys split into two directions, one that became the apes including humans, and one that became modern monkeys. Evolution did not stop for either branch, but only our branch became humans, after several more branchings. Sometimes species adapt and evolve without major changes in morphology, for example modern turtles look a lot like turtles from 100 million years ago, but this doesn't mean they haven't evolved.

The intermediate species are often lost with time as environmental conditions and competition changes. For example, if one early human group found itself competing with a slightly more advanced human group with better tools, the more primitive group would have trouble getting enough food and eventually die off, leaving the more advanced group to pass its genes on.

Now, if those more primitive humans were more suited to a particular niche, they could survive there. Lets say they could climb trees better ( assume REALLY primitive ancestors, barely out of the forest ), they might survive in the forested areas while the more advanced groups become dominant in the grasslands. Something like this is why our ancestors didn't totally displace monkeys, the monkeys were better suited for their forested ecosystem. If those same monkeys had to live on dry savannas we would have eaten them all long ago.


Is there an absolute minimum intensity level to the stimuli we can perceive? By stimuli that we can perceive, I mean what our five senses can perceive.

Is there an absolute minimum for humans, or can we "train" ourselves to perceive stimuli at lower intensity?

And if there is an absolute minimum intensity, do we know what its value is?

There are limits to what a sensory system can detect, which is called the detection threshold. To determine the detection threshold psychophysical methods can be used. A straightforward way to determine the detection threshold is with a yes/no task, where the subject receives stimuli with various intensities. An arbitrary point, mostly the 50% correct-rate, is then defined as the detection threshold. At this point, the subject correctly detects the stimulus 50% of the times. The response curve in a psychophysical task typically takes the shape of a cumulative function such as the one shown in Fig. 1.

Hence, the detection threshold is an arbitrary point, because people are not machines and show variability in their decisions. The detection limit of, e.g., electronic devices is much more precisely defined. The exact values of the detection limits depend on the exact stimulus (visual, tactile etc.) and depend highly on the exact stimulus. For example, in the visual domain the detection limit of light depends on the color, the location in the retina tested, dark adaptation etc etc, and in the tactile domain static pressure stimuli have a different threshold than vibratory, different body parts have different thresholds etc. etc.

Fig. 1. Psychometric curve showing 50% threshold of a visual stimulus. source: Webvision

Training to lower the detection threshold (i.e. improve detection limits) is indeed possible (Sterr et al., 1998).

Reference
Sterr et al., J Neurosci (1998), 18: 4417-23


Synthesis of Fatty Acids Longer than 16 Carbons I understand that the human body when performing Fatty Acid Synthesis can synthesize only until C16 (palmitate). However the ER has desaturases and elongases. I know that desaturases are used to add double bonds, but do humans have elongases to add even more Carbons to a double bond? If so, then this would mean that the human body can synthesize fats longer than C16?

Lets take a hypothetical case and say that humans have both desaturases and elongases. Would it be feasible to add double bonds to palmitate via desaturases, then add more carbons to the chain via elongases and then add more double bonds via desaturases? This way, the resulting fatty acid will have an increased length and more unsaturated character (i.e. more double bonds than the prescribed 4 that humans can add at positions 4, 5, 6, and 9)?

Short Answer: Yes.
Long Answer: See this article:

The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found in Escherichia coli. These reactions are performed by fatty acid synthase II (FASII), which in general contain multiple enzymes that act as one complex. FASII is present in prokaryotes, plants, fungi, and parasites, as well as in mitochondria.
In animals, as well as some fungi such as yeast, these same reactions occur on fatty acid synthase I (FASI), a large dimeric protein that has all of the enzymatic activities required to create a fatty acid. FASI is less efficient than FASII; however, it allows for the formation of more molecules, including "medium-chain" fatty acids via early chain termination.
Once a 16:0 carbon fatty acid has been formed, it can undergo a number of modifications, resulting in desaturation and/or elongation. Elongation, starting with stearate (18:0), is performed mainly in the ER by several membrane-bound enzymes. The enzymatic steps involved in the elongation process are principally the same as those carried out by FAS, but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.

Another article from NCBI states:

Primers for several mouse, rat, and human elongases have been reported elsewhere.

...and cites here for this:

Fatty acid elongases and desaturases play an important role in hepatic and whole body lipid composition. We examined the role that key transcription factors played in the control of hepatic elongase and desaturase expression...In conclusion, these studies establish a role for PPARalpha, LXR, SREBP-1, ChREBP, and MLX in the control of hepatic fatty acid elongase and desaturase expression and lipid composition.

Indeed, humans do synthesize stearic acid (C18) in their body; mainly liver and adipose tissue. See this article:

Fatty acid biosynthesis from acetyl-CoA takes place primarily in the liver, adipose tissue, and mammary glands of higher animals. Successive reduction and dehydration reactions yield saturated fatty acids up to a 16-carbon chain length. Stearic acid is synthesized by the condensation of palmitoyl-CoA and acetyl-CoA in the mitochondria, and oleic acid is formed via a mono-oxygenase system in the endoplasmic reticulum.

Now, would it be feasible or not to synthesize unsaturated fatty acids is a matter of debate. Maybe this could be helpful in this matter.


Can we develop a nucleos(t)ide analogue to cure rabies? Nucleos(t)ide analogues have been successfully used to treat HIV, HBV and HCV. Since rabies virus is also a RNA virus that uses RdRp to replicate. If we develop an nucleos(t)ide against its RdRp, will it be able to save rabies victims? What would be potential obstacles?

In theory that would be possible, as you mentioned the rabies virus does have its particular polymerase, and adequate inhibiting substrates could possibly be found.

On the other hand, the current immunoglobulin and vaccination post-exposure scheme is quite effective, and the incidence of rabies in developped countries is pretty low; so it's unlikely an inhibitor could profitably be developped to the market.  That means rabies-directed nucleoside analogues are not priority target for pharma companies, IMO the biggest obtacle.

Here are some of the technical hurdles a drug candidate would have to overcome, as a nucleoside analogue :

Affinity to the viral polymerase : too low an affinity makes competition with the native substrate difficult
Rate of conversion to triphosphate form : a low affinity of the host nucleoside kinase to the analogue can cause a inadequate concentration of active triphosphated inhibitor. Some virus (HSV) have their own kinase that may be less selective, though that doesn't seem to be the case for the rabies virus.
Selectivity for the viral polymerase (versus the host replication/transcription machinery) : a cause of cytotoxicity and, generally, adverse effects.
Pharmacokinetic problems : the analogue has to be able to be taken in through nucleoside transporters (facilitated transport into the cell), or go through other means of active transport, as that kind of compound is usually quite hydrophilic. One could also use the usual prodrug tricks to pass the membrane (see CP-4055 or sapacitabine). This may be particularly problematic for acute-stage rabies, as there would be the blood-brain barrier to pass.

Some additional perspectives on the development of nucleoside analogues

Advances in the development of nucleoside and nucleotide analogues for cancer and viral diseases -- (http://www.nature.com/nrd/journal/v12/n6/full/nrd4010.html)

Discovery and development of clofarabine: a nucleoside analogue for treating cancer -- (http://www.nature.com/nrd/journal/v5/n10/full/nrd2055.html)


Are there animals that have evolved a resistance to human activity or encroachment? There are countless sources, both peer-reviewed and popular, explaining how overuse and misuse of antibiotics is breeding a new generation of antibiotic-resistant "superbugs" such as MRSA (Methicillin-resistant Staphylococcus aureus) and MDR-TB (multidrug-resistant Tuberculosis). Over in the animal kingdom, the opposite seems to be happening - species after species is becoming endangered and/or extinct as humans destroy or alter their habitat through increased hunting, farming, construction, etc.

Are there any non-human animals that have been found to have evolved resistance to human encroachment into or alteration of their habitat in a way analogous to how bacteria have evolved resistance to human attempts to get rid of them? For example, this could consist of:

an animal that has adapted stronger bones to better survive collisions with vehicles
an animal that has significantly increased its blood coagulation rate to survive gunshot wounds from hunters
an animal that has developed better vision to see in urban environments
an animal that has evolved a skin pigment change that enables them to not take as much damage when they are sprayed with agricultural pesticides

One answer that came to mind is domestic animals - the horse and dog in prehistory, the cat in ancient Egypt, etc. That seems too obvious on one hand, and on the other hand may not really be an answer, as there seems to be no indication that pre-domestic animals were endangered by humans in any meaningful way. Are there animals that have significantly adapted themselves to surviving as wild animals in human-influenced environments?

