Large black caterpillar, cocoon, moth - Los Angeles This is my first visit here, probably the first of many, since I have many species to identify!

The first is a regular resident of my back yard in the Los Angeles neighborhood of Mt. Washington. It's a large black caterpillar that comes out at night to feed on what I assume is native flora. I have seen as many as five or six at a time in a good (wet) year, but the last couple of years have literally seen only one at a time. Note the ant in the lower left for scale:

A couple of years ago, I brought one home and kept it in a terrarium until it pupated and hatched.  I have a picture of the cocoon, but can't post more than 2 links right now. It was dark brownish-red, with strands of silk that looked to anchor it to the ground, with the empty body on top.

It turned into this very pretty moth:

Unfortunately, it beat up its wings a little, as it took me some time to realize it had hatched. It was released at night.

I had a possible ID at one point on another website, but I didn't follow up with them, and have a lot of trouble searching there for my old thread. Found this place, and thought I'd give it a shot. As I say, I have many more species questions, but I'll just start with this one. Many thanks in advance.

Based on the image of the moth, I think this is a Painted Tiger Moth (Arachnis picta). See the image of the moth from the Wikipedia (you can even see the yellow color at the head region):

An image of the caterpillar can be found here, but this is less decisive.
It also fits with the geographic location where you found the moth, see here.


What is the name of this injured species? Location: South India

Size: 2-3cm

looks like injured species, unable to stand.

Well, after a lot of research, I hardy believe that it is a Rhizotrogus aestivus. First of all, the size (2-3cm) you mentioned fits exactly. Secondly, the colour matches fair enough. Finally the antennas and the body shape, may not be seen very well in the picture but I assume that they match. The only thing that I am not sure is the "laziness" of that insect, beacause they are only lazy or clumsy and not active, only when they are about to die.

For more informations check here: https://inpn.mnhn.fr/espece/cd_nom/10907?lg=en


Negative value on linear gene expression in microarrays I am starting to use microarrays and maybe this is a dumb question:

Using Illumina microarrays, linear gene expression can be negative? Or maybe some artefacts have been introduced?

And, in this case, how to correct them? With scaling (adding the absolute value of the minimum negative value) or flooring (converting negative values to zeros)?

Thanks

I'm not personally familiar with Illumina arrays, but I can give some notes here.  This link is a paper which describes the array quality controls specifically. This presentation describes the calculation of the intensities in bioconductor.

The answer is yes: you will find negative numbers sometimes.  They should be rare.  The Intensities numbers from a scanner which essentially takes an image of the bead fluorescence on the glass slide and tries to subtract a background signal.

The background is the typical level of signal you see on a bead with no sample DNA bound to it.  You will get some pixels lighting up a bit even there.

In expression microarrays, this is not a perfect system as each bead has a different nucleotide sequence on it.  Each bead has a specific DNA sequence has non-specific binding which is pretty much unique on the slide.  That is to say, the oligomer on the bead might bind strongly to DNA from your sample which is not its reverse complement to varying degrees.

I think what happened is that there will be a handful of cases you can find a bead which has less fluorescence than the background controls on the slide.  It's possible that the probe has a design flaw but I would generally assume that the negative number means that there is no detectable target cDNA in the sample for that oligo.

I probably wouldn't convert the number to a zero, but you could probably justify it to yourself in some cases.  Most difference experiments are the logarithm of the ratio so zero is not a great number in those cases.

@Luke 's comments are well said.

I think that negative values can still represent signal because of the variance of sequence-dependent effects for the purposes of scaling, and difference experiments.  But I'd tend to think of them as zero signal in any case.  There are probably genes which express at or below detection threshold all the time, which is not zero information, so the number has some value.


What is the meaning of multicellularity? I can't understand what multicellularity is. Wikipedia states that any organism having many cells is multicellular. By this definition bacteria can also be multicellular. For example, cyanobacteria can form filaments made up of specialised cells like spore cells and vegetative cells.

But aren't bacteria supposed to be unicellular only? I would appreciate it if someone could clear up my confusion.

Bacteria are, as a general rule, unicellular.  However, there are some, like the cyanobacteria which you referenced, which are kind of border line.  Wikipedia's definition of multicellularity is a very broad sweeping definition, and its statement that bacteria are unicellular is also a broad sweeping statement.
The fact is, that as a general rule, bacteria are unicellular, but at times, like you said, they can undergo filamentation.  When they do, they end up with several connected cells which are generally considered functionally independent.  In certain circumstances, however, the cells can be dependent on each other for survival, and because they didn't separate completely, it's hard to define whether we're looking at multicellularity or symbiosis.
It is generally accepted that cyaonbacteria are truly multicellular.  In order to be multicellular, an organism generally has to fulfill 5 basic requirements:

More than one cell
Cells stick together
Cells communicate
Cells are dependent on each other
Cells are differentiated

By these requirements, some cyaonbacteria technically are multicellular bacteria, defying frequent claims that all bacteria are unicellular.  That said, wikipedia isn't totally wrong, since as a general rule, bacteria are unicellular.  Cyanobacteria are an odd (debatably) exception to the rule.

Sources:

Bacteria with bodies - multicellular prokaryotes, Gould, S.E.
Multicellularity in Cyanobacteria, Paleontology Podcasts
Introduction to Cyaonbacteria, University of California Museum of Paleontology
Wikipedia: Multicellularity, Cyanobacteria, Filamentation


Single celled organism and immortality My biology book says:

  No individual is immortal,except single celled organisms..

I think that such conclusion aries from the necessity of binary division in many single celled organism to reproduce.

Is the book's conclusion biologically correct and why?

I don't believe this question is an exact duplicate of the question at Do bacteria die of old age?, however all of the comments and answers provided there are relevant, and you should read them before continuing to read this answer because I won't repeat what's stated there.

In addition to bacteria and yeast which produce certain "rejuvinated" cells that can divide indefinitely while other cells become senescent or "aged", all multicellular organisms actually employ a remarkably similar strategy. Under certain culture conditions, embryonic stem cells can propagate indefinitely (1).

During early embryogenesis they divide "symmetrically" to the extent that all of the daughter cells are fully undifferentiated until after gastrulation (2), but there is a certain degree of asymmetry that defines the axis along which gastrulation occurs prior to gastrulation (3). This asymmetry is mediated by a large number of signaling pathways (3), some of which become asymmetric during the very fist cell division of the embryo. Adult stem cells also divide asymmetrically primarily as a precursor to differentiation, but this is thought to also be involved in the asymmetric distribution of damaged components to their more differentiated daughter cells (4), as occurs in yeast and bacteria. Currently there is less research on this in adult or embryonic human stem cells than in bacteria or yeast, but it stands to reason that our embryonic cell line does the same thing beginning at its first division, and our germ line is immortal (we're no "older" at birth than our great-great-great-great-great-great-grandfathers) for the same reasons that unicellular cells are immortal.

References:

(1) https://en.wikipedia.org/wiki/Embryonic_stem_cell#Propagation

(2) https://en.wikipedia.org/wiki/Embryonic_stem_cell#Pluripotent

(3) https://en.wikipedia.org/wiki/Gastrulation#Loss_of_symmetry

(4) http://www.ncbi.nlm.nih.gov/pubmed/25966295


Does anybody knows name of this bird I found in my backyard in India? I found this bird in my backyard in India. I checked several websites but wasn't able to identify it. Any help would be appreciated.

I am pretty sure that this is a  Indian Paradise-flycatcher (Terpsiphone paradisi). Since we cannot see the length of the tail feathers, we cannot distinguish between male and female, the later have a much shorter tail.

See the image (from here) for comparision:

More information can also be found here and here.


Why is it $q^2$ for the individual count in hardy weinberg? My understanding:

In Hardy-Weinberg problems the frequency of a homozygous recessive genetic occurrence in a population is $q^2$. So if 1 in 100 people in a population have albinism (homozygous recessive disorder) then we say the frequency is $q^2=1/100$.

We then say, to find the frequency of the allele count $q$ that $q=\sqrt{1/100}= 1/10$.

I don't understand why we say this. Why would the allele count be the square root of the population frequency? There's 2 alleles per person. Why isn't it x2 or /2 instead?
I suppose my problem is understand what exactly is p and q.

First of, let me correct your equation: $q = \sqrt{\frac{1}{100}} = \frac{1}{10} = 0.1 ≠ 10 $.

From allele frequency to genotype frequency

Imagine you were to randomly sample an allele from a population of allele where the allele A is present at frequency $q$. What is the probability that you draw allele A? Answer: $P(A) = q$. Now, put this allele back in the pool and imagine you have to draw two alleles. What is the probability that the two alleles are A. Well it is the probability that the first allele is A times the probability that the second allele is A, it is $P(A) \cdot P(A) = q \cdot q = q^2$.

From genotype frequency to allele frequency

Therefore, under Hardy-Weinberg conditions, if the allele A is at frequency $q$, then the homozygote genotype AA is at frequency $q \cdot q = q^2$. Now let's denote the frequency of the genotype AA by $f_{AA}$. You know that $f_{AA} = q^2$ from the above though experiment. If you take the square root of both sides, you get $\sqrt{f_{AA}} = \sqrt{q^2} = q$. In words, the frequency of the allele A is the square root of the frequency of the genotype AA.

Recessivity and dominance

Btw, you'll note that those calculations tell nothing about the patterns of dominance/recessivity of alleles (Hardy-Weinberg principle assumes no selection anyway).


Why do we blow when we're out of breath? When people are out of breath from exercising, instead of breathing normally they partially obstruct their expirations by blowing out instead of breathing out.

Why is this?

EDIT: This photo illustrates what I'm referring to.

Trying to rephrase the question

If I understand the question (and what you missunderstand) correctly, I think one could rephrase the post as

When one spends some time under water and come back to the surface, one usually breath out and then breath in. This is surprising to me because I would expect the person to be out of air and therefore wouldn't need to breath out before breathing in.

Let me know if I failed to understand your question and misunderstandings

Answer

We don't incorporate the air we breath in our lungs. We only use the molecules of oxygen $O_2$ from the air (which takes ~20% of the total volume). This molecule goes in the blood, reach the cells and react with sugar to produce energy. The waster of this reaction is another molecule $CO_2$ that needs to be exhaled through the lungs.

So, really the volume and of air that we have in our lungs doesn't vary much (It actually increase a little bit as we had some carbons). Only the composition of the air that we have in our lungs changes. After some time, we need to renew this air and for this purpose we first need to breath out the air that is contain a high density of $CO_2$ before breathing in.

