Why can't C1r cleave C4 proteins? I am researching the complement system, and have ran into something I'm not really sure about. In the past, the C1r2s2 complex was thought to be an 8-like structure tucked inside C1q's collagenous strands. However, this article says that the serine proteases actually protrude away from the core. Originally, it is said the C1s SP cleaves the C4 and C2 proteins because the C1r proteins are hidden in the core. If this new structure is true, however, then the C1s and C1r proteins are close to each other outside the C1q core. If this is the case, what is preventing C4 from being cleaved by C1r instead of C1s? Their serine protease domains should be largely identical.

I have found an answer. The serine proteases on complement proteins actually have very limited enzyme substrate specificity. C1r only has two natural substrates, zymogen C1r and C1s, whereas C1s can only cleave C4, C2 and a few non-complement proteins. This was proven by superimposing the structure of serpins (serine protease inhibitors) with C1r and C1s. This analysis revealed that the access to these substrate-binding sub-sites is severely restricted, compared with digestive serine proteases such as trypsin. The trypsin or chymotrypsin-like pockets were only the primary specificity pockets. The strong preference displayed for Gln residues at P2 and Ile residues at P1 matched those found in physiological substrates of C1r, zymogen C1r and C1s. An example on how these specificity filters work can be seen when we substitute the Gln at P2 with Asn or Gly. To only allow Gln residues, polar or charged molecules will be placed where Gln’s residue’s polar head will be, and hydrophobic residues where the carbon chain will be.  When Asn is substituted for Gln, the shorter carbon chain will cause the polar head to overlap with the hydrophobic residues of C1r, which is highly detrimental for binding. Substituting this with Gly will eliminate the interaction altogether, so it will not be as detrimental, but the stability resulting from the Gln-C1r interaction will be lost.
More information in this article here.


What are the allowed evolution operators (on protein encoding sequences)? What are the evolution operators, meaning allowed actions on the DNA sequence that encodes a protein.

I assume all evolution of genes is a result of duplication errors. So an answer could look somewhat like this: duplication of gene into two identical ones, omitting of nucleotide, addition of nucleotide and so on.

And some followup questions:

Does this mean that originally there were very few genes and they were very short?
If so - how few? How short?

The most frequent mechanisms are

Intragenic mutations: when existing genes mutate modifying gene function.
Gene duplication: leads to related genes in a single cell. A gene duplicates and then as two copies are available, one is free to change
Segment shuffling: leads to hybridisation of different DNA segments.
Horizontal transfer is transfer of DNA from one cell to another
Transduction: infection of cells by viruses or other intracellular pathogens where their DNA can integrate into the genome

You are incorrect to say all evolution occurs due to duplication. Your follow up questions are too vague. Genes can become larger or smaller, but yes as they increase so does their diversity.


What is the purpose of the “No DNA control”? What is the purpose of the “No DNA control”?

Recently I have done a forensic DNA lab experiment and I still cannot understand the use of “No DNA control”

No DNA controls (or water control, also "no sample control") are important to rule out false positives results due to contamination.

If your reagents/pipettes/equipment you use is clean, this reaction (I suppose in PCR) gives you no band. If you have a contamination, this will show up where no band should be and shows that you have a problem. In this case you cannot trust the other results as well.


Reason for seeing grid-like patterns when strobing a solid black-white image? I was trying to do some stimulation for SSVEPs by strobing a solid black square and a solid white square. Weird thing was, I ended up seeing weird grid like patterns that looked like this, always of the inverted color.

  _        _
 / \      / \
 | |      | |
 \ / _--_ \ / _--_
  O |    | O |    |
 / \ ---- / \ ----
 | |      | |
 \_/ _--_ \_/ _--_
  O |    | O |    |
     ----     ----

And that sort of pattern repeats itself around the strobing area (where the convex areas are always of opposite color than the current color on the screen).

I'm inclined to think about light and dark adaptation, but it still seems weird that it'd be shaped like that in particular. So... What's going on?

EDIT: Additional info that I should've realized was necessary >_<:

Strobe area: ~14x10.5 cm
Strobe frequency: 2 frames/half-cycle @ Laptop Vsync (~60 Hz) ~ 15 Hz
Viewing distance: ~55-60 cm and shorter.

Screen is backlit. Not sure about brightness metrics.