Note: This is an answer to the last line of your question.
A classical example of animals adapting to the influence of humans on their environment is the adaption of the Peppered Moth.
Here is a brief summary:
The peppered moth was originally a mostly unpigmented animal (<1800). During the industrial revolution in the southern parts of the UK a lot of coal was burned. This led to soot blackening the countryside. Soon afterwards, a fully pigmented variety was first observed. Only a hundred years later, in 1895, this pigmented variety almost completely displaced the unpigmented variety.
It has been shown that the pigmentation is under strong selective pressure as birds hunt these moths. Since birds rely on their visual system to detect their prey, the variety that blends in with its environment (=camouflage) has a selective advantage over the variety that stands out.
As pointed out by Tim in the comments, since the 1970s there has been a rapid reversal with unpigmented animals being more abundant. As far as I understand, it is accepted that this reversal is due to a decrease in human induced air pollution leading to less sooty barks on trees which makes the unpigmented variety harder to prey upon.
Addendum: genetic basis of adaption
In a beautiful recent study, the causal mutation for the pigmented, or melanic, variety was identified: A ~9kb transposon insertion in the first intron of the gene cortex. The authors calculate that this mutation happened in the year 1819, a few years after the industrial revolution was in full swing. The interpretation is that due to sooty tree bark this mutation, causing pigmented moth, was under strong selection.


Why Can Varied Species Live Together in Particular Ecosystems? Consider the following question:

  The Piney Woods of Eastern Texas is home to a wide variety of organisms ranging from the grass Longleaf Oats to coyotes. Which of the following best explains why these varied specifies can live together in this particular ecosystem?
  A.) Each species lives in a slightly different habitat B.) Each spices occupies a different niche C.) Each species functions at a different trophic level D.) A and B   E.) A, B, and C

I chose answer choice E with the reasoning that: Oats and Coyotes do not share the same habitat; they occupy a different niche -- Coyotes eat organisms, oats use photosynthesis; coyotes are at a completely different trophic level when compared to oats -- oats being primary producers. The answer choice E however is incorrect and I'd like to know why and what the correct answer should be. Is there a flaw in my logic?

The answer should be B "Each spices occupies a different niche" because this is the only answer that reflects a model of species coexistence.  Niche theory proposes a mechanism that allows multiple species to occupy the same space and time any yet avoid competition for limited resources.  Briefly, the model says that a species niche is the total suite of resources that it requires to survice and reproduce and that coexisting species will limit their niche overlap to avoid competition (and its requisite reduction in fitness).  Species can limit niche overlap by preferentially using a subset of resources that are not shared with potentially competing species (this is called the realized niche) or by evolving a new niche that does not overlap with the competitor (this is called character displacement).

Note that your reasoning is incomplete because the question does not specify that the organisms listed are the complete set of organisms  in the community.  For example if the community contained another species of grass, then choice "C" would be false.  Most importantly though, habitat or trophic variation are not mechanisms of coexistence, so they should not be used as general hypotheses explaining coexistence.


Given the number of individuals who have a recessive disorder, how can one calculate the probability that the disorder was inherited? Just to be clear, this is not homework.
Suppose a biological family has five children, two of whom have a certain recessive genetic disorder that is not sex-linked. The parents themselves do not have this disorder.
I want to estimate the probability that the parents are carriers. How can I do that, short of getting this probability directly from a lab study?

This problem appears to be where Bayesian statistics can help. All I need to know is:
1) the probability of the parents being carriers, given they don't have the disorder, but 2/5 of the children do.
2) The probability of the parents being carriers
and 3) The probability of the children having the disorder.

3 I can probably find without too much effort. #2, I'm guessing, is a Hardy-Weinberg problem - I just need to find the relevant statistics for people of the parents' backgrounds. But I have no clue how to start with #1.

Assuming...

The parents are the real biological parents (no cheating allowed!)
There is a purely dominance/recessivity relationship between the alleles and no individual can express the disorder without being homozygous for the disease causes allele
De novo mutations for the disorder are rare enough to be ignored in the calculation of this probability
Trisomy and monosomy is not involved

, then the two parents must necessarily be carrier (both of them) as long as at least one of their children express the disease.

Note, by the way that some of the above assumptions are too strict and could be partially released.

This question does not require any complicated bayesian statistics (or any statistics at all) or any use of Hardy-Weinberg rule. If a children expresses a purely recessive disease, then (s)he is necessarily aa, where a is the recessive allele and A is the dominant allele(s). It means that both parents must have at least one a. Because, no parents express the disease, both parents are necessarily Aa (or aA)


What about 23andMe's SNP test gives it such bad efficacy as a diagnostic tool? The recent news about the FDA stopping the google backed 23andMe service selling any more kits got me thinking. I understand the company may have been selling it as a medical tool prematurely, but what is it about SNP analysis that makes it so poor as at predicting disposition? Even other SNP companies have similar problems with accuracy and can't agree on disease disposition (Tonellato et al., 2011). Why might they differ from 23andMe's predictions?

The long and short of it is that genetic variation is actually not very predictive in comparison to "environmental" effects such as lifestyle.

Only a quarter of the variation in lifespan between twins is attributable to inherited factors (including genetics and epigenetics) [1] - the rest is environmental, from lifestyle to air quality.

Most genetic variants (such as those measured on the chip used by 23andMe) have a very small impact on outcomes such as "Risk of disease X, Y or Z". Many risk loci have been identified, but without a full understand of what this risk means, the results of the 23andMe analysis can be misleading.

Some few rare genetic variants have a larger impact on diseases (such as early onset diabetes), but this comes under the "monogenic" category of genetic variation, rather than the common variants typically observed in large populations.

Basically, genetic risk scores are, at the moment, only indicative of an individuals risk, and to get the real picture a lot more information is required - for instance smoking is a better predictor of early mortality than any "common" (>=5% frequency in a population) genetic variants, likewise a high fat diet is more indicative of cardiovascular disease.

Skytthe A, Pedersen NL, Kaprio J, et al. Longevity studies in
GenomEUtwin. Twin Res. 2003;6(5):448–454. [PubMed link]


Stopping the effect of hormone Many hormones released by endocrine organs travel down in the blood and bind to specific receptors on the target cells. What then breaks that binding of the molecule with the receptor ? ( thus inactivating further stimulation of the target cell )

The binding is reversible typically; part of the potency of a drug is ow well and for how long it binds to its target. There's a natural equilibrium of binding and dissociation. Many drugs, once bound to their cognate receptor, cause a down regulation of their cognate receptor on the target cell. The bound/activated downstream signalling pathways may be inhibited by ubiquitination of the downstream signals themselves or upregulation of antagonists etc. The hormone itself has a half life, which is very important, thus levels naturally decrease and for some hormones this is incredibly rapid. Levels may decrease due to breakdown or excretion. Increase of binding hormones may decrease free hormone thus it's effect also.


By what mechanism is Streptococcus bovis acting as a risk factor for colorectal cancer? Streptococcus bovis bacteremia/endocarditis is considered a risk factor for colorectal cancer. What pathophysiological mechanism may link the two together?

As you probably know, there is a lot of literature on the correlation between Streptococcus bovis and colorectal cancer, but very little on possible mechanisms.

In an editorial (Streptococcus bovis: Causal or incidental involvement in cancer of the colon? in the International Journal of Cancer 119(9):xi-xii), Harald zur Hausen referring to this paper:

  Biarc J, Nguyen IS, Pini A, Gosse F, Richert S, Thierse D, van Dorsselaer A, Leize-Wagner E, Raul F, Klein JP, Scholler-Guinard M. (2004) Carcinogenic properties of proteins with proinflammatory activity from Streptococcus infantarius (formerly S. bovis). Carcinogenesis 25: 1477–84.

comments:

  ...used a partially purified S. bovis S300 fraction representing 12 different proteins and triggered the synthesis of proinflammatory proteins (human interleukin-8 and prostaglandin E2, correlated with the in vitro overexpression of cyclooxygenase-2 [Cox-2]) in human colon carcinoma cells (Caco-2) and in rat colonic mucosa. These data could point to a role of oxygen radicals in colon carcinogenesis induced by a chronic infection with S. bovis. The mechanism could be similar to the one suspected for the development of gastric carcinomas after persisting Helicobacter pylori infections. Presently it would still be important to know whether the increased presence of S. bovis in colonic cancers and polyps results from the preferential bacterial colonization of these cancers and their precursors or whether S. bovis represents a carcinogen that is causally involved in colon cancer.

The last sentence summarises the ongoing debate: does the bacterium promote the cancer, or does the cancer promote the bacterial infection?


Whole Genome Sequencing and B Chromosomes Do whole genome sequencing techniques detect B chromosomes if such chromosomes are present?

My understanding is as follows:

How the DNA material in a B Chromosome is mapped depends on the reference map and not on how the material is packaged into chromosomes for the sample being sequenced.

Is this correct?

