More extreme phenotypes when parents are from diverged populations In quantitative traits we have many loci affecting a trait. If we took a bunch of parents where all mothers and fathers were of a certain value at the upper end of a trait range, and then looked at the offspring would we expect offspring from pairs of parents from more divergent populations to be even more extreme variance in their traits?

For example: if we look at 2 men from East Africa, both 190 cm tall. They each have children with women who are 180 cm, one of whom is from East Africa and the other from Canada. We could assume that the Canadian woman is probably more unrelated to her male than the East African woman. I would therefore expect that it is quite likely that the East Africans in the example are tall because of "tall-alleles" in many of the same loci, whereas there is a greater probability that the Canadian female is tall thanks to mutations at different loci. Therefore would it be reasonable to expect greater variation in the offspring of the Canadian woman?

Is there any evidence of this phenomenon?

Note: Ignore environmental and gene * environment interaction variance, just go with a simple additive model, and assume populations have had some barriers to migration for some time

Yes, it would be reasonable to expect greater variation in the offspring of the Canadian woman.
Human genetic variation is the genetic differences among populations. Populations have access a pool of genes and over-time polymorphisms may arise to create greater variation.
Human populations within a species are defined by, divergence times and rates of gene flow - From mitochondrial, X and Y chromosome re-sequencing data.
Genetic Distance is the genetic divergence between species or between populations within a species (as in your example above). Populations with many similar alleles have small genetic distances. This indicates that they are closely related and have a recent common ancestor.
E.g. Height as you use for your example is a polygene. The inheritance of many genes alter phenotypic height of offspring.
Thus, it would be reasonable to expect a difference in allelic variations pertaining to height from the Canadian woman. The offspring may have a different height profile of alleles, and thus a different phenotypical height.
I should mention that:

"individuals from different populations can be genetically more similar than individuals from the same population"

But the above example - should not be expected.


Is it possible to sequence only the 16S rRNA component? If so, how? There have recently been several papers on using 16S rRNA as a way of identifying species (here, and here). I'm wondering if it's possible to sequence either just that subunit of the ribosome or just the sequence of DNA that it comes from (probably not, I know). That way you can use only the sequence you need to compare against other 16S rRNA sequences to test for novel species.

If so, what is the process involved?

Basically, all 16S genes are highly conserved, i.e., they share much identical bases. This means one can bind the 16S gene piece (after DNA was cut) to a specific other piece of DNA, even if you don't know exactly the 16S gene bases. Everything else is discarded then. Now finally, using PCR the rest is amplified and sequenced. Sequencing 16S only is much less work, so that's how they did it years ago. Today, whole microbiomes are sequenced by professional labs.


Can neurons be inhibited with electric current? It is well known the electricity can be used to fire neurons. But can it be used to inhibit neuronal firing? This is in the context of extracellular stimulation. In extracellular stimulation, it is known that there is a threshold for stimulation and a threshold for damage(electroporation). Is there a threshold in between these two which inhibits neuron firing without any damage? Please provide reference for your answer.

Yes, but maybe not how you think.

It is important to recognize that voltages refer to potential differences. When we say the "a cell is at -65mV" for example, we mean "The potential difference across the cell's membrane to the extracellular space is -65mV." When you stimulate electrically, you create a transient electric field, whereby the extracellular space is no longer effectively isopotential.

Let's imagine for the sake of some neuron that this field strength is on the order of 40 mV across the membrane. If this electric field is perpendicular to some neuronal process, the voltage across the membrane will be about -105mV on one side, and -25mV on the other side. The -25mV side is now depolarized enough to open voltage gated sodium channels, and some current is flowing into the cell. Once the shock has passed, positive current will continue to flow through those open channels and open more channels. It doesn't matter much that the other side is transiently at -105mV, all that matters is that you opened a bunch of voltage gated sodium channels which starts a positive feedback loop.

Therefore, transient electrical simulation will almost always be excitatory. There are two exceptions:

1) Neurochemical inhibition. If you excite a particular brain region that is specifically inhabited by inhibitory projection neurons, you will primarily excite those inhibitory cells and therefore cause excitation elsewhere. Of course, in this case, the electrical stimulation itself is still directly exciting cells, they just happen to have inhibitory effects elsewhere.

2) Depolarization block. If you continually stimulate the same population of neurons with a high-frequency stimulation, you can put neurons in a state called "depolarization block." Voltage-gated sodium channels have a chance to inactivate whenever they are activated. If you inactivate enough channels, there aren't enough available to produce an action potential. Therefore, if you can keep a cell pretty much constantly depolarized by continually stimulating, you can prevent action potential propagation because too many of the voltage gated channels in the axon initial segment are inactivated.


What are the application areas of Pattern formation studies specific to biology? I was reading about reaction-diffusion processes, morphogenesis concept by Alan Turing and works of Murray in describing pattern formation on animals etc. But one question which came to my mind was even if we describe these processes in mathematical and physical contexts, are there any application areas awaiting for the results?

Ok, I'm not quite sure if we are at the repairing an organ phase, but here are a few interesting examples:
1. Philip Maini at Oxford has used pattern formation to give insight into jaguar patterning: Paper. He also has a book chapter Pattern formation and wound healing that could of of interest, although I'm not sure if this is a direct application as much as a heuristic understanding of how wound healing happens.

From the biomedical side, Michael Levin at Tufts is doing amazing work in regenerative medicine, and a lot of what he does is inspired by pattern formation as well, although I am not sure if it explicitly uses the theory - his papers.
This paper is one of my favorite from Ron Weiss - engineered pattern formation. Will most likely have important biomedical applications some day, although not currently.


Can heritability be deduced from a correlation coefficient? I am trying to understand the concept of heritability and from what I can gather, the heritability of a factor (say birth weight) must be closely related to the correlation coefficient of that factor when you do a linear regression of the factor between parent (say mother) and child.

So my question is this - is it possible to calculate the heritability from the correlation coefficient, and if so, what is the formula.

No. But a strong correlation may nevertheless be an indicator for heritability (it makes it more likely).

The reason is, that the correlation in the phenotype (birth weight) is not only due a correlation in the genotype but also a correlation in the environment of the child and its mother (culture, economical situation, genes, etc of their respective mothers).

If you were able to remove the association of the environments and of the genotypes and the environments by an intervention (eg. shuffling the zygotes (ideally of parents who were shuffled as zygotes as well)) then the correlation coefficient of the phenotype between one of two parents and the child would be half the heritability. $corr=\frac{1}{2} H^2$

Phenotype ($P$), Genotype ($G$), Environment ($E$)

$P_{parent}=G_{parent}+E_{parent}$

$P_{child}=G_{child}+E_{child}$

$
\begin{eqnarray*}
corr(P_{parent},P_{child}) &=& \frac{COV(P_{parent},P_{child})}{\sqrt{VAR(P_{parent})}\cdot \sqrt{VAR(P_{child})}} \\
&=& \frac{COV(P_{parent},P_{child})}{ VAR(P)}\\
&=& \frac{COV(G_{par}+E_{par},G_{chi}+E_{chi})}{ VAR(P)}\\
&=& \frac{COV(G_{p},G_{c})+ COV(G_{p},E_{c})+ COV(E_{p},G_{c})+ COV(E_{p},E_{c})}{VAR(P)}\\
&=& \frac{\frac{1}{2}VAR(G)+ COV(G_{p},E_{c})+ COV(E_{p},G_{c})+ COV(E_{p},E_{c})}{VAR(P)}\\
&\overset{(1)}{=}& \frac{\frac{1}{2}VAR(G)}{VAR(P)}\\
&\overset{(2)}{=}&\frac{1}{2}H^2
\end{eqnarray*}
$

$(1): \,\,\,$if you managed to get $COV(G_{p},E_{c}), COV(E_{p},G_{c}),COV(E_{p},E_{c}) = 0 $

$(2): \,\,\,H^2=\frac{VAR(G)}{VAR(P)}$ - the definition  of heritability


Enzymes and plasmids A high school class has analyzed plasmids by the help of restriction enzymes and electrophoresis.

The class got delivered two different plasmids, pBR 322 and pC 508. These two plasmids were going to be clipped by EcoR I and Hind III.

Figure 1 shows the two plasmids with specification of the two cutting points for EcoR I and Hind III.

Furthermore, the cutting points are also shown for the enzyme Pst I.

In figure 2 you can see the result of the restriction analysis.

Questions:

1) Analyze and explain the results in figure 2

2)  What DNA-pieces would be formed if you had clipped with Pst I ?

1) You can see that the figure is showing the result of the restriction-analyzis. As for the plasmid pBR 322, you see that the result of the cutting of Hind III and EcoR I, is that both enzymes have the same size. Figure one shows that Hind III cuts over 0 bases and EcoR I cuts at 0 bases.

In pC508 you see that both enzymes have cut two times. EcoR I have cut at 1200 and 5800 bases, which you can see on figure 1. You can see the result of this in figure 2 (the gel electrophoresis). Hind III cuts at 6400 and 1200 bases, which again is an explanation as why the DNA-molecyles (figure 2) have different size.

2) If Pst I was used instead on the plasmid pBR 322, you would get the same size as Eco and Hind, because they all cut one place. If you had cut in pC508 you would get the bases 4800 and 6700 (as figure 1 shows)

Are these questions correctly answered?

Your estimation of the sizes of the fragments for pC508 are incorrect.

Look at the size of the plasmid at the center of the circle.The size of your fragments has to add up to that number. So if you were sure that one fragment was 1000bp, then the other fragment would need to be 6300bp.

You should also notice that fragment sizes for EcoR1 and HindIII digests should not be the same size.

You also need to say something about the type of DNA you have in the pBR322 lanes. Is it linear, circular, supercoiled?

For question 2, your explanation for pBR322 is okay, you should still mention the type of DNA you have in those lanes.

You need to explain not only where PSTI cut but also the size of the fragments that it produces.