The pattern isn't offset to one corner like I've drawn, it's more evenly spaced. Horizontal bars are more accentuated than vertical ones (and the dark-on-light phenomenon is more visible for me than the light-on-dark). Moving in closer increases the visibility of the effect (I guess that was to be expected), and changes the number of times the pattern repeats across the screen (but it's hard to count them). The larger the area in my visual field the more times the pattern repeats. I'd say that at about 60 cm it's just one box, but with my nose a handful of cm away from the screen (it's hard to measure by myself >_<), there are maybe three in the horizontal direction... Or at least tens of them (increasingly large as it gets toward the center in both dimensions), depending on how focused in on the screen I am.

It's really really hard to count them.

I haven't had the chance to check with other people yet, but I'll try some time (this is just something I saw while working on a personal project).

Seeing in animals is at some level using Gabor wavelets (Marčelja 1980 and later authors). Your images reminds of a combination of two low frequency Gabor basis vectors. Apparently the nervous system does not have time to model the incoming image into Gabor components of other frequencies.

Here is a picture of two low frequency Gabor basis vectors added. (In this image rotated 45 degrees compared to your image.)
http://medicalxpress.com/news/2013-01-feature-combination-perceptual-identification.html

This is a signal processing or a linear algebra question as much as a biology question.

One could argue that even lower frequency Gabor vectors would model the original images even better.


GULO only for mammals? I am not a biology student, but just want to know if GULO gene are present only in mammals or all species possess it ?

And is GULO gene active in human fetus?

GULO encodes L-gulonolactone oxidase which catalyses a step in the biosynthetic pathway to ascorbic acid (vitamin C).

I did a BLAST search at NCBI using the mouse GULO protein as probe, excluding mammals, and I saw highly significant hits in reptiles, birds, sea urchins, fungi and bacteria. I conclude that this enzyme, (or very close relatives) is ubiquitous.

Humans (and other primates; also guinea pigs and the Dalmatian coach hound) have a defective GULO gene and so require dietary ascorbate.

Since the gene is non-functional in humans it isn't expressed in the foetus.


List of the biggest companies that work in selective breeding Looking at this question, I've been wondering, What are the biggest private companies which work in both animal and non-animal selective breeding?

Let me know if Biology.SE is not appropriate for this kind of question.

Thank you

This varies by the kind of animal or plant. I think one company would rarely do both.

For plants Monsanto comes to mind.  And Syngenta.

I'm not sure for animals.  For beef cattle in the US, this is done by individual ranchers (who may be corporations) that collectively share their genetic data creating a market which can predict the value of a bull.  The market for bull semen can be worth hundreds of dollars per impregnation.

Why are bulls valued at such a greater rate than cows?  Because semen can be preserved, transported and used thousands of times while a cow can only calf one at a time.


In plant photosynthesis, in the light dependent reactions, why is 3 ATP produced per 2 H2O? I've been looking at the light-dependent reactions on Wikipedia and Khan Academy.

This is the net reaction:

$$2H_2O + 2NADP^+ + 3ADP + 3P_i \to O_2 + 2NADPH + 3ATP$$

So for every $2H_2O$ I expect $2NADPH$ and $3ATP$. I tried to count:

These are my assumptions:

Cytochrome b6 complex pumps $1H^+$ for each $1e^-$.
FNR makes $1NADPH$ for each $2e^-$.
ATP synthase makes $1ATP$ for each $1H^+$.

If we want to end up with $3ATP$, then $3H^+$ need to diffuse through. The thing is, there's too many $H^+$. $4H^+$ is contributed by the cytochrome b6 complex pumping alone, and another potential $4H^+$ is contributed by the water splitting.

Clearly I'm missing something here that would lead to the correct count.

I remember being confused by the numbers when I first studies it primarily because most sources seem to differ on the stoichiometry. I have tried to explain why is it difficult to comment upon such large equations, hope it helps!

Short Answer

There are two faults in your assumptions.

The plastoquinone-cytochrome cycle actually pumps $2H^+$ per electron (terms and conditions apply)
ATP-synthase requires $\approx 4$ protons per ATP produced

So, 12 protons per 2 water molecules is what is pumped, which makes 3 ATP.

Full Answer

As you might notice, the above scheme does not account for many things. For starters, since the 4$H^+$ from water splitting are produced and not pumped, only 2 of those need to be pumped back via ATP-Synthase to restore equilibrium. So even if you account for the $2H^+$ consumed by $2NADP^+$, there is still something that doesn't quite fit. Furthermore, some sources also try to account for the acidity of the inorganic $Pi$ in the ATP-synthesis which will further allow for changes in the $H^+/e^-$ ratio.