You can use differences in coverage (number of reads mapping to certain regions in reference) to infer if there is a B chromosome.


Biological term for close species rivalry Is there any phenomenon/force in biology when two very close species fiercely fight each other (as a sign of a strong tendency to deepen the difference between species)? If there is, what's the name of the phenomenon or any similar phenomenon? (Question from a layman in biology, thanks for an answer.)

Citing wikipedia

  Character displacement refers to the phenomenon where differences among similar species whose distributions overlap geographically are accentuated in regions where the species co-occur, but are minimized or lost where the species’ distributions do not overlap. This pattern results from evolutionary change driven by competition among species for a limited resource (e.g. food). The rationale for character displacement stems from the competitive exclusion principle, also called Gause's Law, which contends that to coexist in a stable environment two competing species must differ in their respective ecological niche; without differentiation, one species will eliminate or exclude the other through competition.

  In ecology, the competitive exclusion principle, sometimes referred to as Gause's law of competitive exclusion or just Gause's law,[2] is a proposition that states that two species competing for the same resource cannot coexist at constant population values, if other ecological factors remain constant. When one species has even the slightest advantage or edge over another then the one with the advantage will dominate in the long term. One of the two competitors will always overcome the other, leading to either the extinction of this competitor or an evolutionary or behavioral shift toward a different ecological niche. The principle has been paraphrased into the maxim "complete competitors cannot coexist"


Can the human brain be reduced to a binary system? Does the brain really function like a computer as in, ultimately every response is related to a binary sequence based on whether particular neurons fire or not?

First of all, I would like to point out that making analogy between digital computers and the brain is often very misleading.

That being said, my answer is, some scientists believe so, some don't.

Several things to consider:

Some neural systems are not spiking. C. elegans for example has a nervous system that is entirely analogue. Human nervous system also contains neurons with graded responses (mostly in the sensory front-end though).
Spiking neurons may be binary at each time point, but time itself is continuous. Firing at 0.003 seconds later can represent something different. (in contrast to the usual synchronous digital architecture of computers)
The neuron doctrine is sometimes challenged. Glial cells that do not fire may have important functions for information processing. See:

Bullock, T. H., Bennett, M. V. L., Johnston, D., Josephson, R., Marder, E., and Fields, R. D. (2005). The neuron doctrine, redux. Science, 310(5749):791-793.


Why are oceans said to have "low productivity" in terms of photosynthesis? 80% of the world's photosynthesis takes place in the ocean. Despite this, oceans are also said to have low productivity - they cover 75% of the earth's surface, but out of the annual 170 billion tonnes of dry weight fixed by photosynthesis, they contribute to only 55 billion tonnes. Are not these two facts, which I have come across separately, contradictory? If oceans fix 80% of the total $\ce{CO2}$ fixed by photosynthesis on earth and release 80% of the total $\ce{O2}$ released by photosynthesis on earth, they should have accounted for 80% of the dry weight produced as well. Is there any way to reconcile these facts? In any case, if 80% photosynthesis occurs in oceans, that hardly seems low productivity - then why are oceans said to have low primary productivity (a host of reasons are also given for this - that light is not available at all depths in oceans, etc.)? A large amount of photosynthesis taking place should mean a large productivity!

First, we have to know which are the most important criteria for photosynthesis to occur; these are: light, CO2, water, nutrients.
docenti.unicam.it/tmp/2619.ppt
Second, the productivity, you are talking about, it should be called "primary productivity" and it is calculated, dividing the amount of carbon converted per area (m2) by the time.
ww2.unime.it/snchimambiente/PrPriFattMag.doc

So, thanks to the fact that oceans occupy the larger area of the world, the marine microorganisms can convert lots of inorganic carbon into organic (principle of photosynthesis).
A big problem in the oceans is availability of nutrients; these tend to deposit or react with water or other chemical compounds, even though the marine photosynthetic organisms are essentially found on the surface, where, of course, light is present. This reduces as a consequence the  photosynthetic productivity potential of oceans.


Is there any reason an arbitrary DNA sequence such as 5'-ACACACACAC-3' would not exist in nature? I am making a DNA model for my class, and I looked up some examples and they all have different sequences of bases. If I choose an arbitrary sequence like:

5'-ACACACACAC-3'
3'-TGTGTGTGTG-5'

or

5'-ATATATATAT-3'
3'-TATATATATA-5'

Is there any reason it would not exist in nature?

You must first understand a few things:

What are proteins made of
What is DNA made of
What is the relationship between DNA and proteins

From DNA to proteins

DNA is transcribed into RNA which is then translated into protein. The protein, then has some effect (e.g. could be an enzymatic effect) such as affecting the level of sugar in the cell, digesting some lipids or affecting the expression of other genes.

More information on Khan Academy > Central Dogma

What is DNA made of?

DNA (or at least the genetic code) is made 4 different molecules which are called nucleotides. We abbreviate their names by the letters A,T,C and G.

What are proteins made of?

Proteins are made of amino-acids. There are ~20 different amino acids.

Genetic code

For the interest of your question it is now essential to understand how does the succession of nucleotides A,T,C,G in the DNA is reflected in the protein. This is called the genetic code.

We call a series of three nucleotides, a codon. AAT is a codon for example. Each codon (except special codons) correspond to a specific amino acid. This correspondance is called the genetic code. Here is the universal genetic code (where the T has been replaced by U because RNA contains U instead of T)

Consider for example the codon UAU and AUU (where only the order changes) The first one codes for the amino acid Tyr while the other codes for Ile. So yes, the order matters.

Information theory

Globally speaking, for any information the order of a sequence is of fundamental importance! More information on Khan Academy > Information Theory.


How does prolonged exposure to high frequency noise affect hearing? Is there any research showing how prolonged exposure to background noises, particularly high frequency noises, affect hearing abilities? Does constant high pitched noise cause damage even a low volumes? E.g an alarm sounding, noise of an air plane, or noise from road works and building sites.

If so, what is the effect? and why does it happen?

The ear uses a series of hairs to parse out sound frequency in the cochlea.  When the cochlear hairs die, we lose some frequency response.

As we get older, even without exposure to loud noises, the higher frequency responses tend to lose their response first.  But loud noises have been linked to hearing loss and high tones are often lost first.

Hot off the presses: there's been some success in regenerating the cells which respond to sound in our ears.

I want to add @Armatus has a good point.  Ultrasonic sounds - above hearing range - seem to not adversely affect hearing at all.  Will humans and animals be harmed by frequencies outside their hearing range?


E. coli values for [enzymes], [metabolites] and kinetic rates In my attempt to create a metabolic model of E. coli, I have found a comprehensive list of metabolic reactions and their stoichiometry. The one I am currently using is E. coli model iJO1366 (more here). What I have not yet found is a comprehensive list of kinetic rate constants associated with these reactions. I also require a data source of concentrations of these enzymes and metabolites at steady state in E. coli. Where can I find information on concentrations and rate constants?

I would advise you to use the SMBL for iAF1260 E. Coli with a COBRA toolbox on MATLAB. It has all the constants you are looking for optimized for the steady state and have been extensively tested for simulation of single and multiple genes deletion / mutation. Even if you want to stick with your model you will be able to copy the constants from there.

However depending on what you are doing you might not be satisfied by the whole models, since the they are computationally too complicated to simulate and optimize and lead to computationally unstable results, especially when you try to simulate colony collaborative mechanisms.


Has it been confirmed yet that the DNA found in dinosaurs was really DNA? I hear different sources claiming different things, bbc said they did, wikipedia says it hasn't which is it?

Apparently it wasn't. According to Wikipedia, A study that reported Dinosaur DNA was,

  mitochondrial cytochrome b sequences that had apparently been
  extracted from dinosaur bones dating to over 80 million years ago
  (reference).

However, contamination was found in the reported study (reference). Don't expect too much because this is a close to impossible task (reference 1). Most researchers pinned their hopes on DNA surviving trapped in amber resin but even that is not possible (reference).

If interested in cloning a dinosaur, quickly go through this article (or not).