A place where a restriction enzyme cuts is called the restrictions site, so instead of saying cuts in one place, or two places, you should say at a single restriction site, etc.


Predator prey interaction I went through a line in my textbook which read:

  "But for predators, prey species could achieve very high population densities and cause ecosystem instability."

I was not able to understand the meaning 'but for predators'. Can anyone please help me to interpret it's meaning?link to page where this line is mentioned

Edit: In terms of biology, I was unable to understand the meaning of the sentence,  and I wanted to make sure that I don't misunderstand things... And this is why I posted the question.. I feel that the answer given is correct and in case, you find better explanation, please do post.

I disagree with GForce's explanation; the meaning is not that growth of prey populations causes instability in predator species.

The sentence is merely saying that without predation, prey population growth is more likely to be at a level which leads to ecosystem instability. The term "but for predation" means "if it wasn't for the effects of predation". In other words:

  "Ecosystem instability can occur when population growth of some species goes unchecked by predation."

See here for more explanation, where this example comes from in which it says that running a red light caused a crash:

  "but for running the red light, the collision would not have occurred"

Biologically this makes sense in the sentence you show; without predators a species is limited by its supply of resources, and it can use these resources at an unsustainable level, whereas if you add predators to the mix there is additional extrinsic effects on population size, not determined by ecosystem properties such as space or nutrients.


Is there a physiological difference between love and infatuation? I find that people generally distinguish between love and infatuation. Is there a physiological difference between the two? Or are they biologically identical, and the difference is circumstantial?

Assuming that our emotions are the psychological manifestations of chemical changes in our bodies (an assumption I have no trouble with but one that others may take umbrage at), any emotion will be different.

If your brain can distinguish between two emotions, then the underlying chemistry through which these emotions are expressed will be different.

This is not to say that we, as scientists, can quantify this. Definitely not today at any rate. Simply that there will almost certainly be a physiological difference between any emotional state that can be differentiated by your brain. Otherwise the brain would not register different emotions.

UPDATE:

Human language has different words for different feelings. There is often a type of feeling "continuum" with different words representing different ranges on this scale. For example:

Adoration--->Love-->Infatuation-->Affection-->Indifference-->Dislike-->Hate

How you decide to qualify an emotion you are feeling is more a question of semantics than biology. The point I am making here is that each point on that scale (and every point in between that we haven't explicitly assigned a word to) will represent a slightly different mix of various chemical signals in your body.

If your question is more about the English language words love and infatuation, their definition and distinguishing between them, try posting on English.SE.


Question regarding 2 constructs of tobacco plant Six independent transformation experiments of tobacco leaf explants were carried out using
two different constructs - (1) construct I containing only a Hygromycin-resistance gene
$(HYG^R)$ as a selection marker and (2) construct II with the $(HYG^R)$ gene as a selection
marker and a passenger gene encoding a dephosphorylase enzyme $(DEP)$ that inhibits
phosphorylation in cells in which it is expressed. The marker as well as passenger genes
were placed under transcriptional control of a constitutive promoter $(CaMV35S)$, which
expresses in all cells/tissues. The results obtained are tabulated below.

Explain how The $HYG^R$ gene used in construct II lost its functionality probably due to
mutation(s) either in the gene or in the promoter.

My approach: There is a probability that Expression of the $DEP$ gene is lethal to the transformed cells.

Having a toxic product for the cell in an expression vector is a not uncommon problem when overexpressing proteins.

The other possibility is that the selection marker itself is the problem. Here you can have mutations either in the promoter of the gene as well as in the gene itself resulting in a protein which is not capable of protecting the cells from the selection. Both possibilities (no expression and mutated protein) leave to the death of the transfected cells, since there is no protection of them by the resistance protein.


About a mechanical aid to the heart I saw a news story a few years ago (I think) about a girl with a poor heart having a device implant that took over only some of the functioning of her heart ( I think they called it a piggy-back device , or something like that). The extraordinary thing is that it not only helped her live but all the heart functions started to improve. It was as if giving part of the heart a chance to 'rest'  allowed the whole heart to improve. If this procedure works could it be applied to other organs? Could a Piggy-Back device be made for the liver taking over only some of its functions for instance?  Could such a thing help the liver functions to 'regenerate'?

The function of heart is just to pump blood and nothing else. Though, it is a vital organ, its functions are limited. The device that you are talking about is a battery powered mechanical pump that performs the same function as heart.

Liver, however has a more complex function. One of its function is to synthesize and secrete certain molecules. A small artificial device cannot do that (you would need a bioreactor !!!).

We still haven't developed and artificial cell. Perhaps a consortium of bacteria can do some of the liver's functions but to culture them in right proportions and implant them without the risk of infection or their elimination is almost impossible as of now. You can clearly see that there are too many steps to be optimized.


What is the difference between a predator and a parasite? A human encountering a tiger or a malaria plasmodium is likely to suffer, and the tiger/plasmodium is likely to gain from the transaction. Not necessarily a good example, and I am aware that a successful parasite avoids prematurely killing its host, but I can't see any fundamental difference.

Of course it's like pornography: "we know it when we see it". But is there a formal, generally-accepted distinction?

Good question.

There is no fundamental difference between parasites and predators.

Ecological Interaction

In terms of ecological interaction, they are both defined as an interaction where one species benefits and the other suffers from the interaction.

Intuition parasite vs predator

In general predation is viewed as a big individual eating a smaller one while parasitism is when a small individual eats a bigger one. These general intuition however fails to consider a number of cases. Here some cases I can think of

Examples when intuition don't match the above picture

Generally considered as predation but does not fit the above picture-based definition:

social animals attacking in groups preys that are much larger than themselves - non-social animal attacking prey larger than themselves
herbivores browsing on large trees

Generally considered as parasitism but does not fit the above picture-based definition:

indirect effect of habitat modification that would rather be considered as parasitism.
Species that take advantage of parental care of another species by mimicking babies (but being larger)
Individuals of large species stealing the habitat built by a smaller species
Batesian mimicry (see this post; Thank you @WYSIWYG and @NL_Derek for the comments)

Population culture vs science literature

In the popular culture, some people call parasites only endoparasites. This concept is also misleading and not so much in accordance with the general literature in biology.


Mechanisms and Assumptions of the Species-Area Realtionship I would like to choose a model to use to describe a species area relationship based on plant species richness data that I have collected.  Rather than choosing the power model a priori, I am considering all options (eg. exponential, untransformed, etc).

Does anyone know of any good recent synthesis work on how to choose the best model?  Of particular interest are the assumptions behind each model, and the ecological mechanisms that each model might imply.

Dengler 2009 would be a good start.

I'm sure this paper, his citations and papers citing Dengler's paper will get you well on your way.


What is the meaning of a reported OD600 value? I can't find a reference that explains what, for example, OD600 = 0.1 means.

For example, Wikipedia states

  OD600 is an abbreviation indicating the absorbance, or optical density, of a sample measured at a wavelength of 600 nm.

In other words, the OD600 value reports (a function of) what percent of light goes through a sample. But that depends on the thickness of the sample. More light will go through 1 millimeter of fluid than through 1 meter of the same fluid. So what is the thickness of the sample involved when reporting OD600? Or is the OD600 independent of that, so that it actually has units that people simply omit? In that case, what are the units? What is a precise physical interpretation of what is meant by the measurement OD600 = 0.1?

Suppose OD600 = 0.1 for some sample. I shine 1 mW of 600nm laser light through a 1 cm path length of the sample. What is the transmitted power?

For most laboratory spectrophotometers the path length in cuvette that holds your sample is 1 cm, and unless another path length for the light is specified you can always assume that the Beer-Lambert Law for absorption of light is using 1  cm.

When growing a bacterial liquid culture in an incubator, the OD (wavelength is usually 550 nm or 600 nm) is a approximation of the number of cells, or colony forming units, or cfu, per mL of culture.

The recipe, or protocol, will normally specify the bacterial strain to use, and the desired OD (at which point one either harvests the growing cells, or possibly adds something else to the culture, like a drug, or a viral stock).

To actually know the number of cfu/mL for a specific bacterial strain one needs to construct a growth curve by taking aliquots at defined time points, and reading the OD, and also plating out some serial dilutions.  After incubating the plates at the correct temperature one can count the number of cells per mL and plot cfu/mL vs. OD600 (for example).


Why are cats attracted to catnip? According to wikipedia, the active substance is nepetalactone ($\ce{C_{10}H_{14}O_{2}}$) which has weak sedative, antispasmodic, febrifuge, and antibacterial effects in humans. Why are cats so fond of it? Why do they seem to get high on it?
According to the same wikipedia page, the effect is gene-linked but it does not mention which genes, what they code for or any details whatsoever. Are all felines affected in this way or only Felis catus? What is the biochemical mechanism by which cats are attracted to catnip?

Nepeta cataria(Catnip, Catmint, Catnep) is a plant belongs to the family Lamiaceae.It is a  herb that has been recognized for its medicinal properties for many centuries. Over time it has been used in remedies to cure internal cancer, smallpox and scarlet fever.Also it was believed that a dense growth bordering fields helped to protect crops because of its ability to repel rats.