Why the confusion?

Most of what we know of the stoichiometry is based on a conglomerate of experiments, beginning with experiments on isolated chloroplasts. As a result, some experiments give us some parts of the stoichiometry (we know that the $NADPH/ATP$ ratio is around $2/3$) and others give us the reactions. Often times, many possible reactions are proposed, from which, the ones which can best be integrated with results from different experiments are thought to represent the actual truth. But this process is often mangled with complications, unexplained patches in the theory and the like. Furthermore, biological processes often are stochastic and do not have perfect stoichiometries. This is all overlooking the actual disagreements between experiments (the $H^+/ATP$ ratio for the synthase had significant variations in different experiments).

Okay, so now what?

Don't loose hope. We do know quite a bit about photosynthesis. What we currently understand about photosynthesis (light reactions) is thus:

There are three distinct processes that can produce a chemiosmotic gradient of $H^+$.

a. Non-cyclic Photophosphorylation is the main method. This constitutes the popular Z-scheme involving a linear electron transport from water to the final acceptor $NADPH$, and this process pumps about $12H^+$ per $2H_2O$

b. Pseudo-cyclic Photophosphorylation which is basically the same as above, but the final acceptor is an $O_2$ molecule, with similar ratios.

c. Cyclic Photophosphorylation which allows for recycling an electron, that is, proton pumping without there being a final acceptor of electron solely by internal shuffling of the electron between different states (primarily involved Plastoquinone (Q) cycle. This can pump $2H^+$ extra for 1 electron.
The ATP-synthase is slightly different from that found in animal mitochondria. The number of protons per ATP depends on the rotational symmetry of the synthase. (details in the references below). Basically, initially, it was thought to have 12-fold symmetry (needing $12H^+$ per rotation, in which $3ATP$ is produced, hence $4H^+$ per $ATP$) but was later found to have 14-fold symmetry actually needing $14H^+$ for the observed $3/2$ ratio of $ATP/NADPH$.
The number of Photosystem 1 units(where the cyclic version operates) is more than that of Photosystem 2 units. This means, that cyclic photophosphorylation goes on simultaneously at these centres, and will account for the extra $2H^+$ required to meet the experimentally observed ratio (1 in every 5 electron is "recycled").

References

A good overall paper addressing all the main issues. Photosynthesis of ATP—Electrons, Proton Pumps, Rotors, and Poise; John F.Alle; Cell Volume 110, Issue 3, 9 August 2002, Pages 273-276
General resources on these reactions. Here, here and here.
Studies on the $H^+/ATP$ ratio.

a. Petersen, Jan et al. “Comparison of the H+/ATP ratios of the H+-ATP synthases from yeast and from chloroplast” Proceedings of the National Academy of Sciences of the United States of America vol. 109,28 (2012): 11150-5.

b. Watt IN, Montgomery MG, Runswick MJ, Leslie AG, Walker JE. Bioenergetic cost of making an adenosine triphosphate molecule in animal mitochondria. Proc Natl Acad Sci U S A. 2010;107(39):16823-7.
Old studies to illustrate the difficulty of explaining the results of many studies:

a. Function of the Two Cytochrome Components in Chloroplasts: A Working Hypothesis; R. HILL & FAY BENDALL; Nature - volume 186, pages136–137 (1960)

b. Photosynthesis by Isolated Chloroplasts; DANIEL I. ARNON, M. B. ALLEN & F. R. WHATLEY; Nature - volume 174, pages394–396 (1954)


Bradford Reagent Disposal I am a graduate student volunteering in a professor's lab being tasked with finding out how to dispose of certain hazardous materials. I have encountered a problem with disposing of Bradford's Reagent. I have checked online, but am running into problems due to the methanol component of this compound. Can someone help me with the proper disposal procedure? Thank you in advance.

I would strongly suggest to ask someone in your lab about this, they will have a better idea about the different waste disposal methods you have available.

In general you would dispose anything that contains organic solvents like methanol in a waste container for generic solvent waste. You should have something like that somewhere in the lab.

One thing you always have to keep in mind is to never put anything still reactive into your waste container. A popular example would be a strong oxidizing agent, putting that into a solvent waste container is dangerous and could e.g. ignite the waste. This is not an issue in this case, but you should always keep that in mind.