Does ATP production increase with oxygen availability? I'm not a biologist so pardon any ignorance on my part. I'm working on a speculative evolution project and I'm looking to understand how the partial pressure of oxygen effects the maximum aerobic performance of muscle. This paper gives the maximum aerobic performance of 100 Watts per KG of muscle. This limit is stated to be observed for both insects and vertebrate fliers and is in turn used to calculate the aerobic flight capacities of various animals. The paper also mentions that squamate muscle tissue can achieve 450 W/kg anaerobically.
I have used the equations listed in the linked paper to calculate the size limits of my speculative world's fauna. The only problem is that this assumes an aerobic power output of 100W/kg of muscle. It is my understanding that aerobic respiration in muscle cells is driven by ATP production and that ATP production is dependant on a constant supply of oxygen. It seems logical that the maximum aerobic power output should be higher if there is more oxygen available.
For context, the atmosphere of this speculative world contains 13.5% O2 at a pressure of 12atm. This equates to a partial pressure of oxygen of 1.62 - approximately ~8x higher than our current atmosphere. In these conditions, there is 8 times the amount of oxygen available for respiration. If oxygen availability is the sole factor in ATP production (thus aerobic muscle power), then this means the aerobic power output would net 800W/kg of muscle (assuming the biology of these creatures are the same as known animals). This is almost double what lizards can produce anaerobically which doesn't seem likely.
My question is how would ATP production scale with available oxygen? I assume there comes a point where mitochondria simply cannot process ATP any faster, which would imply a maximum aerobic power output. I have read that some athletes breathe canned air to reduce fatigue. Does more oxygen equate to more power or does it simply mean that muscle cells would not fatigue as quickly? If I've made any mistakes in my reasoning then please correct them. Thanks.

The factors limiting ATP production are the rate of fuel (glucose, fats, amino acids, etc.) metabolism and its efficiency (ATP molecules per fuel molecule).
It is possible to produce ATP with zero oxygen by the glycolytic pathway; if this were not true, there would be no anaerobic organisms on Earth (which there clearly are). Muscle can do this too for short periods of time, producing lactic acid. In fact, many researchers believe that this pathway can produce ATP the fastest of any route of glucose consumption, even though it is least efficient. In other words, the number of ATP per glucose is small (only 2), but glucose "flows" through this pathway so fast that it is still generated faster than by respiration, which produces 30-32 ATP per glucose, but can process far fewer molecules of glucose per second. The actual rate of ATP generation by mitchondria is only limited by O2 concentration, in a chemical kinetics sense, in hypoxia, i.e. when a tissue does not have adequate blood supply, as in certain tumors.
The main effect of oxygen availability is likely size scaling--if you have more O2, you can get it through a larger body more easily. It's not that the muscle cells themselves generate more energy, it's that you can supply more muscle fibers that are farther from the lungs/gills/whatever. That's why in the carboniferous period on Earth, where there was considerably more O2, many animals (particularly invertebrates) were much larger than they are today.


Photoperiodism: Short-Day Plants My Campbell's Biology textbook discusses photoperiodism of plants and introduces us to short-day and long-day plants. What I don't understand is why short day plants will not flower if they are exposed to a very brief flash of light during the night, even if that brief period + the actual day's length is still less than their critical day length? Or, put more concisely:

Length of Flash + Length of Day < Critical Period    <-- Why does the short-day plant not flower?

The following diagram is from Campbell's and makes no sense to me, because it also seems like a long-day plant which is exposed to a brief period of light during the dark will flower even if that period of brief light + its actual day's length is not greater than its critical period (i.e. it never fulfilled the pre-requisite for flowering).

I think you are looking at other the wrong way around. There is no critical light period, there is a critical dark period. That long-day flower is also a short-night flower. As long as there is never any period of darkness that exceeds the critical dark period, it will flower.

In that second picture at the bottom, exactly that is the case. The dark period is not long enough to prevent the flowering.

And in the bottom example of the first picture, there is no uninterrupted dark period longer than the critical dark period, so the plant never flowers.


Can songbirds mimic car alarm sounds? A silly question. A few days ago I observed a very vocal bird with impressive vocal variety. It was rapidly switching from one tune to the next. After sometime I realized that the bird might be mimicking the 6-8 tone car alarm (the one that rapidly changes). Is this my imagination, or are birds really know to mimic/compete with car alarms?

You would be amazed at the vocal abilities of the lyrebird.  A car alarm is easy for them; they can mimic much more complicated sounds.

Here's a snippet from a David Attenborough BBC documentary on YouTube (which includes the car alarm example, among others).  They are so skilled, it's hard not to think this video is fake.


Mechanism by which $lacI^{d}$ is a dominant mutation, impairing the function of normal copies of the Lac Repressor Jacob-Monod model for the lac Operon was based on experiments using two strands of bacteria which constitutively expressed $\beta$-gal: $I^{c}$(mutation in the gene lacI , which encodes the repressor) and $O^{c}$(mutation in the operator, the site where the repressor binds).

$I^{c}$ mutants are usually recessive: the Lac Repressor cannot bind to the operator, however, if a wild-copy of the gene is present in a merodiploid, the inducible pattern of expression is restored, because the Lac Repressor acts in trans (that is, it will inhibit expression of both operons when lactose is not present).

However, I've read that there's a strain ($lacI^{d}$) which is dominant, so the expression is constitutive even in the presence of the normal repressor. According to the article linked, abnormal subunits may mix with normal subunits, resulting in a disfunctional tetramer, even if a wild type lacI is also present.
In terms of protein structure, why some mutations may have this effect and be dominant while other mutations do not interfere with normal copies of the protein and are recessive?

The lac repressor act as a tetramere molecule and requires all 4 of the subunit to be able to bind DNA to act on the operon and repress β-galactosidase expression.

The "all 4" is the key here, if any of the 4 subunits is unable to bind DNA then the whole complex cannot attach to the operon. The lacId mutation produces a repressor subunit that cannot attach DNA, yet can tetramerize with other lac repressor subunits, therefore impeding WT subunits to bind the operon.

For your question on the protein structure. Mutations can occur at different locations in a gene and therefore impact different proteins domains. Proteins contain different type of domains, such as an active site for an enzyme or a binding sites for attaching to the DNA. A mutation might act on one of the domain while leaving others fully functional.

In your case this is exactly what happens, the mutation is in the protein region involved in binding DNA but does not affect the region involved in the protein-protein binding with other subunits.


What is the difference between Regulatory Gene and Modifier Gene? If both controls the expression of another gene by physically or genetically interacting with the target gene, which attributes make "Regulatory gene" different from "Modifier gene" or vice-versa?

Different terms in different fields

I think that the two concepts are very similar but are used in different fields. The term "modifier genes" is often used in quantitative genetics and in evolutionary genetics while the term "regulatory gene" is often used in molecular genetics.

Example of a modifier gene that is not a regulatory gene

The concept of modifier gene can also be used in modelling when considering genes that "modify" the recombination rate (e.g. Otto and Barton, 2007; or other properties of the genome) in a quantitative manner. As such, a modifier gene is not really a regulatory gene (as it does not regulate the expression of another gene). As such I consider definitions like this one from ndsu as being too restrictive.

What I think about when I hear these terms

I would tend to think as a modifier as a more general concept than the concept of regulatory gene. Also, when I think of a regulatory gene, I think of this gene by the mechanism by which it affects other genes while when I think of a modifier gene, I think of the statistical effect of this gene on genetic properties of the organism.


Are humans still competing in the same way now that the first life forms did? I'm not sure if this is actually a philosophical question, but I was reading a timeline of life on earth and I came to this:

  4500-3500 Ma The earliest life appears, possibly at Alkaline vents
  with the creation of the Last Universal Common Ancestor, possibly
  derived from self-reproducing RNA molecules.[6][7] The replication of
  these organisms requires resources like energy, space, and smaller
  building blocks, which soon become limited, resulting in competition,
  with natural selection favouring those molecules which are more
  efficient at replication. DNA molecules then take over as the main
  replicators and these archaic genomes soon develop inside enclosing
  membranes which provide a stable physical and chemical environment
  conducive to their replication: proto-cells.

..and I thought to myself, are we still essentially doing that as we live our lives?  I think I'm trying to connect the idea of a human "being competitive" with "evolution".. is there any truth to that?

It's important to realise that evolutionatry competition and the common usage of the word competition do not mean quite the same thing. For example, you could talk about Usain Bolt competing in the 100m but this is only evolutionary competition with the other athletes in they are in competition in terms of evolutionary fitness. Evolutionary fitness encompasses ideas of survival, reproduction and the nurturing of offspring. The only thing that matters, from an evolutionary point of view, is how many successful offspring are produced1. Where human competition does not relate to this, it is not related to competition in the evolutionary sense.

People certainly do still compete in the evolutionary sense for mates, resources, etc. but in the West, in particular, much of human competition has become a very long way removed from anything that relates to evolutionary competition except in the most tangential of ways.

1 - my favoured definition for fitness is number of grandchildren.


Why does SDS-PAGE use for protein, and agarose use for nucleic acid? My question maybe very primary, but after I learned this part, questions always follow me.
SDS-PAGE gel works for detect protein, agarose gel works for detect nucleic acid, so here is my question:
1. Why does SDS-PAGE works for protein, and agarose gel works for nucleic acid? Is it any possible to use SDS-PAGE to detect DNA? Or use agarose to detect protein?