Major Active Constituents of catnip includes a and ß nepetalactone  citronella , a and ß citral , limonene , geraniol , thymol , and carvacrol  epideoxyloganic acid and 7-deoxyloganic acid

  Nepeta cataria has a carminative, anti-spasmodic, astringent and anti-flatulent effect on the gastrointestinal system, particularly on the stomach . It is also a diaphoretic and antipyretic in times of fever . Nepeta cataria is similarly recognized as a tonic, mild nervine, and sedative, with a slightly emmenagogue action . With respects to cats, Nepeta cataria produces an aphrodisiac effect.

http://scu.edu.au/scps/index.php/125/

A research paper published in 1994 states that,

  Catnip was  the most promising candidate lures tested. The 'catnip-response' is
  inherited as an autosomal dominant (Todd 1962). In trials, behavioural observations showed
  that 50% of the subjects (including all four domestic cats and 8 of 20 feral cats) showed the full catnip response (B. K. Clapperton, unpublished data). This includes sniffing, licking, rubbing and head-over rolling (Tucker and Tucker 1988). Nine of the remaining 12 feral cats approached and sniffed at the catnip samples. This suggests that, although not all cats are genetically determined to respond to catnip , these odours may act as more general attractants.

http://www.southwestnrm.org.au/sites/default/files/uploads/ihub/clapperton-bk-et-al-1994-development-and-testing-attractants-feral-cats-felis-catus.pdf

  When cats inhales nepetalactone it stimulates the olfactory bulb, the part of the brain that processes odors. The olfactory bulb then interacts with the amygdala, the brain region associated with emotion and decision-making, and hypothalamus, which controls a variety of bodily functions. From the hypothalamus, nepetalactone stimulates a sexual response in cats that are genetically predisposed to sensitivity to catnip. (About 20 to 30 percent of cats don't seem to react to the plant.)this is why mostly adult cats shows significant addiction to catnip.

http://www.compoundchem.com/2014/06/08/catnip/

  The catnip stimulates an Innate Releasing Mechanism(IRM) in domestic cats that elicits a predictably playful behaviour pattern apparently independent of experience and learning(Ewer,1973 and Leyhausen,1975) ,trans-nepetalactone is reported to produce behavioral respondse in cats.It has been verified by Todd in 1963 that capnip is mediated by Olfactory and not gustatory stimuli.Catnip sensitivity has been related to a dominant autosomal geneand to the estrous cycle by Todd.The reports shows catnip elicits behavioral respondses in domestic and wild cats, but these responses are not shown by female sex.In addition, it has been suggested that catnip mimics a pheromone found in cat urine, however evidence supporting this theory is scant.(Todd 1962)

http://link.springer.com/article/10.1007%2FBF00987747#page-1


8 abdominal muscles but 10 pack Simple question, how is it possible that there are people who appear to have 10 pack abdominal muscles while the human body has only eight?

The only "way" someone can have a 8-pack or 10-pack is due to genetics. Across the rectus abdominis muscle you have either 3 or 4 tendinous bands going over it, consequently resulting in either a 8 or 10 pack.


Special bacteria in infants This question is similar to a previous question, but is not the same.

I was told, you are born with a bacteria in your digestive track that are made by the body. Can a body in development create it's own bacteria from nothing? Also said by the teacher the first time you take an antibiotic it is gone forever?  Can a body in development create it own bacteria from stem cells? Is there such a bacteria, can it be cultured and re-introduced into the body?

No, no human (or any other eukaryote lineage) are able to "create bacteria". The story you were told is wrong.

However and interestingly, female parasitoid wasps seem to "create viruses" (Herniou et al. 2013). The viruses are part of the wasp genome (lysogenic phase) and detach (lytic phase) in the ovaries only. The viruses, then infect the caterpillar in which the mother lay its eggs. The viruses ensure to reduce the immune system of the caterpillar in order to protect the wasp egg (and later larvae) and ensure its development to adulthood.


HapMap 3 phased haplotype I need to get HapMap 3 phased haplotype data. Where can I find it?

Actually I need these data for specific populations and a specific gene. What is the easiest way to find data?

I hope I can find an answer. Thank you!

Here is the FTP address. Inside you will find the phase_3 folder. For other questions check this page (the link to the HelpDesk is at the bottom of the page).


How selfish is Dictyostelium slug formation? Dictyostelium is a slime mold which is well known for having a single cell free living phase and other some conditions (e.g. when food is scarce) for forming communal piles of cells called 'slugs' which migrate as a proto animal.  Eventually the slug can turn into a fruiting body with a stem and a nodule of spore forming cells at the top.  The spores can then be carried off by the air and seed dicty further away.

Apart from being amazed at the seeming ability to form amoebic, animal, plant and seed like forms, there must be a lot decision making happening at the formation of the stalk and fruiting node at the top.

So my question is: what is the current thought about how cells compete in the mexican hat and stalk formation to be at the top of the pile?  Its pretty altruistic of the cells in the stalk to do this - some web pages say they die, is that right?  Links to references after 2007 or so would be appreciated unless it's all been decided.

By analogy its always been pretty altruistic of 99% of our bodies to let our gonads reproduce, but we are (approximately) homogeneous genetically.  In the wild is slug formation heterogeneous?  How does genetic diversity influence slug and fruiting body formation?

Joan Strassman's work is probably the route to go for this.

The short of your answer is that several things mediate who ends up where in the slug:

  Cheaters are limited from exploiting other
  clones by high relatedness, kin discrimination, pleiotropy, noble
  resistance, and lottery-like role assignment.

Here's the most relevant paper:

Strassmann, J. E., & Queller, D. C. (2011). Evolution of cooperation and control of cheating in a social microbe. Proceedings of the National Academy of Sciences, 108(Supplement 2), 10855-10862. [pdf]


Exact average molecular weight of a dsDNA basepair I am trying to calculate the exact weight of a given dsDNA.
On the Internet and the literature, different values for the av. molecular weight of one basepair are given :

660 g/mol (probably wrong),
other sources say 617.96 g/mol
Thermofisher gives 607.4 g/mol
(https://www.thermofisher.com/de/de/home/references/ambion-tech-support/rna-tools-and-calculators/dna-and-rna-molecular-weights-and-conversions.html)

I tried to calculate the average weight using following molecular weights:

molecule
.
weight

2'-Deoxyadenosin- 5'-monophosphate
dAMP
331,22 g/mol

2'-Deoxycytidin- 5'-monophosphate
dCMP
307,197 g/mol

2'-Deoxyguanosine 5'-monophosphate
dGMP
347.2212 g/mol

2'-Deoxythymidine-5'-monophosphate
dTMP
321.2005 g/mol

water
H2O
18,01528 g/mol

adding the matching nucleoside monophosphates together and subtracting one water for each peptide-bond condensation (one on the sense; one on the antisense side);
I get following formula for the average dsDNA basepair weight:
$$
avg.BP.weight = \frac {(dAMP+dTMP-\ce{2H2O})+(dGMP+dCMP-\ce{2H2O})}  {2}
$$
resulting in :
$$
\frac {(331,22+321.2005-36,03056)+(347.2212+307,197 -36,03056)}  {2} = 617.3892 \frac{g}{mol}
$$
which is very close but still 0.57081 short off the "best" literature value.
What am I missing?; Im trying to get this calculation as exact as possible.
Maybe i didn't consider some hydrogen or protons in bonds?
Thank you in advance!

The different protonations forms are considered in the averaged Mw.
Removing two H2O is the step that makes your average different than the traditional 650Da per base pair. But you must remember that the last base pair in the sequence will have it's OH group so you need to add 17.008 gr/mol * 2 = 34.016 gr/mol.
The effect of this changes with the length of your sequence, here is a graph showing it.

Blue line is your calculation and red line is the one from literature.
Literature one is achieved around 60bp (I calculated Mw(63bps) = 617.93) and yours at 10^6.6 (Mw(10^6.6) = 617.3892085)
Why you need this calculation to be so exact? Knowing the length of you sequence and region can help. Remember that some regions are richer in one type of nucleotides (CpG islands, hairpin coding sites)


Did some senses evolve from other senses or are they considered independent? Are there evolutionary connections between different senses, in such a way that one sense is evolved from the other or from a common root, e.g. the possibility that hearing and touch are derived from a common root? If there are such evolutionary paths, are there any attempts to draw a map between different senses?

Hearing and touch are both examples of mechanosensation, i.e. touch receptors are activated by pressure changes and sensory hair cells (hearing) are activated by fluid motion initiated by sound waves. Therefore, I think it makes sense that they evolved from similar origins.

Vision on the other hand is due to photosensation, which has a very different physiology, so I don't think there's any evidence of a similar evolutionary link, but there may be (almost certainly are) similarities in the way our brains have evolved to respond to the different senses.


Absence of cytoplasmic Intermediate Filaments in Arthropods Cytoplasmic intermediate filaments such as vimentins support the architecture of the cell and have been known to aid signaling processes. However, as in this article, it is stated that out of all eumetazoans in Kingdom Animalia, only arthropods do not contain such structures. How is this possible? Are there any replacements to the conventional intermediate filaments present in cells? Do arthropods have special cellular behaviors or signaling networks to correspond with this absence?

It is stated that out of all eumetazoans in Kingdom Animalia, only arthropods do not contain such structures.

I found this paper(1), eliciting an exception (within an exception)- Isotomurus maculatus:

Here, we report the first evidence for the expression of a cytoplasmic IF protein in an arthropod - the basal hexapod Isotomurus maculatus. This new protein, we named it isomin, is a component of the intestinal terminal web and shares with IFs typical biochemical properties, molecular features and reassembly capability.

I would suggest you to read the paper, for more information.

How is this possible? Are there any replacements to the conventional intermediate filaments present in cells?

Both electron microscopy and molecular cloning studies have been unable to detect any cytoplasmic IF protein in these organisms, although they do express a nuclear IF system made of authentic lamins. Other cytoskeletal components have been proposed to have assumed, in arthropods, the mechanical functions that are usually played by cytoplasmic IFs in other organisms. For example, wing epithelial cells are stabilized in insects by a cytoskeletal array consisting of parallel bundles of 15-protofilament microtubules and actin filaments.

Do arthropods have special cellular behaviors or signaling networks to correspond with this absence?

I am not sure if this is what you might be looking for, but the Delta/Notch signalling, which may be involved in posterior elongation in arthropods, does not require IF's.(2)

The Notch cascade consists of Notch and Notch ligands, as well as
intracellular proteins transmitting the notch signal to the cell's
nucleus. The Notch/Lin-12/Glp-1 receptor family was found to be
involved in the specification of cell fates during development in
Drosophila and C. elegans.