This is why when sticking the head out of the water many people first breath out and then breath in. Note, however that one can breath out all its air underwater and then only has to breath in when back at the surface.

EDIT

Are you asking why do we contract our lips during sport?

If yes, I think it very much depend from one person to another. There is probably no physiological advantage/disadvantage at doing so and it probably is just a consequence of expressing pain on our face.


Is Zika suspected of causing birth defects only if contracted during pregnancy? There seems to be growing evidence that a recently spreading strain of Zika virus is in fact linked to microencephaly and other birth defects in newborns (see here, here, and here for examples).

I understand that this is currently an active area of research and a number of questions remain unanswered. However, even given the current uncertainties, I feel any discussion about when a mother gets infected has been largely ignored by all of the news/media/science outlets I've seen.

My question is: does the virus lead to birth defects only if the mother gets infected during pregnancy, or can a previous (or latent) infection lead to similar birth defects? If the former, does timing of infection during different trimesters matter?

As you mentioned, there is evidence that mother-child transmission of Zika virus causes congenital anomalies like microencephaly.
Now your question, if a cleared infection before the pregnancy could affect it? In principle, no. Once the virus is cleared, it should not reactivate, unless there is reinfection. Here's a quote from the Zika article from Uptodate.com:

  Women of childbearing potential — It is uncertain how long women of childbearing potential should wait between Zika virus exposure/infection and conception. Most pregnant women with Zika virus exposure give birth to normal infants [111]. Zika virus usually remains in the blood of an infected person for a few days to a week, and thus far there is no evidence that a fetus conceived after the virus has cleared from the blood would be at risk for Zika infection [94,112]. However, information regarding the persistence of Zika virus following infection is not known. It has been suggested that infection due to other flaviviruses such as West Nile virus may persist years after initial infection [113-115]; these data are controversial. Pending further study, healthcare providers should encourage women to make such decisions based on their individual circumstances, values, and preferences.

  Daniel J Sexton, MD
  Editor-in-Chief — Infectious Diseases Section
  Editor — Bacterial Infections
  Professor of Medicine
  Duke University Medical Center


Why are root hairs mostly unicellular? Most root hairs are unicellular but why is it so? What advantages does a plant derive from a unicellular root hair that it couldn't have if it was multicellular?

A couple reasons come to mind.* The purpose of root hairs is absorbtion. If you consider multiple cells along the length of the hair,  additional cell walls and plasma membranes would somewhat impede the movement of nutrients.

More importantly, the absorbtion is a function of the surface area of the hair. Smaller diameter (one cell thick) hairs provide greater surface area to volume ratio. While it's true that a larger diameter, due to multiple cells, might offer greater overall surface area, it would come at the expense of requiring more volume compared to a greater number of smaller hairs.

For example, suppose you have a certain volume of cutoplasm to spend on making root hairs. For the sake of the example, suppose the hairs are of a fixed length. If you make the hairs half the diameter you will be able to provide twice the overall surface area using the same volume of material.

* By this I mean I don't know the ultimate (evolutionary) reason and I doubt anyone does. This is probabably not an active area of research and you're not likely to find definitive answers with research. So, my answer, if you will, is conjecture.

That said, it is educated conjecture. In 24 years of teaching AP Biology, the relationship of volume versus surface area has arisen multiple times. One of the exercises I gave my students, in preparation for the exam, was to find at least ten examples. Some of the best students found many more.


How good is information transfer between the hemispheres of the brain? I sometimes listen to lectures on my phone using ear buds, but occasionally with only one ear bud in. Is the other half of my brain losing out on any aspect of the lecture? Just how good is the corpus callosum at sharing information between the hemispheres?

Auditory information is routed to cerebral hemispheres via the brainstem and midbrain.  Structures in the midbrain receive information from both ears and combine it (including differencing it for spatial location) before sending the combined information on to both cerebral hemispheres.  Usually only the left hemisphere interprets the sound for language content, but it is doing so based on the sounds perceived from both ears.  The corpus callosum would not be involved in the hearing pathways.  So sound coming from the left ear should work as well as sound from the other if the perception level is adequate and not interfered with by sounds from the other ear.  It is likely the sound perception is somewhat better if both ears are receiving input from the source.


ELISA troubleshooting Hi,

Why does my elisa plate wells gives a brown color after adding the stop solution. I am giving a 4*5 minutes wash after each step. TMB gives it a proper blue color but when I add the stop solution (0.16M H2SO4), the color turns to brown. I am using all the reagents new. Any help will be appreciated.

The full oxidation of TMB ( 3,5,3’,5’-tetramethylbenzidine) is 2-electron process.  The first step (one electron oxidation) gives the blue product, which is then further oxidized to a yellow product (2nd electron) that is stable in acid.  At high concentrations this might appear brown.
You might also not be fully quenching, leading to a mixture of blue and yellow products (should be more greenish though).  In this case add more stop solution.
TMB chemistry:
Josephy, P. David, Thomas Eling, and Ronald P. Mason. "The horseradish peroxidase-catalyzed oxidation of 3, 5, 3', 5'-tetramethylbenzidine. Free radical and charge-transfer complex intermediates." Journal of Biological Chemistry 257.7 (1982): 3669-3675.


How to build a phylogenetic tree without an outgroup? I have whole genome aligned sequences of four beetle populations of same species. I wish to construct a phylogenetic tree with the four. However, I am unable to find a suitable outgroup of the species, so I cannot use an outgroup to root the tree. Is there a particular method that one can use to construct a tree without an outgroup? I found that the MEGA software does this well. What is the theory and understanding of constructing a tree without an outgroup? what are the implications of constructing a tree without an outgroup? Ar the distances between trees measured relative to one another?

Most classic phylogeny reconstruction algorithms root the tree a posteriori, based on the outgroup chosen by the user. The tree is actually inferred and internally represented without root.

Therefore, if you use a program that asks you an outgroup, it is likely that you can just choose an arbitrary one and later "de-root" the obtained tree.


Negative Oxygen Consumption Rate Oxygen consumption rate (OCR) is defined as the rate at which cells consume oxygen. I reason that for cells not capable of photosynthesis, OCR is strictly non-negative.

That was until I read this article which provides a graph with negative OCR values. Could someone enlighten me as to how this might be possible? If the cells are consuming no oxygen, I would expect OCR to be zero, not negative.

Scientific Paper:

http://www.pnas.org/content/108/33/13829.full

The diagram is not clear. They should write "change of oxygen consumption rate".

The caption of the diagram makes it clearer what they are describing:

" In A, a time course for measurement of oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) is shown under basal conditions, [...] ".

So basically they are measuring oxygen consumption rate under basal conditions and apply some chemicals and depict the change in oxygen consumption rate in a diagram, given in percentage.


Can methylation of a promoter induce gene expression in some rare cases? Can methylation of a promoter induce gene expression in some rare cases?

I've read somewhere that methylation of an intron can induce gene expression (eg. Igf2). How is that even possible?

Thank you in advance!

There is nothing intrinsic to DNA methylation itself that requires it to repress transcription. Simply, it affects sequence recognition by proteins. CpG methylation can prevent transcription factor binding and/or recruit proteins that inhibit transcription, either competitively or through chromatin condensation. This is why it's generally associated with transcriptional repression.

I have found some articles which describe methylation in intergenic regions and introns activating transcription but, since you're asking specifically about promoters, I'll limit the examples to methylation in the 5' flanking region. Please note that I'm grossly oversimplifying these articles, you should actually read them to get the full picture.

Bahar HK, Vana T, Walker MD. 2014. Paradoxical role of DNA methylation in activation of FoxA2 gene expression during endoderm development. J Biol Chem 289(34):23882-23892

This study reports that, during development, high levels of methylation of a CpG island in the FoxA2 promoter is present in expressing tissues and absent in non-expressing tissues. Their hypothesis is that CpG methylation prevents binding of a protein that represses transcription by condensing chromatin through histone modifications.

Hantusch B, Kalt R, Krieger S, Puri C, Kerjaschki D. 2007. Sp1/Sp3 and DNA-methylation contribute to basal transcriptional activation of human podoplanin in MG63 versus Saos-2 osteoblastic cells. BMC Mol Bio 8(20)

Here, PDPN expression was associated with CpG methylation. They hypothesize that methylation could affect chromatin state or recruit, what they term, a methylation dependent factor, which activates transcription.

Niesen MI, Osborne AR, Yang H, Rastogi S, Chellappan S, Cheng JQ, Boss JM, Blanck G. 2005. Activation of a methylated promoter mediated by a sequence-specific DNA-binding protein, RFX. J Biol Chem 280(47):38914-38922

This study describes a DNA binding protein (RFX) that can recognize and activate the methylated promoter of MHC. They suggest that RFX can competitively inhibit binding of methyl-DNA binding domain proteins that condense chromatin.


Is it possible to have life that feeds on thermal energy On earth, as far a we know, there are two main ways that bacteria gain energy.

First, there is Photosynthesis, the transition of light into chemical based energies such as ATP.

Second, there are chemical processes in which the cell breaks down a variety of molecules down to gain energy from the reactions. A example of this is Chemosynthesis.

Is it possible for their to be a bacteria or type of organism that gains energy from thermal energy?

For example, there could be a bacteria that lives in a volcanic area, somewhere hot enough that there is a excess of thermal energy. Would there be a way for such a cell to use this thermal energy in much the same way that some cells use Sunlight in Photosynthesis?

It is theoretically possible but no known organisms does it. The problem is you need a pretty strong and persistent temprature gradient to generate usable work out of it, and those are not that common in nature.


What information does the KEGG Module statistics page show? While browsing through the home page of KEGG Module, I clicked the button named Module statistics.
Can someone tell me what does these numbers signify? What are they the statistics of?

My understanding is that these statistics show the coverage for each KEGG Module in the particular phylogenetic group. For example, M00001, is found in 275 of the eukaryotic organisms in KEGG (which represents 90.5% of the eukaryotes in KEGG). The same logic applies for other groups.

An quick example demonstrating this hypothesis, done with the Protists group found in KEGG Organisms (since it is easier to count by eye). There are 43 protists, and in the statistics it says (as of 2015/7/9) that module M00001 is found in 33 of them, hence: $33/43=0.7674419$ which agrees with the 76.7% shown.