Why does the SDS-PAGE gel always runs vertically, and agarose gel runs horizontally? Are they necessary?
Is any other material could be use in gel electrophoresis?

You can use polyacrylamide gels for RNA and DNA, and this is the common way to examine shorter nucleic acids. Agarose gels can be used for larger nucleic acids like plasmids that are a few thousand base pairs long, polyacrylamide gels work better for shorter nucleic acids around a hundred nucleotides long.

You don't need SDS for nucleic acids, they already have a negative charge at the phosphate backbone. Polyacrylamide gels for nucleic acids also don't use a separate stacking gel like in SDS-PAGE, it is just one single gel.


Telling distance with one eye Basic mathematical/logical reasoning makes it clear that you need two eyes to have depth of vision. By seeing an object from two perspectives, our brain can calculate the distance of the object based on the angle from each eye to the object. However even when I close one eye, I am able to judge reasonably well the depth of objects. Furthermore when I look at a picture I can instantly (I tried to be as unbiased as I could about this) tell it was a picture. How are we able to do this?

Depth perception consists of what are called monocular cues and binocular cues. As you mention, binocular vision has a lot of advantages for depth perception, but it is not completely necessary.

Many animals, particularly those that don't need especially precise vision, have little to no binocular vision, opting instead for visual coverage in more directions by having eyes on the side of the head.

The Wikipedia page I linked at the beginning has a whole list of various monocular cues, but I will mention a few of them here as well that I think roughly outline the different "categories" of monocular cues.

Relative size is a simple one: you expect certain objects to be a certain size. You can use that information to approximate distance.

Motion parallax: moving relative to objects gives you more information. Nearby objects move very quickly across the eye when you move, far away objects do not.

Accommodation: when you focus on a nearby object, you can estimate the depth by how much the lens needs to be deformed to bring the object in focus. The brain gets a copy of that muscle signal that it can use to estimate distance for nearby objects.

Although monocular depth perception is actually quite good out in the natural world, it is possible to trick the system with sufficiently clever strategies, like many other types of optical illusions. The Ames room is one of these.


Do Archaea have membrane-bound organelles? From Campbell Ch. 6 Intro to the Cell,

Which of the following statements concerning bacteria and archaea cells is correct?

A) Archaea cells contain small membrane-enclosed organelles; bacteria do not.

B) Archaea cells contain a membrane-bound nucleus; bacteria do not.

C) DNA is present in both archaea cells and bacteria cells.

D) DNA is present in the mitochondria of both bacteria and archaea cells.

(A) is correct. My logic was that Archaea and Bacteria were originally from the same family as they are prokaryotes with membrane-less organelles. Is this thinking correct? If not, where am I wrong?

A) Archaea cells contain small membrane-enclosed organelles; bacteria do not.

FALSE. As you said, Archaea and Bacteria are prokaryotes: that don't have any nucleus nor membrane-bound organelles.

B) Archaea cells contain a membrane-bound nucleus; bacteria do not.

FALSE. See comment above.

C) DNA is present in both archaea cells and bacteria cells.

TRUE. Apart from some kind of viruses, all living organisms* have DNA as the support of their genome. It confirms that other choices are false.

D) DNA is present in the mitochondria of both bacteria and archaea cells.

FALSE. See comment for answer A: neither of them have mitochondria.

More info: Archaea on Wikipedia

(*) Viruses aren't always considered living organisms.


What does a female mosquito need from blood? I have come across many articles stating that female mosquitoes suck blood from vertebrate hosts to develop their eggs. Some also state that they need proteins, carbohydrates, iron etc., from human blood. But none of them (as far as I know) have stated what components exactly are needed from blood for their egg development. If proteins, what kind of proteins?

According to the Introduction to this paper:

  Attractiveness to biting insects is important in medical contexts, mostly in the dynamics of transmission of pathogens by mosquitoes that cause diseases such as dengue and malaria. Blood feeding is an essential part of the lifecycle for most mosquito species as it provides females with the proteins necessary for egg production.

I imagine that the blood protein is simply a rich source of amino acids. This is supported by the finding that an artificial meal consisting of bovine serum albumin can support egg production in Aedes albopictus.

Update following answer from Greg Thatcher

Clearly there is evidence that iron from a blood meal reaches ovaries and eggs, although the paper doesn't provide direct evidence that this iron is essential. However this made me think more deeply about the paper that I cite above about feeding bovine serum albumin as an blood substitute. Could this have also supplied a significant amount of iron? The artificial meal was BSA dissolved in a phosphate-buffered saline. The authors don't specifically address the problem of iron contamination. The main component of PBS is NaCl. If they used AR-grade NaCl then the iron content will have been very low (0.0002% in one example that I found online). However BSA itself can bind metal cations (see here for example) so the protein may have contributed some iron. The authors do quote the source of the BSA that they used but I haven't been able to access a data sheet that might shed light on the level of iron contamination.

Of course it is entirely possible that blood is an essential source of both protein and iron.


Scale up of Bacterial growth from 250mL to 1-5L? I am currently growing up a specific strain of E.Coli with a knockout in 40mL of growth medium (LB) in a 250mL shaker flask... My ultimate goal is to scale up this process to a 1-5L large scale setup for the lab. But for now I'd like to quantitatively characterize this 250mL scale using Monod Kinetics so that the mathematical model can be used to build the aforementioned bio-reactor.

Currently I am making two growth curves of the E.Coli in the current 250mL flask. One is OD vs. time and the other g.Dry mass vs. time. The idea of doing so is to ascertain the $\mu_g^{max}$ (maximum specific growth rate). However, I am stuck as to how to find the saturation constant (Ks). I am also stuck on how to measure the sugar concentration ([S]) at each time-point that I would measure the OD. The idea behind these two variables is to use the equation(s):

$D = \mu_g^{max} . \frac{[S]}{Ks + [S]}\\
D^{\ max} = \mu_g^{max} . \frac{[S^{\ max}]}{Ks + [S^{\ max}]}$

Am I looking for the right variables and/or using the right equations?

Thanks again for your help!

Michaelis-Menten:

$V=V_{max}.\frac{[S]}{Ks+[S]}$

Lineweaver-Burk:

$\frac{1}{V}=\frac{Ks}{V_{max}[S]}+\frac{1}{V_{max}}$

Plot $\frac{1}{V}$ vs $\frac{1}{[S]}$; find the slope and intercept of this plot.

Depending on what you consider as primary substrate (glucose??) measure the concentrations using appropriate assays. Glucose sensors (based on glucose oxidase) are available or you can do conventional biochemical assays (DNSA) for glucose and other reducing sugars. To find the growth rate, measure OD at different time-points and get the differences of OD in a time interval. A better method would be to make a scatter-plot of OD and time and fit a polynomial function. Get rate by taking the tangent of the curve at that time-point.


Barr body in mitosis In early embryonic development, some female cells pass through a process called lionization and one of the X chromosomes get condensed and began to be called Barr body.

What I don't understand is how the Barr body behaves during mitosis. Specifically, if a cell had condensed a paternal X chromosome, all of its children will have a paternal Barr body. But aren't  the barrbodies supposed to decondense to be able to be copied during mitosis? If so, when they recondense, why isn't the choice of which chromosome will condense random?

Thank you!

X inactivation is mediated by several epigenetic marks on DNA that cause condensation into heterochromatin. These include DNA methylation and histone modifications:
https://en.wikipedia.org/wiki/X-inactivation#Silencing

As you suggested, a newly copied DNA strand would be free of the epigenetic marks that mediate heterochromatin condensation. Yet epigenetic modifications are inherited, along with DNA molecules, by the daughter cells during cell division. That is, cells have ways of copying these modifications from the old DNA strands to the new ones. These mechanisms are not all known, and are the subject of much research.

In this fashion, each cell division produces two cells that inherit the X-inactivation status (i.e. heterochromatic state) of the parental cell.

This cycle of epigenetic inheritance only ends when the chromosomes are reactivated in primordial germ cells before meiosis and the production of eggs or sperm. The embryo of the animal's offspring can then make that initial, random X chromosome inactivation that is inherited by all of the cells in its body.


Does SARS-CoV-2 kill its host cell or not? Wikipedia says that

Initial spike protein priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS-CoV-2.After a SARS-CoV-2 virion attaches to a target cell, the cell's protease TMPRSS2 cuts open the spike protein of the virus, exposing a fusion peptide in the S2 subunit, and the host receptor ACE2. After fusion, an endosome forms around the virion, separating it from the rest of the host cell. The virion escapes when the pH of the endosome drops or when cathepsin, a host cysteine protease, cleaves it. The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus, which infect more cells

What happens next? Can this cell stop to produce the virus and start to divide ?
For example this article (SARS-CoV-2 RNA reverse - transcribed and integrated into the human genome) suggests that virus also inserts its portion into DNA so the person can have PCR-positive tests even if "no replication - competent virus was isolated or spread from these PCR-positive patients".