1- https://bmcbiol.biomedcentral.com/articles/10.1186/1741-7007-9-17
2-https://en.wikipedia.org/wiki/Notch_signaling_pathway#Mechanism_of_action


Cyanobacteria pools as carbon sinks According to some scientists, at one point in time in this planet's history cyanobacteria almost drove life to extinction by reducing it to a snowball as they captured vast quantities of carbon and locked it up.

Today we face a different challenge where we have excess carbon dioxide (and other greenhouse gases) in the atmosphere leading to a warmer planet which threatens its current inhabitants.

As someone who studied applied physics I have very little understanding of how cellular and molecular biology work. But is it a viable solution to build artificial sinks of cyanobacteria in controlled environments at various places on the planet to capture this excess carbon dioxide? If not then what stops us?

I could think of some challenges:

As cyanobacteria need sunlight to capture carbon so the reaction will be limited to the surface where we will have most sunlight. But one can improve the efficiency by building columns which have embedded light sources (using solar/renewable energy only) at various points within.
Maintenance of these pools/columns.
An economic model to make this a profitable venture for companies. Can the end products produced by these bacteria be sold for money? Can they serve as an ingredient into some other (profitable) reaction?

The best cyanobacterial pool is the World Ocean.

No man, no amount of venture capital investment, no board of directors, no CEO, no CFO, no CSO, etc. can ever create, on the Earth, an equivalent to the World Ocean.


Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over? To be specific: Assume chromosomes A and B are homologous. They've both replicated into A1, A2 and B1, B2 and have formed a tetrad at the equator (synapsis). Most textbooks show either A1 and B1 OR A2 and B2 exchanging genetic material, but I've never seen an experiment/paper proving that this is actually the case, and now I've come across this figure showing both A1, B1 and A2, B2 crossing over https://web.archive.org/web/20160314020121/http://www.uic.edu/classes/bios/bios100/lecturesf04am/lect16.htm
see ("crossing over" under meiosis)

So which version is correct, or do we simply not know for sure? Thanks in advance.

Yes, it is perfectly possible for both pairs of non-sister chromatids to cross over in a single tetrad. The "standard textbook" depiction is a simplification, true tetrads can sometimes be very complicated and the nested crossing-over would be difficult for entry-level textbooks to cover.

This microscope image clearly shows two chiasmata occurring on two sets of chromatids, with both of the "blue" chromosome's chromatids undergoing crossing over.

In fact, even more complicated chiasmata complexes can form during meiosis. For example, this slide depicts many chiasmata occurring in a single tetrad. More examples can easily be found by searches.


Why use embryonic neurons to study protein knockouts/mutants in long term potentiation? Just wondering if anyone had some ideas about the question in the title. I'm just wondering why some papers use embryonic cultures of specific brain regions for neurones to test the effects of knockouts/mutations on synaptic plasticity (for example, long term potentiation, LTP) instead of adult cultures?

Many thanks

Some suggestions, there may be more:

1) The knockout may not be viable to adulthood (the animals die). Perhaps heterozygotes are viable, but to test the full knockout you need a homozygote.

2) Even if the knockout is viable to adulthood, the brain may develop adaptations to the knockout that aren't specific to the knockout itself: up- or down-regulation of certain channels, for example.

3) Plasticity is upregulated in developing brains compared to adult brains, so the effects may be more pronounced in the young tissue.

4) Younger tissue cultures better - you can keep cells alive longer, more easily.

Also good to note is that undifferentiated stem cells tend to be "neuron-default" - that is, if you just culture embryonic stem cells and you don't do anything special to them, they will tend to generate neuron-like cells. In the adult, neurons are always going to be alongside other types of cells: glia, vascular tissue, etc.


Why are the hormones dopamine, adrenaline, noradrenaline and serotonin so ubiquitous across the animal kingdom? As far as I know there is no reason for the makeup of a given hormone to be universal as it merely serves as a carrier from one part of the brain to another. So why are the above hormones seen across the entirety of the animal kingdom, and used in more or less the same way?

Evolution.

This is not special to hormones: receptors and ligands of all types are highly conserved across not only the animal kingdom, but also to single-celled organisms. The degree of conservation is typically dependent on the closeness of evolutionary relationship: more related organisms share more homology.

Because species evolve from common ancestors, they tend to share a lot of the same 'tools.' Changing the purpose of a hormone would likely require some sort of selective pressure, some new reason to use that molecule in a different way, and if the old and new roles conflict then there needs to be a replacement. This can happen, but it's complex and requires just the right conditions. More often, minor changes occur: among the steroid hormones, for example, you will find many small biochemical tweaks that make new molecules that have different functions.

Certainly the functions of some hormones are not entirely conserved, and if you look at the nervous systems of, for example, insects versus mammals, you will find some major differences, but the closer in evolutionary time you look the more similarity you will find.


How and why can cold inflict pain? I was carrying a can of very cold liquid, had something heavy in my other hand so couldn't switch hands. After a few minutes, I started to feel very intense pain. I was very surprised. cold is just atoms moving slower. This makes more sense if you think about how heat, or burns can cause pain. But heat can cook tissue and disable it, it makes sense it would hurt.

I think your getting confused. Your assuming that it's actually the heat or cold that creates the feelings of pain.

  I was very surprised. cold is just atoms moving slower.

Pain is a warning mechanism, stop doing that or you'll hurt yourself. It is not caused by the atoms in your nerves moving faster or slower in response to heat. Your nerves are triggered by a stimulus that could cause harm to your body and react by passing a pain signal to your nervous system. The heat (or lack of it) does not transmit up your nerves.


Quorum Sensing in Vibrio cholerae This is a figure summarising the quorum sensing mechanism in Vibrio cholerae.

In this video by Bonnie Bassler, she explains how quorum sensing can be targeted to control infections.

At 15:09 she explains why cqsA- mutants show more dramatic effect when external CAI1 is added - because we are not fighting against the endogenously produced autoinducer1.

My question : But won't endogenously produced autoinducer help in controlling virulence, as the more the auto inducer lesser the virulence ? Why should we be fighting against endogenously produced autoinducer 1 ?

First of all I find quorum sensing to be generally facinating, so I'm happy to see the topic brought up here.

Dr. Bassler has many papers on the subject, but I think one of the most relevant ones to this question is here.

Regarding your question, you have the right idea, but you're missing the point of her comment.  The Western shows a more dramatic difference in cqsA- bacteria because they are not inhibiting themseleves (as you suggested).  Thus the lower concentrations have much higher levels of the toxin produced because the only CAI-1 being provided is the synthetic one.  This makes the ramp up in administered CAI-1 seem more drastic because you start at a higher level.

I hope that makes since, if I can find an open writes version of the Western, I'll come back and give further analysis on it.

Regarding @AlanBoyd 's comments, V. cholerae is different because it seeks to create an acute infection, not a persistent one.  Cholera toxin is what causes the majority of diarrhea and virulence from cholera.  V. cholera produces the toxin until it's inhibited by ether auto-inducer (which should be after the pt already has massive diarrhea), then it switches to produce enzymes which detach it from the gut.  The pt still has diarrhea at this point, cholera just doesn't need to make any more toxin for it to continue.  To do so would probably waste energy, and not help the bacteria make it back to a water supply.


Literature about industrial enzyme application Can someone point me out to literature (reviews or better workbooks) describing industrial chemical reactions catalysed by enzymes?

What I'm most interested in are case studies of how the output of a reaction on a big scale is optimized with respect to enzyme activity.

Most of the literature I'm finding is about optimization of cell growth, which is not what I'm looking for.

I'll give you examples I have encountered in talks. There are too many variations and types of applications for me to break out in a comprehensive way.

Example 1: enzyme production.  this sort of application is about optimizing the amount of a desirable enzyme or protein produced from a liquid culture.  Sorry if this is too close to cell growth, but its terribly important.  Small cell cultures are used in research and the genetics of the cells (usually e coli or yeast, but also often a fungus that's been found somewhere) to improve the amount of the desired protein.  The protein may be secreted, which makes it much easier to purify.

Once a good strain is found, the culture is scaled up to thousands of liters, often many kilos of pure enzyme can be produced this way.  Examples: the enzymes that break down fabric for acid washed jeans, the proteases and cutinases which are included in laundry detergent
and insulin.

Example 2: glucose isomerase.  This enzyme is used to produce high fructose corn syrup.  The enzyme itself actually changes fructose into glucose, but by le Chatlier's principle, a glucose syrup under high pressure will be converted to fructose by the enzyme.  This enzyme, produced by an industrial process like that described in example 1 is immobilized onto a resin and packed into large industrial sized columns.  I seem to remember from the talk that they were similar in size to an oil barrel.  Large amounts of glucose rich corn syrup are passed through the column; it comes out about 40% fructose.

Another example (3)  along those lines might be how to use an enzyme with a product.  In an industrial manufacturing process like enzyme denim treatment, the fabric may be washed in a solution including the enzyme.  The process has to be careful to control the amount of enzyme the denim is exposed to and to optimize the conditions so that none of the fabric is ruined but comes out consistently.  The enzyme might be killed by a pH change or heating.  This is essentially chemical engineering and there are courses about this sort of thing at most major chemE departments now.


Why are siblings unidentical? (Which chromosome of the pair do gametes have?) I know that a normal human cell has 23 pairs of chromosomes (total: 46).
On the other hand, a gamete has only 23 chromosomes.
Which chromosome does the gamete choose out of each pair?

And if "One of each pair of chromosomes comes from the mother, the other from the father.", then the chromosomes of a gamete could be an exact copy of the chromosomes in a grandfather's gamete?

The gamete doesn't "choose" one or the other.  Both are made and you get two gametes, one for each.

Also it's unlikely to be an "exact copy" due to recombination and random or independent assortment.  There are also smaller influences on genetic variation, and epigenetics, but at this level of question I think you should focus on those two.

Was this homework?  If so it should be tagged.


What is an "Alternative Sensation"? As far as I know, alternative sensation it's a sensation to distract people from the original stimuli, for example when you have to get an injection, the nurse will pinch you in the other arms so your brain is distracted and will not focus on the original pain in the arms that's got the injection.