Mitochondrial D-Loop I know that the D-loop is  a DNA complex in which the strands of double helix DNA molecule are separated for a stretch and held apart by a third strand of DNA. Usually, this third strand has a base sequence, which is complementary to one of the main strands and pairs in accordance with it. The third strand then sub sequentially displaces the complementary main strand in the region. Im also aware that D-loops occur in many DNA systems, such as in DNA repair, telomere activity, and in mitochondrial circular DNA molecules.  However, my question is why does the D loop only provide information about maternal DNA ancestry?

All the mitochondria of an individual are originating from the mother. This means that if the mother is afflicted by a mitochondrial disease, the offspring will also be affected. This is why the three parent model is being considered in some cases (1).

(1) Pritchard, C. (2014, September 1). The girl with three biological parents. BBC News. From http://www.bbc.com/news/magazine-28986843


Insulin and monoclonal antibody production When producing insulin, the gene for its production is inserted into the plasmid of a bacterium that is allowed to replicate freely.

Why can't the same thing be done with antibodies (as I understand it, currently cancer cells are fused with mammalian cells that produce these antibodies, and now the tumour is allowed to replicate, much like the bacterium, making more antibodies)?

What is different about these two proteins that means fairly distinct processes of production are required for each?

I recommend that you take a look at this:

  Jeong KJ, Jang SH, Velmurugan N. (2011) Recombinant antibodies: engineering and production in yeast and bacterial hosts. Biotechnol J. 6:16-27.

This fairly recent view discusses the progress and prospects for producing functional antibodies in yeast and bacteria. As pointed out by @Nick in the comment to the OP, the main stumbling block in both cases is the engineering that would be necessary to ensure correct glycosylation in the heterologous expression systems. This quotation from the cited review sums up the situation:

  The N-linked glycan structure in the Fc region of antibodies is indispensible for binding to receptors (FcγRs), but glycosylation has been one of the major limitations in choosing possible production hosts. Eukaryotic yeast as well as bacteria, including E. coli, have not been used as the main hosts for the production of recombinant antibodies (full-length IgG format) for use in humans because of glycosylation problems.

They do however go on to discuss some interesting developments such as the expression of a Campylobacter N-glycosylation pathway in E.coli, as well as strategies for the production of functional antibody fragments.


How many copies of a gene? I am studying mathematical models of transcription and translation and I am wondering:

In a particular genome, how many copies of a gene coding for one particular protein should one expect? Are they all transcribed at the same rate?

I know humans have two copies of each chromosome, so the answer would be at least 2 in humans. But I wonder if one particular gene coding for a protein we need in abundance might be present in many copies in the genome to increase expression.

Cell cycle

Talking about physical copies of gene, we would indeed have at least 1 copy during the haploid phase, 2 copies during the diploid phase and 4 copies during the mitosis (and during the first phase of the meiosis). Of course, species having mitosis during the haploid phase would have 2 copies of the gene during the mitosis. I am not talking about polyploid species and am not talking about some fungi and other things that have all kind of crazy reproductions system. I am not talking about mtDNA either. Finally, I am not addressing the case of specialized cells that lose part of their genome or the case of tissues that are basically cells who merged together, so that the concept of cell does not even hold any more such as the Syncytiotrophoblast (in the placenta) (see also cell fusion and syncytium).

In short, the variation in the number of copies during the life-cycle is very dependent on the species of interest, the sequence of interest and may also fall under some semantic issue about what is a cell. Note another potential semantic issue result from the question "how similar two genes have to be to still be called copies?".

Mutations and polymorphism

Now, some genes can be found in several copies. When, in a given population the number of copies of a given gene varies from one individual to another, we talk about Copy-Number Variation (CNV). The increase in the number of copies is called gene duplication (or gene amplification or chromosomal duplication when a very big chunk of DNA gets duplicated). The decrease in the number of copies is called gene deletion. There are a diversity of processes that can cause deletions and duplications such as homologous recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.

Evolution of CNV

What mutation is likely to occur first

Gene duplication does not necessarily yield to an increase in the protein concentration (but it can as it is the case for the Pelizaeus–Merzbacher disease for example). If higher expression is selected for, it "feels more likely to me" that the first mutation(s) allowing for this increased expression will affect the regulatory sequences and will not increase the number of gene copies.

Consequences of gene duplications

Gene duplication (if not loss) can yield to subfunctionalization or neofunctionalization. From wikipedia:

  Subfunctionalization [is a process] in which pairs of genes that originate from duplication, or paralogs, take on separate functions

...In others words, copies are free to accumulate mutations as long as the other copy is still doing its job

  Neofunctionalization, one of the possible outcomes of functional divergence, occurs when one gene copy, or paralog, takes on a totally new function after a gene duplication event

...Basically, one copy gets a totally new function... that can yield to very interesting innovations such as anti-freeze proteins (ref) or snake venom (ref).


Why does the inhibition of translation initiation cause the accumulation of 80S ribosomal monosomes? As I have read in (1), inhibition of translation initiation will increase the number of 80S ribosomes while decreasing the fraction of polysomes due to the polysome-runoff. The net effect is to decrease the polysome/monosome (P/M) ratio and we observe it for example by inducing ER stress by tunicamycin in (2).

I understand the reduction in polysomes - since we don't interefere with elongation, polysomes work as normal, fallling of eventually, but new monosomes cannot proceed to polysomal stage due to inhibited initation.

However, why do the 80S ribosomes accumulate? I have always thought that 80S ribosome is always bound to mRNA, otherwise it dissociates as separate 40S and 60S subunits. Does this effect therefore mean that the accumulated 80S fraction is mRNA-free and therefore "vacant 80S ribosomes", as decribed in (1), can exist?

Thanks a lot!

https://books.google.co.uk/books?id=6sEq1xLu_hcC&pg=PA130&lpg=PA130&dq=polysome+translation+initiation&source=bl&ots=Un6JjImBJX&sig=ln9mn0KoJDJaVOGK8LbrEmMz9XE&hl=cs&sa=X&ei=x2JiVci8N4jX7Ab02YLgBQ&ved=0CGQQ6AEwCw#v=onepage&q=polysome%20translation%20initiation&f=false
http://jcs.biologists.org/content/115/11/2443/F4.large.jpg

It will depend on the drug you are using. There is a pathway that forms the translational initiation complex that starts with binding the mRNA's cap, the small subunit scans to find the AUG, then the large subunit binds, and so on. The 80 S peaks on the density gradients are not vacant, they are poised on mRNAs waiting to initiate (if you removed the inhibitor).


How are haplotype blocks different from genes? According to Cardon et al. 2003, a haplotype block is

  A discrete chromosome region of high linkage disequilibrium and low
  haplotype diversity. It is expected that all pairs of polymorphisms
  within a block will be in strong linkage disequilibrium, whereas other
  pairs will show much weaker association. Blocks are hypothesized to be
  regions of low recombination flanked by recombination hotspots.

It seems obvious that the parts of the genome that compose genes will have a somewhat similar behavior.

So what are the differences between haplotype blocks and genes? Are genes a kind of haplotype block?

Cardon, L. R., and G. R. Abecasis. 2003. Using haplotype blocks to map human complex trait loci. Trends in Genetics 19:135–140.

Haplotype blocks may cover more than just one gene.

While positions within a gene are also in high linkage disequilbrium (or well correlated) with each other, this phenomena of high LD may extend beyond the gene body and overlap with the next gene.  A good visual representation of this comes from Jeffreys et al. in the figure below:

Red means more LD, black means zero LD.  Each point in the heatmap is essentially a pairwise correlation between two points in the genome.  Therefore regions of red represent regions of high LD or haplotype blocks.  Going from left to right we can see that each gene appears to be in its own block of high LD.  However, the genes PSMB9 and TAP1 appear to be in the same block.  Other examples exist as well, a great source is this review.


Could cancer be in itself a evolutionary process? Could cancer be in itself a evolutionary process? Maybe in some way could it be a process of variation? Or would this idea be completely without support, if so, why?

I don't mean that each case would lead to evolution, but that within an entire group of organisms, it could lead to case of of individuals developing ways to resist what caused the cancer, maybe in cases of individuals beating the cancer or in cases of successive generations of off spring from individuals with cancer?

Could it be possible that in rare cases it could lead to the development of new organs or specialized cells?

Interesting question. I believe it definitely is an evolutionary process. unicellularity breaking away from a multicellular life.

There are two examples that I can think of, which can support this argument:

Hela cells: Hela cells have been classified as a different organism because they have the ability to grow outside the host indefinitely and their genome is different from Homo sapiens. Hela cells also have a new scientific name- Helacyton gartleri
Transmissible tumors: two tumors have been known to infect other hosts and therefore can be called obligate pathogenic lifeforms. One is Devil Facial Tumor Disease which infects Tasmanian devils and gets transmitted by biting. Another is Canine Transmissible Venereal Tumor which infects dogs and spreads via sexual route.

  Could it be possible that in rare cases it could lead to the development of new organs or specialized cells?

Cancer as of now has a pathogenic identity. It is a simplistic process which in a thermodynamic point of view can be described as maximization of entropy(disorder) and thereby increasing the stability [like the way solutes diffuse]. If a cancer has to give rise to a new functional organ then it has to be supportive of the ordered lifestyle which it is trying to break away from in the first place. It may adopt a pathogenic lifestyle initially and then may redevelop order. I don't know of any such evolutionary event but it may nonetheless be possible.


Why and how does falsifying sensory information work? Some context, before the question:

Whenever I have a craving to binge on something sugary, I just prepare a cup of extremely bitter green tea (with 3 bags of tea) and I imagine myself binging on something sugary, but at the same time I take a gulp of this bitter stuff and let that sit in my mouth for a few seconds.

The very next moment, I immediately notice that the craving comes down and after a few more sips the craving completely goes away. I feel nauseous if I think about something sugary for another day.

Actual question:

Why and how does this work? Even though I consciously know that I am fooling myself, with a false sensory perception, why does my brain associate sugary treat to be revolting and poisonous(cause of nausea)?

These are learning phenomena you describe. I'll try to explain a simple way to think about this.

By default, sweet foods are appetitive and, for instance, strongly bitter foods are aversive. However, it is possible to condition yourself to associate a stimulus, no matter how it presents originally, with a different valence (appetitive or aversive).

There are several well understood forms conditioning can take. I list a few here, and some subtypes. They are described well on Wikipedia:

Classical conditioning

-- Serial application of classical conditioning can be called second-order conditioning.