The answer is yes, as there is no indication that SARS-COV-2 is an exception to the rule.
Cp., for instance: SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation,   Shufen Li, Yulan Zhang, Zhenqiong Guan, Huiling Li, Meidi Ye, Xi Ch https://www.nature.com/articles/s41392-020-00334-0
On exceptions to the rule cp., for instance
V. Kaminskyy, B. Zhivotovsky, To kill or be killed: how viruses interact with the cell death machinery
https://pubmed.ncbi.nlm.nih.gov/20433575/
In my opinion, only in the context you cited your question seems a still open one:
https://www.sciencemag.org/news/2020/12/coronavirus-may-sometimes-slip-its-genetic-material-human-chromosomes-what-does-mean
"... Baltimore says. “It is also not clear if, in people, the cells that harbor the reverse transcripts stay around for a long time or they die.”
However, this statement does not contradict the general rule that cells infected by viruses finally die.
There is always, as cited, some "staying around" - otherwise the immunogenic mechanism of presenting antigen would not exist.
As for retro viruses, host cells might divide, thereby multiplying the integrated genome of the virus, so one might speak of "no dying" as in such case the cell is still able to divide. However, that should be seen as only "staying around" for a very much longer time, as every infected cell will sooner or later become the retro viruses' friendly host - if that cell hasn't died before  because of other reasons:-) Still, if CoV-2 were a retro virus the answer to question had to be "no" - but it is not, CoV is no retro virus.
Refering to integration by LINE elements: this is different from retro viruses and it might be an open question, see the text passage cited, if the integration as a  coincidental and irregular  one (that should be current common belief)  does interfere with viral replication of CoV-19. In the study cited it is suggested that the RNA of the virus that has been retrotranscribed and integrated into the host's DNA is being read and transcribed to viral RNA. Interestingly, at that point  the study speaks of viral "chimeric RNA" being detected,  not viral proteins that maybe have not been searched for. The study also speaks of antigen that has been transcribed and translated from retro-integrated RNA may still be presented (on MHC) to immune cells. The latter possibility might be ruled out if viral proteins or peptides have not been found - in that case it is much more probable that the expression of viral genes has stopped the host from producing virions which is in line with a known strategy of "restriction" (e.g. by small or large interfering RNA).
In other words: to me it is highly probable that the reading of integrated viral RNA is   a mechanism of "restriction" in  a wider sense in that by activating the transposon after integration  the cell activities that would help the invading virus to replicate are being halted which different from o known defence mechanisms in bacteria/procaryotes leads to cell death probably by apoptosis, but maybe by necrosis.
This indeed seems coherent to "cytokine storm" as a reaction to SARS-Covid not of the adaptive but the innate immune systems that tries to clear up dead cells.
Another argument pro cell death  is the fact that - maybe contrary to common belief - it does not seem a seldom and random event that viral RNS becomes integrated as the study's outcome apparently is a  "first hit - success". To my mind, the  - disputable -  fact that there are no viruses that infect cells of the germ-line with the exception of certain retro(!)-viruses, cp.  https://en.wikipedia.org/wiki/Endogenous_retrovirus, https://www.sciencedirect.com/science/article/pii/S0014579300016069, https://www.sciencedaily.com/releases/2019/10/191010113231.htm  can be reconciled with and thus corroborates my opinion that integration of viral genes as transposons a. is no rare event and  b. leads to cell death in eucaryotes because, otherwise, the  integration of transposons the activation of which leads to apoptotic processes in stem cells  might put the indivual if not the host species at risk.
In my opinion it is a possibility that the LINE insertion is part of a yet rather unknown  "restriction process" of certain infected cells  that interferes with viral replication. The study found viral RNA transcribed from DNA that had been successfully integrated into cell's genome. The RNA found in samples might be some "interfering RNA" of some mechanism of "restriction".  If this is correct, it seems a possibility that  cells stays alive with viral genes integrated and - refering to maybe the gist of your question - divide and multiply, in an attempt to replace other cells who were not successful with this restriction strategy. Moreover, those successful restrictive cells might (seems like a paradox) NOT  present antigen to cytotoxic T-cells, and not get killed by those. However, I think this is highly unlikely. Much more coherent with findings of chimeric RNA is some induction of cell death by expression of integrated viral genes. It is known that active transposons can interact with genes they transpose to, leading to heritable disease (in eukaryotes). That should be - next to adaptive immune system defence -   another way infected cells die altruistically, in order to stop the progression of viral invasion.
In any case, the answer is: yes, cells infected by SARS-CoV-2 die.
Still, it is a possibility that "successful restriction" (integrated RNA becomes interfering RNA) leads to destruction of the virus, as this seems to be a known defence outcome in the bacterial world. However, the findings - RNA detected outside cells  - suggest that apoptosis or necrosis is the way to die for human cells infected by CoV-19.
Hint:  In any case, the fact that killer cells of the immune system lead to apoptosis of infected cells does not imply that a cell would survive an infection (if it were not for the killing by killer cells).


What sort of biofiltration is best for a small, portable, biofiltration unit? I've been exploring the idea of a system to allow re-use (drinking) of RV greywater, or at least the freedom to dump in storm drains (I think the requirements are looser about this, but it still has to be somewhat purified)

Greywater is wastewater that does not contain feces. The primary contaminants would be food waste, various soaps (probably only biodegradable or non-antibacterial), and used shower water. I would also probably add urine, after sterilization to remove pathogens.

I was thinking of pre-filtration to remove larger fragments and detritus. Probably with the highest grade of this

-Processing rate would have to be 10 liters per day absolute minimum. 2x to 3x that would be best.

-Weight and volume are both at premium

Any kind of sponge and pump filters will breed nitro bacteria to remove organic content. Added to a drip filter made from pure mineral sands and clays, you'd have a bacterial sponge and plant aquarium plus a sand filter.

You can make you own activated carbon too.

Urine requires at heavy plant growth to purify. You already have a tank, volume not given so I'll say it's 125 L. Here's a two stage bio filter: one with an incoming and circular bacterial filter to filter incoming water in graded sponges up to about .05 - 1 mm finest incoming particles for foods and stuff.  Use 2 divisions in the tank, one of 100 L, one of 25 L that you can prepare 10 L from every day.

Use 2 fish filters AC of 7 - 20 watts (?) or 12 V (DC) pumps similar to fish ones. Use 500 ml - 1L volume of filter sponges with fast access so you can squeeze out the bacterisl mats periodically because they will fill with nitrogen and phosphate and oxygen based pond organisms.

If you can fill the 100 liter tank with algea, it's ideal.

Put a valve to keep 2nd 25 L tank separate. Filter final 10 L drawn daily through mountain mineral sand from places with great spring water, i.e. dolomites / chalky to add trace elements. It's recommended you use sunlight and lots of plants in the first tank.


What makes/breaks the hydrogen bonds between DNA and RNA during transcription? So I know that RNA polymerase catalyzes the phosphodiester bonds that hold the sugar backbones of a growing mRNA molecule together during transcription. However, I'm less sure about the hydrogen bonds between the nitrogenous bases of the forming RNA and the template DNA strands.

I do assume that hydrogen bonds are forming, but they must be short-lived.
Their existence are confirmed here:

  ribonucleotides containing 3 phosphate groups hydrogen bond through the process of complementary base pairing with the exposed deoxyribonucleotides on the unwound strand that is to be transcribed

and represented in this gif:

Is RNA polymerase responsible for creating the hydrogen bonds between DNA and RNA? Is it, then -- I assume -- also responsible for breaking these bonds? Are the breaking bonds driven by chemical reactions or more due to the physical movement of the polymerase along the DNA template?

This site mentions the transient H-bonds formed by holoenzyme at promoter sites, but I haven't been ale to fnd a reputable source discussing the transient H-bonds between nucleic acid strands.

I'd appreciate if someone can provide a clearer molecular description of what's going on here. Pictures/animations are a plus!

I wouldn't really say RNA polymerase is "creating" the hydrogen bonds so much as it's thermodynamics that creates them. When we talk about an enzyme "creating" a bond, what we're generally referring to is an enzyme facilitating a reaction by lowering its activation energy so that it can proceed.

However, in the hydrogen bonding between base pairs, there's not really much activation energy to overcome. Before the formation, the nucleotide is just floating around in the cell (solvated by water), and forming a base pair is more energetically stable than not being paired. When a ribonucleotide happens to diffuse into contact with the unpaired DNA strand, the hydrogen bond will spontaneously form because it's energetically favorable. The thing about hydrogen bonds, though, is they're fairly weak, so there's an equilibrium between formation and breaking. When a mismatched nucleotide diffuses into that space, the hydrogen bonding isn't as strong, and it might be in an improper orientation, so it'll diffuse out again. When the correct nucleotide enters, the hydrogen bonds will form spontaneously, hold it there longer, and orientate it properly. This properly places the phosphates for backbone formation, which allows RNA polymerase to proceed with making the backbone.