But I also read here, alternative sensation refers to the brains that can process stimuli from multiple senses, for example when the eyesight is bad, the ears will take up and boost the visual system to help and stimulate the visual system (Visual + Auditory) .

Which one is exactly an 'alternative sensation'? Also, what is Time-Frequency in alternative sensation ? I would appreciate any references too.

"Alternative sensation" is not specific terminology in neuroscience - it is just the noun "sensation" with a descriptive adjective "alternative." It just means that it is referring to a different sensation than whatever the "primary" one is.

Knowing what this term means in a given context depends entirely on that context, and may not have any relationship to other contexts.

Time-frequency refers to how something varies in time and frequency. In the context of stimuli, for example, an auditory stimulus can have different "tones" or "notes": those are different sound frequencies, and those frequencies can happen in sequence. To describe a sound visually, one will often present a 'heat map' showing when (time) and at what frequency that sound has energy. Touch stimuli can also have a time-frequency representation, where the frequency indicates the vibration speed of the touch.


Correlation between muscle size and absolute strength Is there a linear connection between muscle size and the power it can produce?
If not, why? And what is the true correlation if any, can it be described with an appropriate function? What other factors modify it? (Red/white fiber for instance?)

The short answer to your question is that the work output from a muscle is a combination of physiological cross-sectional area, length, fiber type, and recruitment (how many motor units are activated).

Read on for more details.

Force output (tension) of a muscle is proportional to its physiological cross sectional area (Fundamental of Medical Physiology), and shortening is proportional to the length of the muscle. Work output (force X length) is a function of both. Power (work / time) involves both force, length change, and the shortening velocity. Shortening velocity is related to muscle fiber types.

There is a complex relationship between force output and length. In the graph below, the x-axis is relative length (1.0 being resting). When muscles operate outside a relatively narrow range (gray box), the cross-bridges are either too close together or too far apart to optimally generate force. When the muscle gets really stretched, force goes up, but only because passive tension (the intramuscular connective tissue is getting stretched) increases.

The force-velocity curve below relates relative force output to how fast the muscle is shortening (which can be negative; i.e., lengthening contraction). The green part of the curve is muscle shortening. As velocity approaches 0, the muscle produces maximal shortening force. When the muscle goes into the red part of the curve, force is even higher. In order for a muscle to shorten very quickly, it can't produce a lot of force (far right).

Muscle fiber type generally relates to both the force output of a muscle fiber and it's shortening velocity. There are different ways to classify muscle fibers (enzyme activity, myosin isoform, or the "classical" method):

SO ("slow oxidative"; the dark meat of a chicken) fibers contract slowly, produce lower force but are fuelled by oxidative reactions and thus have good endurance. At the other end of the spectrum, FG ("fast glycolytic"; the white meat of a chicken) fibers contract quickly with high force, but fatigue easily because they get energy from glucose, which is rapidly depleted. FOG fibers are intermediate between the two.


Is there a word for the assumption that a sufficiently complex and refined organ must be the result of natural selection on a large time scale? Is there a term for the valid assumption that a sufficiently complex and refined organ must be the result of natural selection on a large time scale?

Example:
A biologist exists in a world where nothing has eyes.  They find a creature with an eye as developed as a modern mammal's in our reality.  Assuming this biologist understood what the eye was able to do as far as limiting and focusing incoming light and sending visual information to the brain, etc - it would go without saying that this was a gradually evolved system.

It would be impossible for a parent from a completely eyeless ancestry to spawn a child that had the equivalent of a fully developed modern mammalian eye, both because of the statistically improbability of that happening, and possibly even because of limitations in the way dna works.

Is there a word for this assumption? e.g. "As per the Axiom of Reliable Intuitive Ancestry Determination for Sufficiently Complex and Refined Traits, we will start our genetic research confident that the eye must be the result of iterative natural selection on a large scale of time."

Preferably a term that acknowledges the validity or reliability of this assumption when it comes to very complex and refined organs or systems, such as the eye, the brain, or the circulatory system.

The 'term' you are looking for is actually gradual change or gradual evolution. If you want to make clear that this is an assumption or a theoretical consideration, you could say assumption of gradual change or theory of gradual change, replacing change with evolution if you like.

The idea comes from Darwin directly and was challenged in the 1970's by biologists like Stephen Jay Gould that suggested that evolution is not driven by gradual accumulation of changes but rather by morphological equilibria disturbed by many rapid adaptations forming new species, a concept called punctuated equilibrium.

It speaks for itself that these concepts are opposing but not mutually exclusive. They are rather two extreme states in a continuum.

Edit: As pointed out in a comment by Daniel Weissmann gradual changes also occur in neutral evolution; this is what we call accumulation of mutations - in fact, it also applies to (at least slightly) deleterious variants, especially in populations with small effective population sizes. This means, that the concept of gradual evolution can be generalised to neutral evolutionary processes. However, it does not mean, that the process involving natural selection cannot also be described by gradual evolution. You just have to specify what you are actually talking about. When talking about obviously complex adaptations, you would assume that they have not evolved neutrally.


What are these (eggs?) ? ( Location - India ) The picture can be zoomed in on clicking

Description:

There are 24 of them, each ovoid, 1mm long and attached to the switch's frame by suction cups connected by tubes. They are secured to the base and couldn't be brushed off with a stick. Found them in East of India.

UPDATE

The ovoid heads have reduced in number (17) and have turned brownish (10.04.2017). The number of ovoid heads are 11 now and two of them have a black spot at the proximal end (could be the eye spots of developing embryos) (13.04.2017). The bunch has 4 of them now (24.04.2017).

Research & Question:

Assuming those are eggs (resemble those of Green lacewing and with the changes observed it is evident), what group of arthropods have such stalked eggs other than Green lacewing?

The group of insects called Neuropterans have several species that lay eggs on stalks. This group includes lacewings, owlflies and antlions, however stalked eggs are not a defining trait of the group. In addition to the Green lacewing, the Blue-eyed lacewing from Australia lays stalked eggs while owlflies do not. Mantidflies also have stalked eggs which are members of the Neuroptera order, but the stalks are relatively short compared to lacewings.

This thread provides some interesting discussion.

P.S. While not an arthropod, at least one Genus of Molluscs (Nucella), lay stalked eggs too.

These are certainly eggs from this order (Neuroptera). Incubation time for these type of eggs can be anywhere from 2-7 days so you may already be having hatching if there are less eggs than what was initially there.


Why is there an apparent reduction of reptile species near the Mississippi River? The USGS Gap Analysis Program published a map of reptile species richness in the U.S. There is a conspicuous reduction in reptile richness along the Mississippi River corridor. Why might this be?

From USGS:

  This map of reptile species richness in the U.S. is derived from the
  USGS Gap Analysis Program’s (GAP) national reptile ranges dataset. The
  map represents the total number of reptile species summarized by
  12-digit hydrological units (HUCs). Light blue HUCs have the lowest
  number of species while red HUCs have the highest.

The reptiles mostly were ploughed away and replaced with soy beans.

The low reptile diversity zone matches the Mississippi Alluvial Plain which includes the Mississippi Floodplain. The Mississipi drains nearly half of the USA's geographic area, so the flood plain is massive.

The Silt Plain is very flat, mostly has hills left by oxbow lakes and river meanders. If you put your hand in the ground, it consists of organic matter/silt/clay/mud/fine sand, and it is very fertile until it is depleted by modern agricultural practices.

It's one of the more productive agricultural regions in the USA, and it's mostly giant square fields and mono cultures.

zoom in: http://gokml.net/maps#ll=32.163208,-91.720681&z=11&t=h&q=winnsboro

Here is a quote from the Discussion at the end of this review:

  traditional agricultural landscapes, typically characterized by
  mosaic–like structures, intermediate levels of disturbance, and able
  to host great biodiversity levels (Bignal & McCracken, 1996), have
  undergone profound transformations in last decades. The rapid
  extension of intensively cultivated fields and the reduction and
  fragmentation of the original habitats have led to the creation of
  more uniform and depleted landscapes, with significant loss of
  biodiversity (Whittaker, 1975; Bull & Skovlin, 1982; Burel et al.,
  1998; Zechmeister & Moser, 2001; Moser et al., 2002; Pfiffner & Luka,
  2003). In accordance with these changes, our analysis of reptile
  assemblages in an agricultural area mainly devoted to the intensive
  cultivation of arable lands found the landscape to be relatively poor
  in biodiversity. Four out of five agricultural land uses hosted only
  one species, while most of the recorded reptiles occurred inside a few
  patches of semi–natural habitats and, above all, in the grid of
  vegetated buffer strips interspersed among the cultivated lands. In
  addition, during field activity, we observed only seven of the
  eighteen species of terrestrial reptiles reported for the province
  where the sites are located, and most records were ascribable to a
  single species.

Reptiles and Amphibians are at the top of the insect food chain, and studies have shown that they are sensitive to pesticides, especially when their numbers are low:

  By using three evaluation factors - (i) pesticide exposure, (ii)
  physiology and (iii) life history - a taxon-specific pesticide
  exposure risk factor (ERF) was created. The results suggest that about
  half of all evaluated species, and thus at least 1/3 of all European
  species exhibited a high exposure risk. Previously the region would
  have been host to a very tall high growth forests, because of the high
  temperatures, available water table of the area and fertility.

you can check pics 6 and 8 from this page to see the productivity of the region. It suggests that the reptile biomass was replaced with obese humans.

That forest has been reduced to the swamp forests where the roots are covered in stagnant water for most of the year, where some large aquatic reptiles take refuge, and which is completely different than the lost forests of the Mississippi plains.

The old forests would have perhaps been similar to florida's inland forest, and perhaps very different, because of the available water table, and much more productive silt, than florida's ground allows for. I didn't manage to find photos of the lost forests of Mississippi plain regions, they would have been dense, producing 3-7 times more biomass than normal forests.