-- You can also condition yourself through self-evaluation, called evaluative conditioning
Covert conditioning is a technique more than a type of conditioning, it may directly apply to your question. It involves the use of imagery.
Operant conditioning

Operant and classical conditioning are the two major paradigms to know. Classical or Pavlovian conditioning involves pairing an "unconditioned" stimulus with a neutral "conditioned" stimulus. Operant conditioning involves providing a feedback, usually a reward or punishment, to reinforce learning.

You can self-learn or condition yourself. This does not mean necessarily it is intentional or conscious on your part, often things can be subconscious or unconscious. For instance, if you associate eating crisps with watching a movie, watching movies without crisps can become uneasy, in spite of the fact that watching a movie was originally a pleasurable activity. In a neuroscience seminar involving conditioning in fruit flies, I once recorded a saying which captured the spirit of the experiment quite well: An expected reward, not experienced, can feel like a punishment, and vice versa. Rewarding yourself after doing chores can also be a easy and practicable way to build good habits with doing chores.


Modern reference for Kropotkin's lazy bees I have been reading through Peter Kropotkin's Mutual Aid: A Factor of Evolution and he mentions a curious fact about bees (bolding by me for emphasis):

  predatory instincts and laziness continue to exist among the bees as well, and reappear each. time that their growth is favoured by some circumstances. It is well known that there always are a number of bees which prefer a life of robbery to the laborious life of a worker; and that both periods of scarcity and periods of an unusually rich
  supply of food lead to an increase of the robbing class. When our crops are in and there remains but little to gather in our meadows and fields, robbing bees become of more frequent occurrence; while, on the other side, about the sugar plantations of the West Indies and the sugar refineries of Europe, robbery, laziness, and very often drunkenness become quite usual with the bees. We thus see that anti-social instincts continue to exist amidst the bees as well;

He does not provide a citation for this (and even if he did, it would be something from the late 1800s). Is there a good modern reference for the above behavior?

I would in particular be interested in something like a graph of %-robber-bees vs. plentiness-of-food (in some abstract measure of the latter) so that I could intuitively see the increase in lazy/robber bees as the environment is low on food, or as it is overly abundant and compare it to 'typical levels'.

Theories that explain this behavior are of interest, as well, but I am primarily after experimental measures/observations to support and quantify the above quote.

The quote refers to 'robber' bees, but in today's terminology, there are actually three separate phenomena. "Cheating" in bees and other social animals refers to the exploitation of a social contract for one's own benefit. Example: bee workers lay their own eggs rather than tending those of the queen. "Laziness" or "inactivity" of bee or other social insect workers is incredibly widespread, but it is not clear that it is selfish: it may be a side-effect of imperfect task allocation, or those individuals may be a reserve work force. "Robbing" in bees usually refers to removal of nectar or pollen from flowers without pollinating them.

"Cheating" associated with illicit reproduction is widespread in social insects, including in bees, and there's a broad literature on it (search terms "anarchist" "queenright", "policing") but it sounds like your question concerns differential effort and environmental resources specifically.

Differential effort in labor ("laziness vs. busynesss") has been seen in many social animals. The way you frame the question seems to be in terms of:

  "how many lazy individuals can a society tolerate given environmental
  conditions?"

Most observational/experimental studies seem to have approached the question in terms of:

  "how can what appears to be cheating actually be adaptive?"

For instance, Kukuk et al. suggest that in Halictine bees, lazy bees who avoid the high-mortality-risk foraging tasks are actually acting as caretakers and orphan-rearers for the brood of the foraging busy bees. It's also been proposed that apparently lazy insects act as a "defensive reserve" for the nest, although at least in Bombus impatiens, experiments show no evidence that lazy bees defend any more than busy bees (Jandt et al.)

Lazy individuals could also be acting a labor reserve ("substitute helpers"), in case of food or colony depletion. To me, this scenario is the closest to what you mention – the idea that lazy individuals become busier, either voluntarily or through coercion, in time of need. Baglione et al. show that this is the case for carrion crows, and quantify it to some degree along the terms you suggest. On the other hand, Cartar (cited in Jandt and Dornhaus) shows that for a number of bumblebee species, it was more likely that busy bees would work harder or switch tasks than it was that the lazy bees would become busy!

In sum, what you/Kropotkin suggest exists in all social insects, although the mechanisms of sociality and of laziness are diverse and various among species.

 Baglione V, Canestrari D, Chiarati E, Vera R, Marcos JM. 2010. Lazy group members are substitute helpers in carrion crows. Proc Biol Sci 277: 3275–3282. (free)
Cartar RV. 1992. Adjustment of foraging effort and task switching in energy-manipulated wild bumblebee colonies. Animal Behaviour. (full text not online?)
Jandt JM, Robins NS, Moore RE, Dornhaus A. 2012. Individual bumblebees vary in response to disturbance: a test of the defensive reserve hypothesis. Insectes sociaux. (behind paywall, buy Jandt kindly has uploaded for free on her site)
 Jandt, Dornhaus. 2009. Spatial organization and division of labour in the bumblebee Bombus impatiens. Animal Behaviour 77: 11–11. (behind paywall, but also free on Jandt's site)
Kukuk PF, Ward SA, Jozwiak A. 1998. Mutualistic benefits generate an unequal distribution of risky activities among unrelated group members. Naturwissenschaften. (Behind paywall, but this free article by Forbes et al. reports similar information)

Also see:
Jandt JM, Dornhaus A 2011 ‘Competition and cooperation: bumblebee spatial organization and division of labor may affect worker reproduction late in life’, Behavioral Ecology and Sociobiology 65: 2341-2349.
- shows that selfishness/cheating may actually play a role

Dornhaus A, Holley J-A, Pook VG, Worswick G, Franks NR 2008 'Why do not all workers work? Colony size and workload during emigrations in the ant Temnothorax albipennis' Behavioral Ecology and Sociobiology 63: 43-51
- this paper reviews other literature about how many bees/ants in a colony are lazy; up to 75% or even more at a time!


What's the exact meaning of and how to derive the coefficient of the path from sire to offspring? According to Wright's Coefficients of Inbreeding and Relationship,

the coefficient of the path from sire to offspring is given as

$p_{o \cdot s}=\frac{1}{2}\frac{\sqrt{1+F_s}}{\sqrt{1+F_o}}$

But how to get this formula?

And what is the  exact　meaning of this path? It's the path from sire's genetype to offspring's corresponding genetype, or just from one allele in sire's locus to offspring's one allele in the corresponding?

Furthermore, Wright gives
$F_o=\frac{1}{2}r_{sd}\sqrt{1+F_s}\sqrt{1+F_d}$

From Wright's another paper Correlation and Causation we know
$d_{o \cdot s}+d_{o \cdot d}+d_{o \cdot \bar{sd}}=1$

in which

$d_{o \cdot s}=p_{o \cdot s}^2$,

$d_{o \cdot d}=p_{o \cdot d}^2$,

$d_{o \cdot \bar{sd}}=2p_{o \cdot s}p_{o \cdot d}r_{sd}$

Thus

$\frac{1}{4}(1+F_s)+\frac{1}{4}(1+F_d)+\frac{1}{2}r_{sd}\sqrt{1+F_s}\sqrt{1+F_d}=1+F_o$

$\implies F_s+F_d=2$

Since $F_s,F_d\le 1$,
we have $F_s=F_d=1$......

Incredible. But what's wrong with it?

In The Method of Path Coefficients(Wright1934) Wright showed that the path linked two objects is the path linked their genetic constructions. Probabily "genetic construction" means sequences of loci rather than a locus. However, if we consider a genotype of a locus as a random varible, the total genetic construction of a germ cell will be a random vector. Hence something like correlation or covariance between genetic constructions of germ cells is usually in form of matrix or tensor rather than a real number $F$(which is Wright actually showed). Moreover, if germ cells are made of several chromosomes, the correlation between corresponded pairs of loci in two germ cells may be not equal to each other. (e.g. chromosomeI of $G_1$ and $G_2$ are from the same ancestor, but chromosomeII are not)

So I guess things were worked out in this way.

Suppose $G_1=(g_0,g_1,\dots,g_n)$,$G_2=(g'_0,g'_1,\dots,g'_n)$. If $g_i$ is mth chromosome's kth locus and original from an ancestor germ cell $G_A$. And let us only modify $G_A$'s mth chromosome's kth locus, then $g_i$ would get modified; $g'_i$ would also get modified if only $g'_i$ is also original from $G_A$; loci on $G_1$ or $G_2$ in other chromosomes or in mth chromosome but other loci would not get modified anyway.  Hence $\rho(g_i,g_j)=\rho(g_i,g'_j)$ for any $j \neq i$. Therefore $$cor(G_1,G_1)=cor(G_2,G_2)=\mathcal{I}\dots(1)$$ $$cor(G_1,G_2)=diag(\rho_{g_0,g'_0},\rho_{g_1,g'_1},\dots,\rho_{g_n,g'_n})\dots(2)$$

Since $1=\sum\limits_{i}{p^2_{G_1\cdot g_i}}+\sum\limits_{i\neq j}p_{G_1\cdot g_i}\rho_{g_i,g_j}p_{G_1\cdot g_j}$ and by $(1)$, $1=\sum\limits_{i}{p^2_{G_1\cdot g_i}}$. hence $p_{G_1\cdot g_i}=\frac{1}{\sqrt{n}}$ if we weighted every $g_i$ the same. And $p_{g_i\cdot G_1}=\rho_{g_i, G_1}=\rho_{G_1, g_i}=p_{G_1\cdot g_i}=\frac{1}{\sqrt{n}}$, Analogously to $G_2$.

Therefore $\rho_{G_2,G_1}=\sum\limits_{i,j}p_{g_i\cdot G_1}\rho_{g'_j, g_i}p_{G_2\cdot g'_j}=\sum\limits_{i}\frac{1}{n}\rho_{g'_i, g_i}=E(\rho_{g'_i, g_i})$. i.e. in this case the correlation between germ cells are just the mean of correlations between their corresponding loci.

So similarly the coefficient of the path from a sire to its offspring is also the coefficient of the path linked their genetic constructions. and in detail is from sire's  genetic construction to its components, then from components to offspring's construction's components, then to offspring's construction.

The derivation was given in the article. In fig6 the coefficient of the path from a sire to its offspring can be gotten from the product $p_{o \cdot G_s}p_{G_s \cdot s}$.