As for the breaking of the hydrogen bonds, it's the energy released from the phosphodiester bond formation that causes the bonds to break at the other end of the RNA-DNA hybrid. To simplify things a lot, it's kind of like a zipper, where forward translocation of RNA polymerase along the DNA strand is driven by phosphodiester bond formation, which breaks the hydrogen bonds of the RNA-DNA hybrid somewhat mechanically, as the nascent RNA strand leaves through a different channel than the DNA does.

References:

Structural Model of RNA Polymerase II Elongation Complex with Complete Transcription Bubble Reveals NTP Entry Route

Transcription elongation: Heterogeneous tracking of RNA polymerase and its biological implications


Normal ECG/EKG Measurement? I'm getting started using ECG using a 3 lead system by iWorx. I have place the leads on my two wrists and the ground on my ankle and have recorded some data into the provided LabScribe 3 software using the ECG template. Can anyone help me interpret what I'm seeing?

It doesn't look like the standard QRS I see in my textbook, but it's so regular (this is just a snippet) that I don't believe I'm seeing artifacts.

Any insight would be greatly appreciated.

Thanks!

If you're looking for an explanation of the parts of the waveform you recorded, here's an annotated version:

I hope that helps you map it back to the "standard" QRS you saw. The AV delay is the time between the depolarization of the atria and the ventricles.

I agree, the T-wave is too intense. I'm not familiar with a 3-lead ECG that connects to the wrists--I'm more familiar with chest ECGs. I'm guessing the large T-wave is an artifact of measuring through the wrists (hopefully it's not indicative of a health condition such as Hyperkalemia). It looks like your resting heart rate is around 52 BPM--that's healthy.

The signal itself comes from the heart muscles. It takes a number of milliseconds for the electrical impulse to travel from the sinoatrial (SA) node to the atrioventricular (AV) node, down the His bundle, and finally to the Purkinje fibers in the ventricles. It takes this long because the movement of charge is caused by ions in the cells physically moving. That change in charge is conducted (via normal electrical conduction, such as you see in a wire) through the tissue and muscle to the electrodes on the wrists--this conduction is effectively instantaneous (in this case, it's electrons "pushing" each other, not ions moving within cells as in the case of the heart's electrical system). ECGpedia has some good background on this.

The ECG system takes the voltage from your right wrist (call this VRA), and subtracts it from the voltage at your left wrist (call this VLA), so that Vlead I = VLA - VRA.

So, in summary, the signal you're seeing is produced by the heart's conduction system, not the muscles in your wrists. Muscle noise would manifest itself as noise or random spikes in the ECG.


Are all prokaryotic promotor regions the same, or do they differ depending on the product of the transcript? Are all prokaryotic promotor regions the same or do they differ depending on the protein encoded by the mRNA being transcribed?

What I am thinking is that if activator proteins are a method of transcription regulation, then shouldn't promoter regions differ so that activator proteins have an effect on the  expression of a specific gene?

Please tell me if this is correct, or if I misunderstand something.

Definitely not. There is a ton of variation from gene to gene, otherwise, as you say, regulation wouldn't work.

That said, the word "promoter" sometimes gets used in different ways. Especially in eukaryotic systems, people will sometimes say "promoter" to mean the entire region upstream of the gene where transcription factors can bind (for yeast, typically within a few hundred base pairs, for mammals, could be many kb away). These regions are extremely variable from gene to gene in all organisms. But for bacteria, the word is more commonly used in a much stricter sense, to mean the region where the polymerase and the associated sigma factor binds -- this is typically one or two very short stretches of DNA (maybe 5-10 base pairs) very precisely located at a specific position from the start of the gene. These regions are much more conserved, but there will still be some variation. Check out http://nar.oxfordjournals.org/content/40/7/2907.full for a very detailed characterization of some of these sequences in E. coli.


Help with understanding XKCD's “How Vaccine Failure due to Viral Vector Immunity Works” Why is this response a failure exactly? Full disclosure; no biology since 9th grade, so please go easy on me!
XKCD's 2406 shows a literal wooden Trojan Horse outside a castle, but instead of bringing it inside the castle walls, the soldiers recognize the shape as horse-like:

Look! It's a statue of that horrible animal that trampled Steve!

and the soldiers decide to destroy and dispose of it rather than to let it in.
The title of this XKCD is

Viral Vector Immunity

with the subtitle

How Vaccine Failure Due to Viral Vector Immunity Works

Wikipedia's Viral_vector; Vaccines explains the basic idea, which is (I think) that the viral vector's genome is modified so that it includes a new protein on its surface that serves as an antigen, and the host builds and learns an immune response to this antigen that will then immunize the host against an infection by another organism that also presents this antigen.
Question: The XKCD shows recognition and an analogy of an immune response, so why does the subtitle call this a "Vaccine Failure"?

XKCD image License

Yes, the cartoon is a description of immune action.
Traditionally shown is first exposure being a vaccine, and the second exposure being the bad virus being destroyed.
However, this cartoon is describing viral vector immunity.
The first exposure is a viral vaccine. This alerts and educates the immune system about not just the intended antigen, but also the (harmless) carrier virus which is represented by a horse.
The second exposure is a different viral vaccine.
The immune system immediately mounts a successful response against the vaccine because is recognises the carrier virus.
So the immune system doesn't get the chance to learn about the antigen associated with the second virus.
A example of viral vaccine failure would be useful - I will see if I can find one if no-one else does.


Definition of "Regime of selection" How would you define Regime of selection (or Selection regime)?

In addition to a accurate definition, a developped example would be very welcome!

I'll kick this off with an attempt at a definition: a selection regime is

the set of selective pressures on a population

As in, "alteration of selection regime resulting from harvest" (Mooney & McGraw 2007)

or "Human-induced nutrient input can change the selection regime and lead to the loss of biodiversity. For example, eutrophication caused speciation reversal in polymorphic whitefish populations through a flattening of littoral–pelagic selection gradients." (Hirsch et al 2013)

 Hirsch PE, Eckmann R, Oppelt C, Behrmann-Godel J. 2013. Phenotypic and genetic divergence within a single whitefish form - detecting the potential for future divergence. Evolutionary Applications 6: 1119–1132.
 Mooney E, McGraw J. 2007. Alteration of selection regime resulting from harvest of American ginseng, Panax quinquefolius. Conserv Genet 8: 57–67.


Systematic difference of diversity between sister taxa? When looking broadly at the tree of life, my feeling is that, after a divergence there is almost systematically one taxon that speciates way more than the other.

(There will have some approximations below it is not really the point of my question to discuss whether the urochordata is a sister group to the vertebrates or not.) Let's look at the kingdom Animalia for example:

Chaonflagellata vs "the others"
Sponges vs "the others"
Cnidaire and cténaire vs "the others"
Protostomia vs Deuterostomia (both are fairly equally diverse diverse! Some might not be happy with this claim!)...let's continue with the Deuterostomata
echinodermata vs chordata
cephalocordata vs vertebrata

etc ...

My questions:

Is there really a systematic difference in diversity between the branches?
Is this difference can be explained by chance?
Is it only a bias due to out ability to recognize more species in animals that look more like us (or a bias due to something else)?
Does it make sense to say: the more diverse is a taxon, the more likely it is that it gets even more diverse (because each species might have an equal chance to speciate or something like this)?

Bond and Oppell address your question points one, two and three empirically by looking for what they call "unbalanced bifurcations" as a sign of adaptive radiations in a well-resolved phylogenetic tree (spiders), and find that the number of unbalanced bifurcations does indeed exceed what they would expect to occur by chance.

As you mention and as I suggested in the comment, there are some serious problems that arise in trying to answer your question. Many of these are well presented in Cracraft, including assuming that higher taxa are comparable with one another, making arbitrary choices about what rank of taxa to compare, ignoring counterexamples, and qualifying rather than quantifying diversity. I think that Bond and Oppell effectively address most of these problems through rigorous, apriori definitions.