Can someone identify this plant I saw in NYC (might not be native idk) I've never seen a plant with these type of leaves before and was wondering if anyone recognized/can figure out the species.

That looks like it is probably a single leaf coming up from a tuber.

That fact combined with the mottled pattern on the petiole (leaf stalk) and the shape and branching pattern of the leaflets makes me guess it was something in the genus Amorphophallus.

Example image:

Other images for the "voodoo lily".


What determines if an allele is dominant or recessive? Going back to my high school days we were taught about dominant and recessive genes. We were taught how to calculate the geneotype and pheneotype of potential offspring using a small table (forgotten the actual table name). But it never occurred to me then what determines if a gene is dominant or recessive and how this is carried out biologically.

Take my example below, there is a 50% change that an offspring will carry both the tall (T) and short (t) genes. What determines that the tall gene T has a dominant effect over the short gene t.

Now, I know that there is going to be differences between the different genes (i.e. eye colour), but is there a general description any one and provide which states how a gene becomes dominant and how the dominant effect is carried out biologically.

Dominance is seldom complete. Owing to effects like co-dominance, incomplete dominance, collaborative (additive) effects of polygenes, our classical concept of dominance doesn't work. Having said that, there are certain ways in which a gene, if showing complete dominance can be analysed from the molecular level.

In an individual heterozygous for a certain trait, the following possibilities exist:

Both the alleles, though different, code for a protein (which might be an enzyme or a regulatory protein) which is functional and is indistinguishable atleast in terms of its functions. In this case, no matter if the person is heterozygous or homozygous for either allele, the concerned protein will be in sufficient amounts and will always be functional. These alleles can be treated as the same allele while performing Mendelian analysis though their products might differ slightly, leading to formation of two (or more) functionally similar Alloenzymes (as opposed to Isozymes which are similar enzymes produced by genes at different loci).
Haplosufficiency. In this case, one of the two alleles codes for a functional protein and the other either codes for a non-functional protein (or does not code at all). But, even in heterozygous condition where only one allele producing functional protein is present, the amount of protein produced is sufficient to show the phenotype and hence, even in heterozygous individuals, enough protein is coded for by the single functional allele exhibiting the normal phenotype. If the two non-functional alleles are present as a homozygous pair, no functional protein is synthesised and hence the phenotype is not shown (i.e a different phenotype is shown). Here, the functional allele is Haplosufficient (able to produce enough protein in heterozygous condition) and is called the dominant since it expresses its phenotype both in heterozygous and homozygous conditions. this is pretty common.
Complete Haploinsufficiency. Here again one allele codes for a functional protein while the other does not. But this time, if the functional allele is present in heterozygous condition, then the amount of the protein produced is not at all sufficient and hence the phenotype is not exhibited. Here the non-functional allele is said to be dominant because heterozygous phenotype resembles the phenotype of homozygous non-functional allele (where no protein is synthesized) since the functional allele is completely haploinsufficient (unable to produce enough protein in heterozygous condition). This method is pretty rare.(e.g rare autosomal dominant dyskeratosis congenita)

If there is partial haplosufficiency /partial haploinsufficiency, the phenomenon of incomplete dominance can be explained. (heterozygous individual produces protein not sufficient for a full-blown phenotype but just a partial expression of the phenotype)

Here, "functional" refers to being actually "functional" as in case of flower colour (anthocyanin synthesis) or just performing certain kind of a conversion leading to a particular effect on thephenotype.


What is this animal? Reminds me of a crab because of the way it crawls but it looks like a plant. Crablike animal however it looks like a plant. Doesn't seem that fast when it comes to speed.

It looks like a clump of seaweed to me. But I can pick out pairs of legs.

It is a species of "seaweed crab" or "decorator crab": a crab that camouflages itself with bits of seaweed it picks up, so its appearance can vary depending on its surroundings. Here's a video, and as you say, in the speed department, it's a bit lacking.

It is identified as Naxia tumida as opposed to the larger decorator crabs. The cephalothorax is that round brown bump in the middle, and in front of it (in the middle below the long axis) are the pincer legs. The second and third pairs of legs have quite a lot of seaweed attached (making up what I've described as the 'long axis'.)

Here is a screenshot from the video of a Naxia tumida.


Why is Mus Musculus a good model organism? I'm reading through a number of articles that use partial hepatectomy in Mus Musculus to study the mechanisms for liver regeneration (1, 2, 3). I have no doubt that a better understanding of hepatocyte regeneration mechanisms will allow scientists to discover/create new theurapetic targets that would improve liver regeneration in mice. However, these articles seem to imply that the results of the research will be applicable to liver regeneration in humans as well.

What makes Mus Musculus a good model organism? I'm inclined to think that some mouse genes might have homological human genes; is there more to that? Bonus points for answers that would show how research on non-coding RNAs, as compared to protein-coding genes, in mice would apply to humans.

Mice are mammals, like humans, so their proteins tend to show more homology with human proteins than non-mammalian options. They are also actually more closely related to humans than cats or dogs due to the relatively recent (~80 million year) separation of lineages that led to modern rodents and primates.

Mice breed fairly quickly year-round and have relatively large litters. Laboratory strains are also quite tolerant of research lab conditions.

Mice are inexpensive to keep: they are small, require little food and care, etc.

People tend to have less opposition to research in mice due to their status as pest species.

Many genetic tools are available for mice, which makes them better models for the next generation of science, which means there are more genetic tools available for the generation that follows, etc. There are now many specialized mouse lines, some for particular diseases, some for particular techniques, etc.

Mice are well-studied, so experiments in mice can be easily compared to other experiments, and there are a lot of standards for protocols. Most experiments are done on inbred mice, which have the advantage of being nearly genetically identical to each other, so experiments done in different labs are done in (nearly) genetically identical subjects which can help with reproducibility and comparisons across studies (though there are also downsides to inbred animals; see below).

None of these factors make mice perfect model organisms. Many successful experiments and treatments in mice have not translated to human outcomes. Laboratory mice are typically highly inbred and may display characteristics thought to be "normal" that are actually the result of genetic drift, founder effects, etc. These can include preferences for alcohol, tendencies toward obesity, poor immune systems compared to wild mice, etc. Some get particular tumors early. Some have seizures. Some lab mice are blind at birth or shortly after. Others have hearing problems.

References

Abolins, S. R., Pocock, M. J., Hafalla, J. C., Riley, E. M., & Viney, M. E. (2011). Measures of immune function of wild mice, Mus musculus. Molecular Ecology, 20(5), 881-892.

Beck, J. A., Lloyd, S., Hafezparast, M., Lennon-Pierce, M., Eppig, J. T., Festing, M. F., & Fisher, E. M. (2000). Genealogies of mouse inbred strains. Nature genetics, 24(1), 23.

Battey, J., Jordan, E., Cox, D., & Dove, W. (1999). An action plan for mouse genomics. Nature genetics, 21(1), 73-75.

Gordon, J. W., Scangos, G. A., Plotkin, D. J., Barbosa, J. A., & Ruddle, F. H. (1980). Genetic transformation of mouse embryos by microinjection of purified DNA. Proceedings of the National Academy of Sciences, 77(12), 7380-7384.

Justice, M. J., & Dhillon, P. (2016). Using the mouse to model human disease: increasing validity and reproducibility.

Kurien, B. T., Gross, T., & Scofield, R. H. (2005). Barbering in mice: a model for trichotillomania. Bmj, 331(7531), 1503-1505.

Lynch, V. J. (2009). Use with caution: Developmental systems divergence and potential pitfalls of animal models. The Yale journal of biology and medicine, 82(2), 53.

Martin, B., Ji, S., Maudsley, S., & Mattson, M. P. (2010). “Control” laboratory rodents are metabolically morbid: why it matters. Proceedings of the National Academy of Sciences, 107(14), 6127-6133.


If plants "alternate generations" between sporophytes and gametophytes, why don't we say the same of humans? I've been reading on Wikipedia about how plants alternate generations between a diploid sporophyte (usually the dominant part) and haploid gametophyte (in flowering plants, the pollen and ovule sacs).

Mammals also produce haploid gametes. But in mammals we don't describe the gametes as a separate generation that alternates with the dominant "sporoid." The gametes are just the organism's means of reproduction.

What is it about plant reproduction that warrants describing their gametes as a separate "generation" or "phase"?

The big difference is that in humans, there is no mitosis in the haploid phase.

There are three terms that are important here:

Haplontic: Most of the life is spent in the haploid phase
Diplontic: Most of the life is spent in the diploid phase
Haplodiplontic (aka. diplohaplontic): About as much time is spent in the haploid phase than in the diploid phase

At the extreme, when there is absolutely no mitosis in one of the phase, then the organism is clearly not haplodiplontic. Haplodiplontic organisms have an alternation of generations.

Note that the term alternation of generations is also used for systems that are much more complex than haplodiplontie. Examples of such complex alternation of generation include many parasites such as the giant liver fluke


Is [O2] different in a 5 mL liquid media? Is there a drastic difference between top and bottom of the tube, with no stirring?

I believe there is. As you can see in the image below, strictly anaerobic bacteria can survive in liquid medium in test tubes, herefore they will migrate to the bodem of the medium to avoid Oxygen. Also you can see that microaerophiles, which require an oxygen percentage of approximately 2-10% (versus approximately 20% in normal air), will be able to survive below the surface of the medium.

So yes, there is a drastic change, seeing as obligate aerobic bacteria can surive at the surface of the medium, and obligate anaerobic bacteria can survive at the bodem.

To this I have one caveat to add. Namely that these tests are normally done in standard test tubes (approximately 9, 22 or 28mL depending on size), which would most likely contain more medium. So I am not absolutely sure, nor have I found any specific information on oxygen gradients in 5mL tubes. You could test this by performing the experiment in described in the figure in your tubes with 5mL medium and see what happens. Then you will definitely know.

Hope this helps!