$p_{G_s \cdot s}=\sqrt{\frac{1+F_s}{2}}$; $p_{o \cdot G_s}=\sqrt{\frac{1}{2(1+F_o)}}$.
So $p_{o \cdot s}=\frac{1}{2}\frac{\sqrt{1+F_s}}{\sqrt{1+F_o}}$

If $F_s=F_d=F_o=r_{sd}=0$, then $d_{o \cdot s}=p^2_{o\cdot s}=d_{o\cdot d}=\frac{1}{4}$, $d_{o \cdot \bar{sd}}=0$ . Thus
$d_{o \cdot s}+d_{o \cdot d}+d_{o \cdot \bar{sd}}=\frac{1}{2}<1$. This result means  parents' genetic constructions are not sufficient to determine their offsprings'. But it is very normal the same parents have both sons and daughters. Which causes their difference in gender are random factors.


Why do we see a different color when we mix two colors? The compounds responsible for a color do not change when they are mixed with another material. The same compounds are there after mixing. However, when we mix colors such as blue and yellow we see green.

BUT we are able to tell where a color starts and ends in pictures. For example, if we hold a yellow piece of paper up to the sky, we can tell that the paper is yellow and the sky is blue. We can distinguish where the paper ends. And where the sky starts. We do not see a green outline near the paper.

I believe that  how we perceive colors may explain this. But I am not sure how. Is it because how the brain integrates information. Or is it because of how the cones cannot register two signals at the same time. Why do we see green instead of a blue and yellow?

I am not sure if this is entirely correct, its just a scientific guess. But it might actually play some role in this phenomenon. This is actually the physics part part of answer rather than the biology part.

Rayleigh criterion for angular resolution is the minimum angle which two bodies should subtend on an object so that they can be viewed as distinct bodies by that object.

Suppose there are 2 bodies, (right now) with same color of wavelength $\lambda$. Now, they are viewed from a lens of aperture $d$. Thus, from Rayleigh's equation, the minimum angle which these bodies should subtend with each other on the lens is given by:

$\theta = 1.22 \lambda/d$

Now I'm not sure if this is correct, but if the 2 bodies have different colors, of wavelengths $\lambda_1$ and $\lambda_2$ then the equation becomes:

$\theta = 1.22\times (\lambda_2 - \lambda_1)/d$

$\theta = 1.22 \times \Delta\lambda/d$

Now, putting values in this equation:

$\lambda_2 = 597 nm$

$\lambda_1 = 492 nm$

$d = 5 mm = 5 \times 10^{-3} m$

Answer comes out as:

$\theta = \underline{1.22 \times 105 \times 10^{-9}}$
$\hspace{15mm}5 \times 10^{-3}$

$\theta = 2.56 \times 10^{-5} rad = 1.4 6\times 10^{-3\circ}$

So, if these 2 bodies subtend an angle less than $2.56\times10^{-5}$ radian, then they will appear as a single object with green color.

Now, solving it by a common formula:

$\theta = a/l$

$l = a/\theta$

$l = \underline{\hspace{7mm}10^{-2}\hspace{7mm}}$
$\hspace{8mm}2.56 \times 10^{-5}$

$l = 390.625 m$

It means if yould hold two 5 cm x 2 cm papers together (i.e. total 10 cm2), one with blue color and the other with yellow color, then you would see a single paper of green color if you keep these papers $\approx$391 m away (if my calculations are correct ;).

This, in part, explains that it is not the fault of only our eyes, but of light and physical laws too.

References:

Angular resolution
Wavelengths of different colors
Resolving power of imaging instruments


Cloning a coding gene into a non-expression vector Does it make any sense to clone a CODING gene into a NON-expression vector?
doing this will only give us multiple copies of the gene, while we could run  PCR instead (Let's say we know the gene sequence)

In principle, you can amplify any gene with PCR and then clone it into a vector of choice. However, it is often not as easy. Most things can be done with expression vectors, but sometimes it is easier to clone a sequence first and then subclone it.

Some sequences are hard to amplify, especially when they get long or very long. Amplifying 2,5kb can be tricky, digesting and subcloning such a piece might be easier. Additionally yields of PCR can be low, while you get a lot of DNA from a miniprep.

You might want to introduce additional restriction enzyme recognition sites (one can easily be done via PCR, but more again is tricky), linker or additional tags, which are not present in all expression vectors. Then it is easier to simply do a first cloning step into the non-expression vector and then take the complete insert into the expression vector.


Why is oxaloacetate made in the mitochondria? I'm looking at the gluconeogenic pathway:

Pyruvate is shuttled into the mitochondria from the cytosol, converted to oxaloacetate by pyruvate carboxylase, converted to malate which is then shuttled out of the mitochondria, and then converted back to oxaloacetate in the cytosol.  Why is the mitochondrial step necessary?  Why can't pyruvate just be made into oxaloacetate in the cytosol?

Got it.  The ratio of [NADH]/[NAD+] is about 100000 lower in the cytosol than it is in the mitochondria.  The conversion of malate to OAA reduces a molecule of NAD+ to NADH, and that NADH can be used for the later step in gluconeogenesis: the conversion of 1,3-bisphosphoglycerate to glyceraldehyde 3-phosphate requires a molecule of NADH.


Who would win in a fight: an amoeba or a leukocyte? (sorry, I couldn't resist the rhyming, silly title)

I find it facinating that humans can suffer from an amoeba infestation. Amoeba must reproduce far more slowly than bacteria. In size, they seem to be approximately the same size as the various leukocyte cell types (I see estimates ranging from 10μm to 30μm in diameter). I would assume that they are slow-moving, or, at least no more motile than a leukocyte.

How is it, then, that a population of amoeba can take up residence (and a particularly dangerous one, at that) in a human body without them being wiped out by the immune system? Do we know much about the pathology of such an infection? Do the amoeba actually consume the leukocytes by phagocytosis before they can be consumed themselves?

Assuming you don't mean a single leukocyte as I doubt That a lone leukocyte could do much. Macrophages and neutrophils can release their lytic/degrading enzymes spewing them on to the amoeba. Antibodies produced by BCells, particularly the IgE type can coat amoeba and cause histamine release from mast cells recruiting more neutrophils and macrophages. Eosinophils are also important. Finally one must not forget the complement system, a series of proteins that could kill by making pores in the amoeba membrane. Amoeba have however developed many techniques for immune evasion, such as diverting the immune system via cell signalling (cytokines) such as IL10 which dampens the immune system or coating themselves or activating the "wrong" immune system.


The Eye, and Camera Lenses How do near sightedness, farsightedness, and normal sightedness work? If the eye is accustomed to one small focal point, how can it manage a wall of light? And also, how does it process the small pinpoint that it normally does?

I think I understand what your issue is here.

Often, in diagrams of lens systems and eyes, the diagram will only show rays parallel to the optical axis (see here). Although many optical systems are designed so they are optimal for this axis, off axis rays respond in a fairly predictable way too. This figure shows an off-axis point source, which focuses at a corresponding off-axis point on the other side of the lens.

So, there is "one focal point", as you say, for each position of the object relative to the optical axis. In optics we generally talk about a focal plane rather than a point, as the focal point only refers to cases of idealized point sources, lasers etc.

Now, the aperture (pupil) is a completely different matter. This provides a limit to how well an optical system can focus. When the aperture is small, it can focus really well, but not much light can get in. When it is large, the ability to focus is reduced but it allows one to see better in the dark (increasing the signal to noise ratio). Focusing requires all the rays from a source to end up at the same point on the retina/film, the aperture, when it is as small as possible "selects" only those rays that will end up focusing at exactly the right place (assuming the lens focuses to the right place, which it does not in the case of the short or long sighted). This selection cuts out a lot of the light, and often it is good to trade off the ability to focus for the amount of light. Without going into detail, this large aperture results in the focal ability of the optical being strongly dependent on how far away the object is (see this).

Your question is rather open ended, but I hope this is what you were getting at.


In what ways have plants and animals evolved to support each other throughout history? I'm curious about how plant and animal life have been able support each other throughout time and how each has evolved in a way that would help the other?

For example I have heard that plants have evolved to attract animals, such as bees in order to allow for pollination.  These plants produce smelly flowers that are usually white....  or colorful, non-smelling flowers.  By allowing bees to collect nectar for themselves and their hive, the plants are able to be pollinated in the process.

Earlier today I was noticing a bird hopping up branches of a tightly branched tree, which made me think of how plants and animals would support each other throughout time.  Trees are usually homes for a lot of animals, including birds, so I was curious about the evolution of trees to allow for tigher canopies to protect animals from the weather/elements.

My question is, how have plants and animals influenced each other's evolution, by helping each other throughout history?

There are probably a few cases of this and exactly how animals and plants co-evolve probably differs between different scenarios. One 'famous' example I like is between ants and acacia plants. The acacia plant has evolved to produce food for a particular species of ant and in return the ants protect it from the grazing of herbivores.

Explained better here: http://bioblog.biotunes.org/bioblog/2007/10/02/cool-bug-9-acacia-ants/


Can humans survive without consuming life? Some people say that it's awful that humans eat animals.  They feel that it's barbaric, because you're killing life and then on top of that, you're eating it, and that you should eat vegetation instead.

But isn't vegetation life too?  Personally, I see no difference between animals and veg as all life has cells, dna etc

So my question is, is it possible for humans to live healthy long lives without eating any type of life, i.e no animals, no plants, no cells (dead or alive) etc? If it is possible, how would it be done?

The answer to your question is yes it is certainly possible.

At one time it was thought that there was something special about "organic" chemicals which meant that they could not be artificially synthesised out of fundamental elements. In 1828 Frederick Wöhler synthesised urea (CO(NH2)2) which is often taken as the first demonstration that the organic v inorganic distinction was not a sound one (for more on this see the Wikipedia article on Wöhler synthesis.

As far as we know all essential human nutrients can be synthesised from inorganic ingredients, even complex molecules such as Vitamin B12.

Other contributors have pointed out that organic pathways for synthesising our food have evolved over long periods to be very efficient - at least in the conditions prevailing on Earth. You haven't ruled out copying biochemical pathways using chemicals that are entirely of inorganic origin. Anyone trying to do this seriously could create glucose (for example) by artificially creating enzymes (perhaps via artificial DNA) to do the job. The thing is that we already have self-replicating and repairing machines to do that already (plants).