There's a diversity of opinions and evidence from biological systems on your fourth question point. Bond and Oppell connect these significantly unbalanced bifurcations to key traits (like orb-weaving) that open up new adaptive zones. I suppose therefore they might say that there's a fundamental factor (a key trait, and therefore open adaptive zones) driving diversification, and therefore might not agree with you that diversification would necessarily beget more diversification (at least, not in the absence of open adaptive zones). For instance, in Hawaiian tetragnathid spiders, ecomorph niches on an island are filled either through immigration from another island or through adaptive diversification (Gillespie). No ecomorph is represented by two sympatric species, so a niche filled by immigration will presumably not spur adaptive radiation. However, species radiations in Andean lupines (Hughes and Eastwood) and plethodontid salamanders (Kozak et al) seem not to have been accompanied by any key traits or particular ecological opportunity, and could theoretically be driven by the self-reinforcing mechanism you propose. As a related point, I suppose more diverse lineages could be less likely to go extinct; which could support diverse lineages becoming more diverse.

 Bond JE, Opell BD. 1998. Testing adaptive radiation and key innovation hypotheses in spiders. Evolution 52: 403–415. (Behind paywall, free pdf here).
 Gillespie R. 2004. Community assembly through adaptive radiation in Hawaiian spiders. Science 303: 356–359. (Behind paywall, free pdf here)
Cracraft J. 1990. Origin of evolutionary novelties: pattern and process at different hierarchical levels. p. 21-44 in Evolutionary Innovations, ed. M. Nitecki, U Chicago Press.
Hughes C, Eastwood R. 2006. Island radiation on a continental scale: exceptional rates of plant diversification after uplift of the Andes.
 Kozak KH, Weisrock DW, Larson A. 2006. Rapid lineage accumulation in a non-adaptive radiation: phylogenetic analysis of diversification rates in eastern North American woodland salamanders (Plethodontidae: Plethodon). Proceedings of the Royal Society B: Biological Sciences 273: 539–546.


How do cells age and die if they are dividing into new cells? If cells in our body keep on dividing into new cells how do they ever grow old?

The only cells to grow old would be defunct cells or those who won't divide into new cells like nerve cells.

What am I missing here?

Human chromosomes contain certain DNA regions called telomeres. These regions are shortened on each cell division and once they are gone, the cell cannot divide. Therefore an average cell in our body can divide only about 50 times.

There are indications that longer telomeres may increase lifespan, however this remains controversial. Telomeres are believed to be a method of higher organisms to prevent uncontrolled cell division and cancer, therefore artificially increasing telomere length may not lengthen but shorten lifespan because of increased cancer risks.

Also, ageing is not (only) caused by individual cells growing old. Often it is the organization between the cells that breaks down. Scarring is a good example for this. The wound is closed but the tissue inside the wound was not able to organize into functional skin tissue again but rather "patched up" the wound with comparatively unorganized tissue.

The brain is another extreme example of ageing by disorganization. It has been shown that even adult brains contain neuron progenitor cells (albeit fewer than other tissues) so even adults can regrow neurons in the brain. However, while the cell body of the neuron can be replaced, all its (sometimes thousands) of connections to other neurons are lost. Therefore, brain tissue can be regenerated in principle, but the information it contained cannot.


What is the difference between a circular and a cat's-eye (slit) pupil? I've been to local zoo the other day and one lizard caught my attention: its pupils are circular, which, I thought, is not usual for reptiles. Turns out it is, but now I can't find any explanation on why some animals have one kind of pupil and others have the other. Lizards can have both, and so can snakes. The only difference I have found is that circular pupil can't shrink quite as much as a cat's-eye pupil, but that hardly explains why circular pupil even evolved in the first place as I don't see any advantage to it.

Ideas?

P. S. Fish only have circular pupils so that shape is older, right?..

Circular pupils are always functionally superior to vertical pupils; a slit does not correctly focus light from all directions whereas a circular pupil does. If you observe cats when they're hunting at dawn and dusk*, they have big, circular pupils; it's only when they're in bright light that the pupil shrinks to a slit. So why have vertical pupils at all? Because, as you mention they're capable of letting a more controlled range of light into the eye.

Thus vertical slits let you be active in a wider range of light conditions at the cost of poorer vision in bright light; whilst circular pupils continue to function well in brighter light but at the cost of not allowing such a large range of control over the amount of light entering the eye.

It is then easy to see why you get both kinds of pupil: circular pupils are favoured by animals that are typically active in bright light and need good vision under these circumstances; vertical pupils are favoured by animals that are primarily active in low light but need some ability to see in bright light.

*- it's often stated that cats are nocturnal, this is untrue; cats are crepuscular - that is they are most active at dawn and dusk.


Are tumor-associated antigens unique to cancerous cells? Are tumor-associated antigens found only on the membrane of cancerous cells or just over-expressed on the membrane of carcinogenic cells?

In other words, are these antigens also found on healthy cells?

Carcinogenic tumor associated antigens correspond to any peptide chain (antigen) which triggers an immune response from the host. This means that they can be found anywhere inside, at the membrane, and outside of the cell: inside the cell (intracellular), at the cellular membrane and exposed to the extracellular environment, or even secreted.

Depending on the oncogene, they can be also eventually be over-expressed (anywhere there are supposed to be, including the membrane of cells).


Is extreme cladism a mainstream position in the species debate? In the philosophy of biology it has been claimed many times that a popular position regarding the question of what species are, among biologists, is cladism. For my current purposes, the defining trait of cladism is captured in the following quote:

According to cladism, a species becomes extinct whenever it sends forth a new side species. (LaPorte 2004, 54)

So, for example, if Homo floresiensis is truly a species, and it derives, via a speciation event, from Homo sapiens, then, after the speciation, there is no Homo sapiens: there is Homo floresiensis and a new species, very similar to sapiens. In general, whenever there is speciation the mother species disappears.

I am under the impression that this description of the situation is not the one most mainstream biologists would endorse. I take it that a more common description would be one under which, if a number of Homo sapiens get isolated in an island and go on to form a new species, Homo sapiens exists both before and after this speciation event. I would like to know whether cladism, described as above, is really a popular position, or whether I am right about what most biologists would say about the relation between floresiensis and sapiens.

It might also be that biologists declare themselves cladists when explicitly theorizing about the nature of species, but fall back to a less extreme form of cladism in the actual practice. Evidence in favour of or against this possibility (coming from biology, not the philosophy of biology) would also be appreciated.

As Noah has pointed below, what I have called extreme cladism might be very far from cladism, as usually interpreted. This is precisely the kind of claim I would like to see substantiated.

  LaPorte, Joseph. 2004. Natural Kinds and Conceptual Change. Cambridge University Press.

I've never heard of it, actually - though I can't speak for my professors or researchers I know, none have ever presented the Cladism argument as an argument for the delineation of species.

As far as I'm aware, the attempts to define a species fall along three lines:

The ability to produce fertile offspring in the wild.

Distinct physical characteristics.

An arbitrary amount of genetic divergence.


Where are eosinophils and basophils phagocytic? It seems known that neutrophils circulate and are phagocytic within the blood stream, but I'm having trouble finding similar conconclusions about where eosinophils and basophils are phagocytic which are less common.

Also to add to this - lets not forget that these cells can function differently in circulation, compared to when they enter in tissue. They look morphologically different, and often one can see phagocytic vacuoles present in the cytoplasms..meaning they probably do participate in some minor "cleaning up" , but like the above poster mentioned, primarily they release granules into the environment wherever they detect damage, or antibody reactions.


Confused with gamete sorting problem A man has the genotype AaBbCc, in other words he is heterozygous in three uncoupled loci on three different chromosomes. A, B and C are the dominant alleles while a, b and c are the recessive alleles.

1. How many gametes can he form?

The answer is 8 and I can see how you derive that by just manually writing each and every one down but what is the mathematical method to derive this? I tried permutations but none I came up with worked.

2. He has a child with a woman of the same genotype (AaBbCc) how many different genotypes can the offspring have?

Here the answer is 27. I'm not sure how they came to this conclusion either?

3. What is the probability that the offspring has the genotype AaBbCc?

This is about the time I start flipping tables because it seems to me that it's 1 out of 27. There are 27 different genotypes and this is ONE of them?!

But the answer is 1/8 as there's a 50% chance of Aa, Bb and Cc when mixing apparently so it becomes 1/2*1/2*1/2. Why isn't it just 1 of the possible genotypes?

Since there are 2 alleles of each gene and 3 different genes, 2EE3 = 8? Let's test this by making a table, for 1 gene there are two different kinds of gametes, so 2EE1 = 2, for 2 genes there are 4 different kinds of gametes (AB, Ab, aB, ab) so 2EE2 = 4, and you already did the calculation yourself for 3 genes, and 2EE3 =  8.

Why don't you try working it out yourself for 4 genes and see if you come up with 16 different kinds of gametes?

Two words: Punnett Square. In this case for a trihybrid cross:

That is a Bernoulli coin-flipping probability. If you are flipping a true coin three times in a row, how often will you get three heads in a row? 1/8? All the events are independent, right? what about the Punnett square? Does it give the same result somehow?

Here is the answer worked out for you.