Why can cats interpret things on a monitor/tv, but dogs cannot? E.g. you can see a lot of videos where cats are smashing some mouse or spider on an ipad, but I have never seen it with a dog. I have a dog myself and I know that he sometimes responds to the sounds from the TV, but not to the images.

Why is that?

Cats and dogs can both view tv screens & monitors ... though their viewing experience is a little different to ours thanks to differences in cone structure leaving them color blind and giving low acuity.

Both species have lower levels of color vision than humans. Cats see slightly more color (in the blue green and yellow end of the spectrum) than dogs do so they may get more of an immersive experience from watching TV.

Further, cats and dogs need a higher frame rate than humans to make it appear as a smooth film, a phenomenon known as flicker fusion, in humans we require 15-20 frames per second, dogs require 70fps and cats about 100. Before the frame rate of televisions increased in recent years it would appeared to them to be flashing images, similar to when you point a digital camera at a screen which may explain why the dog is not interested in the TV, it'd be like staring at a strobe for hours on end. Here is a paper which discusses flicker rates and color vision in dogs.

To summarize there are several factors which influence the "enjoyment" an animal can take from watching a TV - their response to TV imagery will depend on the frames per second, colors, contrast, clarity, movement, subject matter, and (perhaps most importantly in my opinion) the temperament of the animal, for all of which there are difference between the species.

From sciencenordic.com:

  "We humans need about 16 to 20 images a second to perceive what we see
  as continuous film, whereas dogs need about 70 images per second.

  So a few years ago, Fido was probably confounded by his master's
  behaviour of sitting for hours staring at a flashing succession of
  images. With modern resolution and quicker imaging, dogs have become
  potential television viewers.

  This has not gone unrecognised in the USA, for example, where hopeful
  TV producers have started special TV channels for dogs.

  If you have other pets, however, you need to think twice before
  placing them in front of the TV.

  Birds need at least 100 frames per second to see TV images as a moving
  picture. Having a bird in the same room as a TV with a lower frame
  rate than that will be very stressful for the creature."


Anyone know what this it? More than 1 washed up on a beach in Ireland..close to some big jellyfish

Gooseneck barnacles
It appears to be a cluster of goose barnacles washed up onshore. This is based on the thick, distinct pedicle and the general shape of the asymmetrical valves. Without more information, that’s as accurate as I can probably get you.


Can we produce synthetic red blood cells lacking antigens? I had an idea come to me during Biology class and I immediately asked my teacher, but she couldn't really answer the question, so I'll ask it here.

What are the limiting factors in the production of synthetic red blood cells with no antigens? I mean, we do have the human genome mapped, but am I naive to think that we have genetic technology capable of doing this?

If red blood cells are too complex to manufacture, is it feasible to manufacture much smaller particles of just hemoglobin inside small spheres of cell membrane and use that as a temporary replacement for red blood cells?

(I was at a medical research talk a while ago and one professor was explaining that there are many other proteins bound onto a red blood cell that aren't of the ABO or RH system. Normally this isn't a problem for recipients who only occasionally received transfusions but for people who need a long-term supply of blood, their bodies do get sensitized to the foreign proteins and will eventually start attacking the foreign red blood cells).

Actually there are such particles. It is estimated that about 20% of the hemoglobin (HGB hereafter) is in HGB vesicles (HbV hereafter) formed by RBCs. So sure, it is possible to use small particles instead of RBCs, but these vesicles have major and minor antigens on their surface. According to some of the articles they cause other complications too by blood transfusions and they are destroyed by the immune system within 3 to 7 days. So they don't solve the problem.

In Vivo Volume and Hemoglobin Dynamics of Human Red Blood Cells
Artificial Oxygen Carriers (Hemoglobin-Vesicles) as a Transfusion Alternative and for Oxygen Therapeutics
Red blood cell vesiculation in hereditary hemolytic anemia
The red cell revisited--matters of life and death.
Red blood cell microparticles and blood group antigens: an analysis by flow cytometry
Hemoglobin-Vesicles as Oxygen Carriers
Physiological Capacity of the Reticuloendothelial System for the Degradation of Hemoglobin Vesicles (Artificial Oxygen Carriers) after Massive Intravenous Doses by Daily Repeated Infusions for 14 Days

HGB vesicles without major and minor antigens are not a perfect solution either (I think), because the immune system tends to attack such things. For example by viral infections the MHC1 levels are low (in cells with nucleus) to avoid T cell response and the NK cells does not like that, so they destroy such cells. I am almost sure something similar would happen with this kind of vesicles as well. At least afaik. the immune system checks not just the presence of these antigens, but their composition as well. So if a RBC is under stress, then it changes the antigen composition on its surface and the leukocytes destroy it if necessary. According to some of the experiments PEG can cover HbV antigens and increase immune compatibility, so having less surface antigens seems to be a better choice than having more.

Development of a Synthetic Blood Substitute Utilizing Hemoglobin Vesicles
Biocompatibility of Hemoglobin Vesicles, a Cellular-Type Artificial Oxygen Carrier, on Blood Cells and Plasma Proteins In Vitro and In Vivo
Artificial Oxygen Carriers, Hemoglobin Vesicles and Albumin−Hemes, Based on Bioconjugate Chemistry
Hemoglobin Vesicles, Polyethylene Glycol (PEG)ylated Liposomes Developed as a Red Blood Cell Substitute, Do Not Induce the Accelerated Blood Clearance Phenomenon in Mice

HGB vesicles have another problem. The HGB inactivates in them without reduction (metHb formation). Only Fe2+ HGB can carry oxygen. This can be solved with methylene blue according to this study.

Red Blood Cells Donate Electrons to Methylene Blue Mediated Chemical Reduction of Methemoglobin Compartmentalized in Liposomes in Blood
Inhibition of methemoglobin formation in aqueous solutions under aerobic conditions by the addition of amino acids

We cannot use free HGB either, because it would decrease the NO levels and lead to endothelial dysfunction. I think to small particles would have the same effect because of increased surface.

Mechanisms of Slower Nitric Oxide Uptake by Red Blood Cells and Other Hemoglobin-containing Vesicles
Microparticles in stored red blood cells as potential mediators of transfusion complications
Removal of Cellular-Type Hemoglobin-Based Oxygen Carrier (Hemoglobin-Vesicles) From Blood Using Centrifugation and Ultrafiltration

According to other studies RHSA-heme (serum albumin bound to synthetic heme) is another option. It seems to be safe if you replace only 20% of blood volume (of rats). I think a complete transfusion is not safe, because it would reduce the NO levels as we already discussed. I have not found an experiment which does complete transfusion.

Safety evaluation of an artificial O2 carrier as a red blood cell substitute by blood biochemical tests and histopathology observations.
Exchange transfusion with synthetic oxygen-carrying plasma protein “albumin-heme” into an acute anemia rat model after seventy-percent hemodilution

So there is ongoing research in the topic. There is progress, but none of the current solutions is perfect I think.


How to identify the genes that distal enhancers pair? I am writing a project proposal and I have to talk about this problem: how to identify the genes that distal enhancers pair?

I am really new to this topic and I don't know what it is all about. I have been searching the literature but I did not find anything useful. Can someone explain to me what it is all about?
Maybe suggest some papers to me.

Check this technique called Chromosome Conformation Capture (3C). Its variants exist such as 4C, Hi-C etc.

Basically, the principle of this technique is based on the physical interaction between the enhancer and promoter that is bridged by a transcriptional modulator(protein).

The chromatin is crosslinked
DNA is sheared
The protein is pulled down (Optional)
The fragments of the promoter and enhancer are ligated together and then sequencing/qRTPCR is done.

Sequencing (low throughput- sanger) can be used to identify enhancers of a given promoter. qRTPCR can be used to quantify the strength of the association.

What I just said is not a high throughput technique. Hi-C is high throughput variant of 3C. See the protocol here.


Can the mating of a couple with Rhesus positive and negative blood types result in miscarriage? Can the combination of $+ve$ and $-ve$ blood groups of a couple be a cause of miscarriage in pregnancy?

I want to know can +ve and -ve blood group of a couple could be a cause of miscarriage in pregnancy?

Yes. In extreme cases, it can. You are talking about Rh Incompatibility, and can become a big issue when the mother has Rh(-) blood and the father has Rh(+) blood (such as the case with your cousin and his wife).

What could have happened (but definitely won't say for sure) is that your cousin's wife had a natural miscarriage which exposed her to the Rh proteins of the child, and then the subsequent pregnancy had complications due to the previous exposure and mother's development of antibodies which lead to the second miscarriage. However, I am not a licensed physician and you should consult a physician before pursuing any sort of treatments!!!

Rh factor is the presence of surface proteins on Erythrocytes (Red Blood Cells or "RBC"). If Leukocytes (White Blood Cells - most commonly reported as "T-cells") encounter Erythrocytes that do not share the Rh factor of their host, then they can develop antibodies to it - which help identify Antigens (foreign proteins and molecules). Once the Antibodies have been generated the Immune System can attack any foreign Erythrocytes.

In this way, the mother's Immune System can actually attack the RBCs of her child.

You can find out more here: http://kidshealth.org/parent/pregnancy_center/your_pregnancy/rh.html

And a few select quotations:

  Rh incompatibility usually isn't a problem if it's the mother's first pregnancy because, unless there's some sort of abnormality, the fetus's blood does not normally enter the mother's circulatory system during the course of the pregnancy...

  ...Other ways Rh-negative pregnant women can be exposed to the Rh protein that might cause antibody production include blood transfusions with Rh-positive blood, miscarriage, and ectopic pregnancy...