There might be circumstances when we needed to use artificial synthesis. I can think of two science-fiction stories that deal with this question, the first of which goes into some detail:

The Moon is Hell by John W. Campbell, in which astronauts are stranded on the moon and forced to make food from what they find there.
Technical Error by Arthur C. Clarke, in which a man is accidentally rotated through the fourth dimension. His employers contemplate the difficulty caused by the "handedness" of many biological molecules meaning they would have to artificially synthesise many of his foods.

It may be that a future expedition to Mars (say) might have to think about these things.

A little searching fails to come up with standard inorganic syntheses of glucose and similar substances. The reason for this is almost certainly because it is so easy to use organic inputs. Glucose is easily made by the hydrolysis of starch. Starch is very common and cheap. Even l-glucose is usually made out of organically derived precursors (or sometimes even using d-glucose).

UPDATE: sources etc
One problematic question is: where do you get your input for making nutrients? As others have pointed out, exactly where to draw the line is difficult.

This problem starts in defining what is alive in the first place. Do you count viruses (which can go down to a few thousand base pairs of RNA) or satellite viruses (STobRV has only 359 base pairs) or prions? In a sense these are "just" very large molecules. But then really simple bacteria are not many orders of magnitude more complex. As an aside most systems of ethics that do not permit eating meat do not make an alive/non-alive distinction, choosing some other aspect such as sentience, though Jainism comes close to doing so.

The second problem is, if we reject living things as sources of food, how far removed from those living things are we allowed to get? You say no cells in any state including "dead". That would exclude (say) fruit even though most fruits are expressly created by plants in order to be eaten (and in some cases must be eaten) - something that vegans, jains, fruitarians and others would be happy with eating. If we could use dead material things would be much easier.

But would you also include hydrocarbons (coal, oil, gas) which were once living organisms? If you do, then you are in difficulty because terrestrial carbon is recycled through the biosphere. All CO2 was (to a close approximation) once a part of a living thing. If you take that position then of course you are going to have to go off-planet to find your source chemicals and your problem becomes very much harder.

I was assuming that you were restricting yourself to consuming cells that retain some of their cell structure but had not completely degraded. If that is where you draw the line then there are ample sources of raw materials on earth.

Genetic modification is much more science fiction though not entirely impossible. Some nutrients could be made by humans without much difficulty. Our inability to manufacture vitamin C is down to one missing enzyme (L-gulono-gamma-lactone oxidase) which is present in most vertebrates (I think of mammals only guinea pigs, humans and some bats are unable to synthesise it). You could certainly imagine some very careful genetic modification changing humans so they no longer need to consume vitamin C.

But photosynthesis would be much harder. Chloroplasts (which do the job in most plants) are really a very primitive form of life living in plant cells which may independently reproduce  (and for that reason might be excluded by you - they aren't "cells" but they have membranes). They could easily end up in conflict with our mitochondria (since intracellular conflict between organelles is possible) and you would need to do enormous amounts of work to make human cells co-operate with them properly.

More in keeping with your theme would be adding photosynthetic systems directly to human cells along with a suite of enzymes to manufacture all the things we cannot. That is of course in principle scientifically possible (since plants do it) but much harder than it looks. Living systems are very complicated and small changes can have unexpected consequences. Even very minor genetic modifications are problematic. The human autotroph is likely to be some way off.


How can the leakage of mitochondrial protons generate heat? I read the following about thermogenin:

  "When thermogenin is
  inserted into the inner mitochondrial membrane, it
  accentuates mitochondrial proton leak and dissipates
  the proton motive force. Since oxidation is no
  longer coupled to phosphorylation, thermogenin is
  said to cause uncoupling. In the presence of thermogenin,
  oxidation and proton pumping continue
  at high rates but with low rates of ATP synthesis. So Thermogenin enhances
  mitochondrial proton leak so there would be heat."

Why does proton pumping without ATP synthesis generate heat?

Uncoupling ATP synthesis from the ETC (electron transfer chain; this is where oxidation takes place) by thermogenin or any other method means that the energy used to generate or uphold the proton gradient gets 'lost'.

Since physics teaches us that energy is only transferred and never truly lost, the energy consumed by the ETC must most go somewhere - heat / thermal energy is the easiest and therefore most likely option.

References

Wikipedia article on Uncoupling Proteins
Uncoupling article written in chemical terms
Short general article about brown fat and heat production


Are humans more adapted to "light mode" or "dark mode"? I was discussing with a colleague about using dark-mode vs. light mode and remembered an article arguing that humans vision is more adapted to light-mode rather than dark-mode:

I know that the trend “du jour” is to have a dark mode for pretty much
everything, but look around the world is not dark with a bit of light,
it’s actually the contrary. And as the human has evolved its vision to
adapt to this reality, it’s asking extra efforts on many people.

Unfortunately, no reference is provided to support this claim, so I am wondering if this is just an opinion or there are some studies to support this.
Wikipedia seems to confirm this somewhat since we are adapting much faster to "light mode" transition than to dark mode one:

This adaptation period is different between rod and cone cells and
results from the regeneration of photopigments to increase retinal
sensitivity. Light adaptation, in contrast, works very quickly, within
seconds.

Also, some studies confirm that working using light mode is on average more efficient than using dark mode:

light mode won across all dimensions: irrespective of age, the
positive contrast polarity was better for both visual-acuity tasks and
for proofreading tasks.

I am looking for arguments coming from evolutionary biology to confirm (or not) the assumption that human evolution favors light mode.

A question that requires quite a lot of guts to ask on this site :) Nonetheless, and risking sparking a debate, there are a few arguments that spring to (my!) mind that can support the notion that we thrive better in 'day mode' (i.e., photopic conditions).

To start with a controversial assumption, humans are diurnal animals, meaning we are probably, but arguably, best adapted to photopic (a lot of light) conditions.
A safer and less philosophical way to approach your question is by looking at the physiology and anatomy of the photosensitive organ of humans, i.e., the retina. The photosensitive cells in the retina are the rods and cones. Photopic conditions favor cone receptors that mediate the perception of color. Scotopic (little light) conditions favor rod activity, which are much more sensitive to photons, but operate on a gray scale only. The highest density of photoreceptors is found in the macular region, which is stacked with cones and confers high-acuity color vision. The periphery of the retina contains mostly rods, which mediate low-visual acuity only. Since highest densities of photoreceptors are situated at the most important spot located at approximately 0 degrees, i.e., our point of focus, and since these are mainly cones, we apparently are best adapted to photopic conditions Kolb, 2012).
An evolutionary approach would be to start with the fact that (most) humans are trichromats (barred folks with some sort of color blindness), meaning we synthesize our color palette using 3 cone receptors sensitive to red (long wavelength), green (intermediate) and blue (short). Humans are thought to have evolved from apes. Those apes are thought to have been dichromats, which have only a long/intermediate cone and a blue cone.  It has been put forward that the splitting of the short/intermediate cone in our ape ancestors to a separate red/green cone was favorable because we could better distinguish ripe from unripe fruits. Since cones operate in the light, we apparently were selected for cone activity and thus photopic conditions (Bompas et al, 2013).

Literature
- Bompas et al., Iperception (2013); 4(2): 84–94
- Kolb, Webvision - The Organization of the Retina and Visual System (2012), Moran Eye Center
Further reading
- Why does a light object appear lighter in your peripheral vision when it's dark?


Ciliated Epithelium & Goblet Cells Lining The Trachea My book states this - The cells produce mucus that traps particles of dirt and bacteria in the air breathed in. The cilia on these cells move this debris up the trachea and into the stomach. Isn't the stomach below the trachea? Wouldn't it move the dirt and debris up the throat so it can be removed via the mouth? My book does also state that the debris is pushed up the throat as well so does it do both?

There are two pipes from your throat, downwards. A foodpipe and a windpipe. One, called the trachea, feeds air into the lungs, i.e. connects your head with your lungs. Another pipe, called the esophagus, leads to the stomach.

Both pipes meet and share the same passageway in your throat and oral/nasal cavities. Let's call this the common pipe.

The lining of the trachea, made up of ciliated cells and mucus-producing cells, does indeed move debris UP and OUT of the trachea, away from the lungs. Once this debris is at the common pipe, it can go to the stomach or into the mouth or into your nose for clearance.


What would happen if a cell is poked by a fine needle? I had seen this question in an exam:

A living cell has a protoplasm which is water based and demarcated by a lipid bilayer membrane. If a cell is pierced to 1/5th of its diameter with a very sharp needle, after taking the needle out
(a) no effect will be observed.
(b) protoplasm will leak out from the hole made by the needle for a few minutes until the cell heals the wound.
(c) protoplasm will keep on leaking out till the cell is dead
(d) the cell will burst like a balloon.

I understand that the answer is option (a) as the cell membrane will reseal itself after getting pierced.
But my doubt is that if in the question 1/5th was replaced by 1/2 or by any number greater than 1/2, will the answer be different.
Or in other words, I want to know whether the number 1/5 significant in this question.

Generally speaking, there is no effect in microinjections.
This is relevant in the real world example of micro-injections. A video of a pronucleus injection can be seen here, or here is a more thoroughly explained procedure involving cloning. As you can see in the video the membrane, almost no effect will be observed - molecular dynamic simulations show that the membrane can spontaneously reform from fragments in the tens-of-nanoseconds timescale.
1/5 refers to  the question "is the needle small enough?"
The question does include the term "1/5", which is a bit unusual. I guess they want you to recall a specific piece of information about the correct ratio size of needle should be. Here is a video of a microinjection at approximately that ratio. However the exit hole is unintentionally filled with the inserted material and cannot close immediately. The cell disappears out of frame before we can confirm the hole is closed.
Cell diameters are very variable
Cell sizes vary greatly.

From using these values, assuming a cell is a sphere an oocyte has a diameter of approximately 196µm, whereas a neutrophil has a diameter of 8µm. It's a bizarre question given this range because usually micro-needles are between 0.5 and 5 µm diameter in length, except in the case of oocytes where larger needles are used (according to wikipedia). I don't think this is relevant, and it is just arbitrarily picking a needle size that wouldn't completely maul the cell!


Insect ID. Montreal, Qc (Canada) I've found this bug in my appartment today and I was wondering what insect it is? Thank you.

This is a "click beetle" (Coleoptera, Elateridae). They have this name because of the loud click sound they produce. They are related to fireflies (Lampyridae), and some click beetle species are themselves luminescent.

According to the link above:

  A spine on the prosternum can be snapped into a corresponding notch on the mesosternum, producing a violent "click" that can bounce the beetle into the air.

I don't know about those North American beetles, but in South America I've seen click beetles jumping more than 30cm in the air.