Another aspect is the pH of the waste, in many cases the waste disposal facility will only accept reasonably neutral waste, so you should neutralize your waste before putting it into a container. Neutralizing it inside the container can be much more annoying. This might not be necessary if you have a dedicated acidic waste, you'll have to ask someone in your lab about that. The Bradford reagent is strongly acidic, so you'll have to pay attention to this aspect.


Does DNA have a phosphate group or phosphoric acid? I am confused about the structure of nucleotide of a DNA. I have seen that it has a phosphate group(PO₄³⁻) in some books but phosphoric acid(H₃PO₄) in other ones. Which one is right?

The phosphate ion has a negative formal charge and in an acidic solution its appears as a conjugate base of a phosphoric acid. That is the wey the phosphate group found in cells. The nucleotide synthesis can occur de novo or recovery ways. De novo way use phosphoribosyl pyrophosphate, which simple molecules such as amino acid, tetrahydrofolate and carbon dioxide are added.


Calories burn rate calculation — scientific studies There are many online calculators for measuring walking/running/bicycling calories burn rate. They differ in input parameters like some might need my weight as well as height and some don't. Almost none take into account duration of the exercise (and this is crucial in my opinion).

So my question here is: Where are these formulas (used in these calculators) coming from? Any scientific studies perhaps? Are they reliable?

Also I would like to know what is the most accurate method available for measuring the burn rate (I'm only interested in the scientific part, not going to do this myself).

Disclaimer: Not my field but I'm doing my best.

We often measure the calories consumed indirectly by measuring the quantity of oxygen consumed. As we have a reserve of ATP(ATP is a molecule, a stock of ATP is some kind of battery of our body) in our body, at very short term the oxygen consumption is not necessarily perfectly correlated with energy use but at a longer term it works perfectly fine. Seek for further information on the Citric Acid Cycle to understand why the oxygen consumption is directly related to the energy created (which is itself at a long enough term directly related to energy use). If I am not mistaken a bunch of seconds should probably be a long enough term (time to consume all ATP at the start of an important effort) but I would appreciate if someone could give a reference for that.

For small animals we often put the animal in a chamber and calculate the energy consumption by measuring the volume of CO2 that they expire. For this purpose we have to measure the volume of CO2 at the entrance and at the exit (of the chamber) to measure the difference. For humans, we often put a mask on the face of the "cobaye". We allow him to breath normally without doing any effort for a while and then we ask him to run/bike/whatever on a home trainer.

I don't know much about such studies but it is important to 1) know the variance in energy consumption in the population for a typical exercice 2) understand that lab condition probably differ in various ways from person-to-person real life condition (no wind, no dust, stress of the experimentator, discomfort of the mask, ...).

As I have no idea concerning the variance in the population I cannot tell how representative are the summary values that we can find on many popular websites but I would tend to think that given the experimentation, these numbers has probably been fairly accurately measured.


Improving Gel Extraction yields How can I improve my Gel Extraction yields. We use the standard protocol from Qiagen, gel extraction, dissolve in QG buffer at 42C and purify via anion exchange columns. However, with 500 ng we ultimately get 100 ng for a 20% yield. I was curious what else has been tried for gel extraction.

We also add IPA and NaOAc to the dissolved mixture prior to the column purification.

When I optimized gel extraction in my hands, two factors turned out to be critical in maximizing gel extraction yield:

The pH of the eluting solution. I used to elute the final product with DEPC-treated water initially, but the yield would vary a lot as the pH of the water changed. Using buffer EB is better, since it maintains a stable pH 8.

Most importantly, *incubate the eluting solution with the column as long a possible (and also elute twice). * I incubate for about 10 min, which is longer than what they recommend but it works much better.


How are the two mating types, a and α, for S. cerevisiae pronounced? In reading about S. cerevisiae there are two mating types, one being the Latin letter a and the other being the Greek letter α.

How are these two types pronounced such that they can be differentiated?

In other words when I pronounce the text I don't want to say 'a' for both of them; there should be a different word or phrase for each one so that they are known to be different.

Is it simply that a is pronounced as a and α is pronounced as alpha?

Correct.

Haploid mating types in Saccharomyces cerevisiae are MATa (pronouce a as in day) and MATα (i.e. MAT-alpha).