  ...Rh antibodies are harmless until the mother's second or later pregnancies. If she is ever carrying another Rh-positive child, her Rh antibodies will recognize the Rh proteins on the surface of the baby's blood cells as foreign, and pass into the baby's bloodstream and attack those cells. This can lead to swelling and rupture of the baby's RBCs. A baby's blood count can get dangerously low when this condition, known as hemolytic or Rh disease of the newborn, occurs.*

And you are correct that there is a treatment via injection, but the Doctor is also correct in that administering it past the first pregnancy does little for future fetuses:

  Today, when a woman with the potential to develop Rh incompatibility is pregnant, doctors administer a series of two Rh immune-globulin shots during her first pregnancy. The first shot is given around the 28th week of pregnancy and the second within 72 hours after giving birth. Rh immune-globulin acts like a vaccine, preventing the mother's body from producing any potentially dangerous Rh antibodies that can cause serious complications in the newborn or complicate any future pregnancies.

And the ultimate effects of missing the shots and having very unfortunate luck:

  Rh incompatibility rarely causes complications in a first pregnancy and does not affect the health of the mother. But Rh antibodies that develop during subsequent pregnancies can be potentially dangerous to mother and child. Rh disease can result in severe anemia, jaundice, brain damage, and heart failure in a newborn. In extreme cases, it can cause the death of the fetus because too many RBCs have been destroyed.

Is there a cure? No. Once the antibodies have been developed, the Rh(+) protein is known to the mother's Immune System. Nothing short of wiping out the mother's Immune System would act as a cure.

However, in extreme cases, there are treatments:

  If a doctor determines that a woman has already developed Rh antibodies, then the pregnancy will be closely monitored to make sure that those levels are not too high. In rare cases, if the incompatibility is severe and the baby is in danger, a series of special blood transfusions (called exchange transfusions) can be performed either while the baby is still in the uterus or after delivery.

But don't fret yet!

Rh surface proteins are determined by genetics, and each time a child is conceived there is a chance that the Rh protein will be (-) if the exact genotype of the (+) parent allows it. So if your cousin's wife were to get pregnant again (and each time she does) it's a chance that the Rh Incompatibility (aka - "Hemolytic Disease", aka - "Rhesus Disease") won't show up.

So there are some reasons to stay positive.


What causes adenosine build up in the brain when awake? Adenosine is an important hormone in sleep regulation.  It is postulated that when a person is awake, there is a build up of adenosine in the brain, which inhibits the neurons in the brain, and produces tiredness.  (See answer for more information:  What causes humans to be sleepy?)

However, I am wondering what specifically causes this adenosine build up.  I understand ATP (adenosine tri-phosphate) is broken down to ADP in the brain to produce energy.  I thought this ADP would then be used to re-generate ATP again etc, so I'm not sure how adenosine is built up in the brain over a day.

Basically I am unsure how Adenosine itself, as opposed to ATP or ADP, is produced during the waking state?

My theory is that during the high demand waking state there is insufficient energy to convert ADP back to ATP, and the excess ADP is broken down to adenosine somehow.

I would appreciate an explanation of how this build up occurs, and also an explanation of how this in turn how it induces sleepiness would be a plus.

Adenosine causes humans to become sleepy. But how ?

During day time we consume food which is broken down into glucose. This glucose is broken down by "Glycolysis" in cell's cytoplasm during which ATP is produced. This produced ATP is is then used by body as an energy supplier. ATP breaks down into ADP and then AMP with the release of energy which our body consumes for doing work.

(Fig 1- Structure of Adenosine to ATP)

Adenosine is produced continuously and starts to accumulate around and in Adenosine receptors such as A1, A2a, A2b and A3 (as shown in fig below).Adenosine inhibit signal propagation and energy production in at least A1. (Not all the receptors induce sleep when they receive Adenosine.) "A1 receptor" receives adenosine and induces sleep. A1 receptors are implicated in sleep promotion by inhibiting wake-promoting cholinergic neurons in the basal forebrain.

Continuous inhibition of A1 receptor by Adenosine slowly induces sleep by relaxing the brain and muscles but without substantially weakening their abilities!

How is Adenosine metabolized ?

During sleep the accumulated Adenosine is metabolized by Adenosine deaminase enzyme which catalyzes the irreversible deamination of 2'-deoxyadenosine and adenosine to deoxyinosine and inosine. With the reduction in the Adenosine content the body is excited from sleep slowly.

So in short summarize:

  The accumulation of adenosine during waking periods is thus associated
  with the depletion of the ATP reserves stored as glycogen in the
  brain. The increased adenosine levels trigger non-REM sleep, during
  which the brain is less active, thus placing it in a recovery phase
  that is absolutely essential—among other things, to let it rebuild its
  stores of glycogen.

  Because adenosine is continuously metabolized by the enzyme adenosine
  desaminase, the decline in adenosine production during sleep quickly
  causes a general decline in adenosine concentrations in the brain,
  eventually producing conditions more favourable to awakening.

(Refer this page: MOLECULES THAT BUILD UP AND MAKE YOU SLEEP)


Do Fatty Acid Synthase Inhibitors Selectively induce Apoptosis in Cancer cells without inducing the same in healthy human cells? Do Fatty Acid Synthase (FAS) Inhibitors (e.g. cerulenin) selectively induce apoptosis in cancer cells without inducing the same in healthy human cells?

I found this reference: "Inhibition of fatty acid synthase (FAS) suppresses HER2/neu (erbB-2) oncogene overexpression in cancer cells".   Cerulenin is not a magic bullet, but in some cases it may help.


What's the difference between prions and prion-like proteins? If I added a prion domain to a protein, does that make the protein a prion-like protein or would it be considered a prion at that point?

I'm trying to understand what prions are, how they aggregate and what macroscopic shapes they conform to (i.e. a ring vs smaller micelles).

Thank you very much!

My understanding is that the principal quality of a prion is that it behaves like a prion in cells- the logic is a little circular.

A few of these criteria for acting like a prion (in yeast, where prions are most common):

Reproduces itself by "templating" (refolding of non-prion versions of itself into prion versions)
Sensitive to protein denaturing agents (which get rid of the prion protein conformation).
Dependence on protein chaperones which reproduce prions by releasing prion oligomers from larger prion aggregates. These oligomers go on to "seed" new prion aggregates.
Forms insoluble protein aggregates consisting of many copies of the prion protein.

An important subtlety here is that proteins with identical amino acid sequence can be both prion and non-prion in the same cell. It is a biochemical consequence of a specific protein structure, rather than simply a feature of the protein sequence. Thus, a prion domain confers the ability to become a prion, not necessarily "prion-ness" itself. This Scientific American article might be helpful regarding this point.

As an example of how these criteria are applied, this paper uses some biochemical and genetic methods to screen for the presence of new prions in wild yeast.

As a review of how prions oligomerize and form their classic aggregates, this paper might be helpful.

It is certainly true that creating fusion proteins with candidate prion domains is a common way of confirming that those domains are competent to become prions (see e.g. this paper). But there is usually a higher standard of evidence to show that some protein actually is a prion- usually by demonstrating the existence of heritable protein aggregates mentioned in point (4).

Hope that helps.


Is Einstein's mass energy equivalence ($E=mc^2$) relevant to biological systems? I'm more than 100% sure that the kilograms I eat don't get directly converted to feces and urine.

I'm sure some of it goes to regenerating tissue that is constantly being disposed as well, and maybe some of it is  also being exhaled.

But I have a feeling that $E=mc^2$ might have something to do with the disposal of ingested kilograms.

We are constantly radiating electromagnetic waves in the nonvisible spectrum, we generate heat, we generate chemical bonds, all of these processes can convert mass to energy.

So I was wondering if $E=mc^2$ is relevant to biology?

Thanks.

Short answer

Any law of physics will of course be applicable to living beings. However, in the absence of mass gain and mass loss, the input = output equation for matter holds true and does not require any spontaneous creation and destruction of matter to equate. In other words, the effects of Einstein's discovery has no measurable/practical consequence on biological system (it is here but it is negligible) and the law of conservation of mass applies nicely.

Input and outputs of matter

There are two main sources of matter input:

Eating and drinking
inhaling (gas through the trachea and the lungs)

There are three main sources of matter output

excretion (urine and feces)
exhaling
sweating

The importance of inhaling and exhaling

Just to get an intuition about the importance of inhaling and exhaling matter in this input = output balance, note that when one make sport to lose weight, she/he principally lose weight through exhaling (see this popular video from SciHow). Similarly, trees mass mainly comes from  what they inhale (see this popular video form Veritasium)

Possible duplicate on Physics.SE

You might also want to read the How does mass leave the body when you lose weight? on Physics.SE.


Do all Viruses have the same RNA Let's take the Influenzavirus as an example, and I have 5 of it. Would all 5 viruses have the same RNA with the same base order? Or would the RNA base order differ from eachother?

A person infected with a strain of a pathogenic virus will have copies of that virus in their body.

Virus particle genomes could contain a number of substitution, insertion, and deletion mutations. The surface proteins on enveloped and non-enveloped virus copies could contain mutations. Most mutations are deleterious and those particles will not be infectious.

But the genome sequence of that virus will be largely identical, these mutations aside, and copies will be packaged so as to attempt to reinfect and reproduce.

Actual mutation rates depend on the virus type (RNA, DNA, single- or double-stranded, sense; see Figure 12.1 about the Baltimore classification of viruses), and how it uses reverse transcriptase, RNA, or DNA polymerase to make copies of its genome for use in expression (to make viral proteins) and reproduction (to make viral genomes).

For instance, RNA-dependent RNA polymerase has a lower fidelity rate — makes more copying mistakes — than DNA polymerase. Reverse transcriptase can also introduce mutations when turning the viral RNA genome into DNA, and vice versa. These processes can also introduce errors in expression of membranous or capsid proteins in enveloped and non-enveloped viruses.

The RNA virus family Orthomyxoviridae contains the strains of influenza that infect humans. These are enveloped, negative-sense, single-stranded RNA viruses. They use RNA polymerase to turn their genome into forward-stranded RNA molecules that can act as both mRNA (messenger RNA that is translated into viral proteins) and as a template (again, using RNA polymerase) for making copies of the influenza genome, itself.

Errors introduced at these two steps will result in copies that are different from the parent.