Here is a photo of a click beetle in Montreal, from the Pest Control Canada website, which looks like your specimen:

Unfortunately, the entomologist that identified the animal in the photo above didn't narrow it down to Genus or Species.


Do T-cells express MHC molecules? T-cells recognize the MHC molecules and body's own peptides. When it doesn't, it alarms the immune system. But do T-cells express MHC molecules ? If so, how are they using it? If not, what happens when a virus infects T-cells? (Yes, I am confused about HIV infection mechanism too. They escape from immune response by altering their genes and disrupting the MHC-peptide bonding. I can see that this can work in macrophages. But what is the situation in T-cells ?)

There are two types of MHC molecules:

All nucleated cells express MHC class 1 proteins.  A sample of all proteins produced within the cell are 'sliced' into their constituents which are then presented by MHC-I receptors.  This means that if a virus infects a cell, the foreign proteins the cell is induced to make are expressed on the cell membrane by MHC-I.  This is important as antibodies can not cross cell membranes, therefore this is the method by which a cell signals that it is infected by a virus.

MHC II are the special molecules that are only expressed in antigen-presenting cells, which I think is what you are referring to.  As neither CD4 or CD8 T-cells present antigens, they do not express MHC-II themselves.  Instead CD4 have receptors for MHCII  (while CD8 have receptors for MHCI), allowing them to interact with antigens presented by other immune cells.

If a virus infects T-cells, the viral proteins are sampled by the MHC-I pathway and presented via MHC-I on the surface of the infected T-Cell.  The immune response then progresses as for any other virally infected cell, destruction by CD8 T-Killers that destroy the cell by non-phagocytic means.


Reading and Understanding profile bands in DNA Fingerprinting I have very limited knowledge when it comes to DNA fingerprinting. I know about the technique gel electrophoresis and how everything is carried out. But I don't know how to read the result or understand that. Can anyone please explain me how to read the result  [profile of bands]?

Because of my lack of knowledge, I can't solve problems like this one.
Please explain me using this one so that I can get a clear idea about DNA profiling. This seems like home-work problem but the thing is I want to understand the technique of restriction mapping by reading the result of restriction digestion on electrophoresis and my intention is to understand the topic. Please Help.

And I can't describe how I tried to solve this question because I don't have any kind of knowledge about this technique [Restriction Mapping] so my efforts are very silly to mention and I have improper way of approach to this as I don't know how to do the Restriction Mapping.

But I am given the answer which I tried to make sense by working on it but I just couldn't help it. It seems easy after seeing the Map but I don't get the relation between the profile of bands and the Map so if I am given a different problem I will fail to come up with a reasonable answer.

What I am trying to say is, by seeing this map and working on it I get to agree that this is the correct mapping for the data given but I have some doubts, like, why we keep 3Kb distance between BamHI and EcoRI sites. Working out in some another way will end up with wrong answer. How these inticacies are understood? By reading the profile of bands [data given] right? So that's what I am asking for you to explain to me. I don't know anything about it.

Thank you always.

How you would determine the plasmid map from just the restriction digest data

The thought process behind doing this is a bit involved.

From the question you are told that the Gene is 8kb and does not contain an EcoRI site inside of the gene

I say not inside because the ends of the gene were made with EcoRI cuts, but digesting in EcoRI will only produce the 8kb fragment of the gene

The vector is 6kb and you know that they have EcoRI sites at either end, but you are not told what other cut sites there are.
When you digest the plasmid in BamHI you get 3 fragments, meaning that your plasmid has 3 BamHI sites somewhere in it.
You know that your total plasmid size is 14kb (easiest way to know is just look and see that they tell you that there is an 8kb gene and a 6kb vector). Looking at the Double Restriction Digest, you can see that the five fragments add up to 14kb, which implies that there are only one of each fragment in the plasmid, and they are produced by 5 separate cuts.

This is an important piece of information because this tells you that you do not have 2 fragments of the same size making up different parts of the plasmid.
Remember that when you do a restriction digest on a circular piece of DNA, the number of fragment you get equals the number of cuts (restriction sites) in the plasmid. So because there were 5 fragments, you have 5 separate restriction sites
From the Double Digest data, you also know that the smallest fragment of DNA that you have is 1kb and the largest is 4kb.

Since the 4kb site is common to both the BamHI only and the the Double Digest, as since you do not have a 0.5kb or 1.5kb fragment (the remainders if the Double Digest 4kb fragment had been produced from the 4.5kb or 5.5kb fragments in the BamHI digest) in the Double Digest, you know that the 4kb fragment is the same in both the BamHI digest and the Double Digest, and is produced by 2 BamHI cuts.

You can now work on roughly placing where the 4kb fragment should be in the map.
If you try to place that 4kb fragment in the vector, then you would either generate a 2kb fragment, or something less than 2kb and a very small fragment.
Since you do not have a 2kb fragment or fragments smaller than 1kb, you know that it cannot be in the vector region. Also in order to get a 2kb fragment from the 6kb vector the 4kb fragment would have needed to be cut once with EcoRI and from the description, above, we worked out that the 4kb fragment is produced by two BamHI cuts
It could have been that the vector was 1kb + 4kb + 1kb, however from point 4 you determined that you only had one of each fragment, so you can't have two 1kb fragments.

All of that tells you that it has to be in the 8kb gene portion, though you need some more information to determine exactly where.

Remember that you do know that the 4kb fragment was produced by 2 BamHI cuts, which means that it cannot be at the very end of the gene region, as that would require it to be cut once with EcoRI
This also tells you that you have at least two BamHI cut sights in the gene.

What I would do here is draw two circles, the first having an 8kb arc and a 6kb arc, then draw second circle and make three cuts in it.

From 6 we worked out that the 4kb piece will overlap somewhere in the 8kb area, that it cannot be at an end and that there need to be 2 BamHI restriction sites within the gene.
You also have to consider the 4.5kb and 5.5kb parts from the BamHI digest. Since 4kb plus either of those two are greater than 8kb, then you know that the cut that separates 4.5kb from 5.5kb will be somewhere in the 6kb vector. This is how you know that the third BamHI site is in the vector.

Now that you have determine that the 4kb fragment is in the gene you can start to work out the other pieces.
You had 2 fragments from the BamHI digest that were 5.5kb and 4.5kb and in the double digest you have fragments that are 1.0kb, 2.5kb, 3.0kb, and 3.5kb.

Since you have already determine that that 4kb piece is the same for both digests, then at this point you can tell yourself that the 1.0kb and 3.5kb fragments made up the 4.5kb fragments and the 2.5kb and 3.0kb fragments made up the 5.5kb fragment.

Since you know that there has to be two EcoRI cuts that make the 6kb fragment, you are going to need two fragments that add up to 6kb.

The only way to get this with the four fragments that you have from the double digest is with the 2.5kb piece and the 3.5 kb piece.
So you have now determined the exact position of one of the BamHI cut sites. It is in the Vector, 2.5kb from one of the EcoRI sites and 3.5kb from the other EcoRI sites.

Now that you determined where one of the sites is, you know that the 2.5kb fragment was paired with the 3.0kb fragment, so this tells you that there is a BamHI site 3kb away from the EcoRI site in the Gene.
From there you can connect the 4.0kb piece to the end of the 3.0kb piece because you know that the 3.5kb piece has to be attached to the 1kb piece and cannot be attached to the 3kb piece.
All that is left is to close the circle. You know that you have 1.0kb more of the gene that needs to be place and this will connect the 7.0kb that you determine of the gene in step 11 to the 3.5kb fragment in the vector. You have that 1.0kb fragment, and that is the one.

So that is how you determine how to construct the plasmid map from the restriction digests.

What the distances between the cut sites tell you

The cut sites are determined by the sequence of the DNA that the Restriction Enzyme recognizes.

EcoRI recognizes GAATTC
BamHI recognizes GGATCC

You will notice that these are palindromic sequences, so 5'-GAATTC-3' is 3'-CTTAAG-5' on the complimentary strand.

All that the distances are telling you is that in the areas in between the cut sites, the sequences GAATTC and GGATCC do not appear. If they did, then the Restriction Endonuclease would recognize that position and cut the DNA, and you would have an additional cut site at that location.

Assuming that you were given the plasmid map, this should be the answer.

The answer should be C. The 1kb and 3kb fragments are the DNA fragments from the gene that are generated from the EcoRI / BamHI digest. So one end of the fragment was produced with EcoRI and the other end of the fragment was produced with BamHI

The 4kb fragment is the result of BamHI restriction alone. So both ends of the fragment were produced by BamHI so it cannot be the answer to a fragment produced by EcoRI / BamHI restriction.

If they are saying that they also want answer A as well, then their question is very poorly worded, in my opinion.


Is pith a ground tissue with no specialized function? Here is a question from the book My Max Score SAT Biology E/M Subject Test (where the SAT is the exam taken by American high school students):

  Ground tissue with no specialized function
  A. Xylem
  B. Phloem
  C. Cambium
  D. Bark
  E. Pith

Here, I can eliminate A, B, and D because these are dermal and vascular tissues while a ground tissue is what's between those.

As for the remaining variants, cambium is a tissue that gives rise to other tissues and is responsible for the plant's growth up and to the sides. Pith is a tissue in the very center of the plant stem and is responsible for storage of nutrients. While trying to understand the question, I even found info that it is a type of vascular tissue because it is involved in plant transport (https://www.quora.com/What-are-the-functions-of-piths-in-a-plant) although I'm not sure if it's correct (yeah, I know that Quora is not the website with absolutely credible info).

So, as I can see, both cambium and pith have their function.
Then, I decided to determine whether they are a kind of ground tissue. Pith definitely is a ground tissue, according to its definitions. However, I could not find what kind of tissue cambium was considered to be.
With all that said, I can't be sure to choose either answer. First, both tissues have their functions. Second, pith is a ground tissue, and cambium is undetermined for me.
Here is the answer, however:

  E. Pith is a source of unspecialized ground tissue that adds structure
  to a stem at the very center.

I can't be sure about this answer because unspecialized means "not designed for a particular purpose." But, as I've pointed out, both pith and cambium have their purposes/functions.
Please explain why pith is written to be unspecialized. Is it because "storage" is not an "active" function like growth or transport; this tissue just exists and is able to store different substances in addition to that?

Also, is cambium a ground tissue or some other type (dermal, vascular)?

Short answer: it's not the greatest question.

Long Answer:

So there are three primary tissues in a plant: ground tissue, dermal tissue, and vascular tissue. See below for how they sort out:

However, some sources refer to the tissues of plants slightly differently, and indicate that the three basic tissue types are parenchyma, collenchyma, and schlerenchyma.

Example: "Botany: A Lab Manual" by Pfluger 2014:

  The three fundemental tissues of plants are parenchyma, collenchyma, and sclerenchyma

Since these are all "ground" tissues, this approach to classifying plant tissues would suggest that all plant parts consist of some kind of ground tissue (including all the plant parts you mention in your post). In fact, this is often the case...

Again, from Pfluger 2014:

  They [parenchyma] can be found in virtually any part of the plant and are the most common cell type in a plant.

Of the parts you mention, xylem is "specialized" to move water through the plant via tracheids, pits, and vessel elements; phloem moves sugars/sap through sieve tube cells which are supported by companion cells; cambium acts in secondary growth of wood and bark via the vascular and cork cambia; and bark is a water-proof protective layer.

However, "pith" is simply the central parenchyma cells in the stem, and therefore are primarily just used for storage like "all unspecialized" ground tissue.

As for cambium: from here:

  Interfascicular cambium differentiates from parenchyma or collenchyma cells located between the vascular bundles (mainly in stem)


Why is mRNA used as a biomarker for cancer over tRNA or rRNA? I cannot find a clear explanation for why mRNA is used as cancer biomarker and not tRNA or rRNA. Is there something peculiar about mRNA which cannot be fulfilled by tRNA or rRNA?

mRNAs encode specific genes and perform specific functions whereas the other two perform housekeeping functions in all cells. Changes in their expression are related to global changes in the cell.

The expression of rRNA and tRNA is affected in certain conditions such as stress and also possibly cancer (may be due to high replication rates). However, even if they are affected in cancer you cannot use them as markers for specific cancers as they are present and highly expressed in all cells.

Therefore specific tumour suppressor genes and oncogenes are studied.


Is nutrient absorption different in Hypersensitive I patients? I am thinking how the nutrient absorption differs between between patients with allergies (Hypersensitivity I) and those not.

The current guideline about number of eggs in diet is one daily regularly.
My professor says that 1-4 eggs daily can be also ok because cholesterol is inhibited.

However, I am thinking if we have Hypersensitive (allergic) person, what the recommendation should be then.
My hypothesis says that more cholesterol would be absorbed and less inhibited.
However, I cannot find any evidence for this hypothesis.

Hypersensitive response is fast.
I am interested in many responses during long term.

How does nutrient absorption differ in hypersensitive patient and normal patient?

The absorption is itself not different, but the rate of absorbed substances is different because of greater amounts of proteins in the allergic lymphatic circulation.
So less capacity stays for circulation of nutrients and so less absorption in time.


Can Taq polymerase be used instead of polymerase Vent exo (-)? Instead of using  polymerase Vent  exo (-), can I go with the usual Taq polymerase?

Do the PCR conditions change (the temperature and master mix concentrations ) in the these two conditions? Do the primers (sequence and concentrations) change if we use vent exo instead of Taq polymerase and vice versa? If the primers are designed specifically for Vent exo (-) how can I modify the PCR conditions so that I can use the same primers (meant for vent exo) using Taq polymerase?

I haven't done ARMS PCR myself, so my answer is based on theory and there might be other practical factors I overlooked.

The characteristic feature of the Vent exo(-) polymerase is the lack of exonuclease activity compared to the regular Vent polymerase. ARMS uses the fact that a mismatch at the 3' position prevents primer extension. For this to work it is important to use a polymerase without exonuclease activity, as such a polymerase could "repair" the mismatch and the whole method would not work. Taq polymerase also doesn't have any exonuclease activity, so in theory you should be able to use it for this experiment.

The primers don't have to be changed for different polymerases, the polymerase buffer though is different and I wouldn't recommend using the wrong one.


Test question regarding botany I'm having a hard time understanding what exactly those letters and numbers in the task in the photo below represent, also the task says "Is the blossom formula written correctly?" translated from Lithuanian to English. I would appreciate some guidance.

These are floral formulas, a way to succinctly describe how many petals/sepals/pistils/... the flower contains, and their relations (free, fused, ...). The wikipedia page describe the meaning of each symbol.

For example, for the first one :

Up arrow : symmetry along the vertical axis
K(6) : 6 sepals (K), which are joined (parenthesis)
C(2.3) : Two large petals, three smaller, joined. (not sure on the exact signification of 2.3)
A2 : Two stamen, not joined
[C(2.3) A2] : the petals and stamen are fused
G(2) : two fused carpels

Continuing with that example, it seems to me the first formula is not correct given the schematics below : there are 4 carpels. Though I'm no botanist.


How do C. elegans manage nutrition? If there is ample amount of food, do C. elegans worms know when to stop eating or do they store extra energy? Could they put this extra energy to use by moving faster or putting more eggs?

The answers are:

Yes, they know when to stop eating. See this paper.
Yes, they store extra energy as fat in the intestine.
This one is a little more complicated. They can use extra energy, but not to move faster. Movement doesn't take much energy, and until they're close to death from starvation, they continue to move quite well. As for eggs, they do indeed slow down the rate of embryo production when nutrition is inadequate. But the total number of eggs is limited by the supply of sperm, so there is an upper limit on how many they can produce, even in unlimited food. Probably the main benefit of stored nutrients is to allow them to survive longer if the food runs out. They are very, very good at dealing with a variable food supply -- much better than you, for instance -- and they do it partly by storing up extra energy. This paper and references therein describe some starvation responses. You can also look up L1 diapause, the dauer larva, and adult reproductive diapause.


What is the meaning behind Kcat / Km? I'm trying to understand enzyme kinetics, the formula for Km and Kcat make sense to me.

  Km , the substrate concentration at which the reaction rate is half of Vmax

  Kcat, used to describe the limiting rate of any enzyme-catalyzed reaction at saturation. Most of the time
  Kcat just equals K2 (NOT the case when there are
  more reaction steps)

I can find information about the calculation of the specificity constant (Kcat / Km) and what it means:

  specificity constant,the rate constant for the conversion of E + S to E + P

However I can't find any detailed explanation WHY you should devide the Kcat by Km. Secondly Km is HALF of Vmax (so actullay at half saturation) but Kcat is at full saturation, deviding these two numbers makes no sense to me. So to summerize I'm asking : What is the "meaning" of the division of these two consants?

definitions are derived/edited from Lehninger principles of biochemistry

Just as $k_{cat}$ represents the rate of reaction at saturating substrate concentration, $k_{cat} / K_m$ represents the rate of the reaction at negligible substrate concentration.

If we take a look at the standard one substrate/one product Michaelis–Menten kinetics rate equation:

$$v = \frac{k_{cat}[E][S]}{K_m + [S]}$$

We can imagine what happens when $[S] \to 0$, we see that when $[S] \ll K_m$, the denomiator can be reduced to $K_m$, and thus the rate equation becomes

$$v = \frac{k_{cat}}{K_m}[E][S]$$

Or in other words, $k_{cat} / K_m$ is the (pseudo-)second order rate constant between the enzyme and the substrate, when $[S] \ll K_m$.

In fact, when you get into more complex rate equations (like inhibitors, pH effects, and kinetic isotope effects) there's a decent argument (one often made by W.W. Cleland) to be made that the two key constants for enzymatic reactions are $k_{cat}$ and $k_{cat} / K_m$, and it's $K_m$ that should be thought of as the "derived" constant. (The fact that we write the rate equation in terms of $k_{cat}$ and $K_m$ is a historical accident - we could have just as easily had $ v = \frac{k_{cat}\Phi [E][S]}{K_m + \Phi [S]}$, where I've arbitrarily chosen $\Phi$ as the symbol for $k_{cat}/K_m$.)

This still leaves the issue of why $k_{cat} / K_m$ is often referred to as the "specificity constant" of the enzyme. The reason for this is that if you have a single enzyme in the presence of two different substrates, you have a competitive inhibition setup. The math is a little dense (see here or here for examples), but the end result is that the ratio of reaction rates for the two substrates is related to the ratio of their respective $k_{cat} / K_m$'s:

$$\frac{v_a}{v_b} = \frac{k_{cat,A} / K_{m,A}}{k_{cat,B} / K_{m,B}}\frac{[A]}{[B]}$$

This actually makes intuitive sense, with the right mindset - the only stage where the two substrates are competing (where you make the decision to do reaction A versus reaction B) is when they're binding to free enzyme. "The rate when you only care about free enzyme" is equivalent to the negligible substrate case. With negligible substrate, all you have is free enzyme - there isn't enough substrate to have appreciable amounts of substrate-bound form, and the rate of enzyme-substrate encounter is much lower than the rate of product formation, meaning that in the steady state you don't have appreciable amounts of product-bound form, either. Thus the $k_{cat} / K_m$ for a particular substrate is representing how good the free enzyme is at performing that reaction.


What will happen if a foetus is Rh- and the mother is Rh+? If a mother has Rh-negative blood and her foetus has Rh-positive blood it will result in rhesus incompatibility and lead to erythroblastosis fetalis. What will happen if the reverse occurs, when a mother is Rh+ and the foetus is Rh-?

Nothing. Rhesus incompatibility results when people who are Rh- develop antibodies against Rh+ blood after exposure. People with Rh+ blood do not show any such reaction to Rh- blood.

In a way, it's comparable to blood types in that regard. People with the blood group O can develop antibodies against type (for example) B blood. People with type B don't develop antibodies against type O blood, and can thus receive blood donations of type O.

Also, rhesus incompatibility during pregnancy is only a concern in second or subsequent pregnancies (or after miscarriages). The antibodies develop through the blood being "mixed" during the birth (or miscarriage) and are then an issue if the next fetus also has Rh+ blood, which is just assumed if the father is Rh+ or has an unknown blood type to be on the safe side, and can be addressed medically.

  Injections of a medicine called Rh immune globulin can keep your body from making Rh antibodies. This medicine helps prevent the problems of Rh incompatibility. If you're Rh-negative, you'll need this medicine every time you have a baby with Rh-positive blood.

-What is Rh Incompatibility

Also, as you can read in my answer to a similar question about blood groups and pregnancy
How does a fetus retain a blood group different from its mother? the maternal and fetal blood usually only mix during birth due to the placental blood barrier. If you are wondering whether the fetus should have a reaction, the immediate functions necessary for that don't develop until more than six months after birth.