For convenience you could also refer to the corresponding alleles as MATa or MATalpha (see also here)


Why do both the mango and the bee have "Indica" in their binomial name? In my textbook, it is written that the binomial name of mango is Mangifera indica and the binomial name of a bee is Apis indica. Now in the name the second part is the name of species. But mango and bee are not the same species. One is a tree and the o,ther is an animal. Then why is their second name the same?

In short, we do not think about the uniqueness of the second part of the binomial (the species epithet) but about the uniqueness of the binomial itself (the genus and the species epithet). Thus, the unique binomial of mango is Mangifera indica and the unique binomial of bee is Apis indica. For more detail, see this question.

To complicate matters  slightly, plants and animals are governed by different nomenclatural codes. So it is possible for a plant to have the exact same binomial as an animal. These are called "hemihomonyms." For more detail, see this question. However, a plant cannot have the same binomial as another plant, and an animal cannot have the same binomial as another animal.

In this specific case, the authors probably chose to give both species the epithet indica because they are associated with the Indian subcontinent, which is the root of that word.


Has the human body the greatest total length of nerves of all animals? I've read that a human body contains about 150,000-180,000 km (Pakkenberg et al., 1997; 2003) of nerve wiring in the whole body. But does this length increase with the size of the animal? For example, an elephant is much bigger than a human and perhaps even his brain is bigger but is an elephant also the animal with the longest nerve cells in total?

There is no reason to believe that total nerve "wiring" (or combined length) does not increase with the size of the animal, although the number of neurons in the brain (and the number of connections they make via dendrites) matters as well.

Animals with long necks, legs and tails have long nerves. Ancient sauropods may have had the longest nerves (referring not only to nerve bundles but single neurons) in history. Their brains were not as large compared to their body size, however, as humans.

But whales - the largest animals on earth - do have larger brains. Modern cetacean brains are among the largest in both absolute size and in relation to body size of all mammals. The brain of an average adult sperm whale weighs 8 Kg; by comparison, the average adult human brain weighs about 1.3 Kg.

Blue whales are the largest animals in existence today. With a large brain (3.6 Kg) and a long body, I can't see a particular reason to believe that the total amount of "wiring" in a blue whale doesn't exceed that present in a human.

[Normal weight of the brain in adults in relation to age, sex, body height and weight]
Normal organ weights in men: part II-the brain, lungs, liver, spleen, and kidneys.
Cortical complexity in cetacean brains


How are vaccines mass-produced? I have a background in product design and so am familiar with with how most things are mass-produced — food, machines, etc.  But I've been able to find very little information on how vaccines are mass-produced.
It looks like there are 4 types of vaccines, all of which include pieces or byproducts of the virus they're intended to counteract.
If you're producing billions of vaccines, I imagine you need a tremendous amount of the virus.
How is such a mass of virus obtained? Do they just fill up tanks with a culturing agent and a sample of the virus and wait for it to grow, like a giant petri dish? Are there big vats of Coronavirus sitting in factories somewhere?

Per Wikipedia, typically when one needs a lot of virus, it is grown in a controlled cell environment. This used to be eggs, but is moving toward cell cultures instead.  So basically yes, factories full of virus (though more like in nice discrete bioreactors than big Joker-friendly vats).
Synthetic vaccines, such as the mRNA vaccines for COVID, do not need this step at all, since they do not actually use the virus, but can be done through cell-free biochemical reactions that replicate the mRNA directly.


Full Sequence for Plasmid pMG101 I am trying to find the full plasmid sequence for pMG101. I have been looking through other papers that have sequenced this plasmid. The GenBank access numbers I got are the following: AY009372–AY009396, ASRI00000000. However, when I go on genbank it gives me a result saying it is not there..... I am stuck and not sure how I am suppose to find this full plasmid sequence. Does anyone know another way to find it?

Looks as if you'll have to do some reconstruction work building the full sequence from the information here and elsewhere in this paper:

  Nucleotide sequence accession numbers.The DDBJ/EMBL/GenBank accession numbers for the sequences reported in this paper are AB031076(the SalI-XhoI 3.0-kb fragment of pMG101), D84187(rDNA for strain S55), D86354 (rDNA for USDA 4362), D86355 (rDNA for USDA 4377), AB031077 (plasmid pMG103), and AB031078 (plasmid pMG105).

--Sequence Analysis of the Cryptic Plasmid pMG101 from Rhodopseudomonas palustris and Construction of Stable Cloning Vectors


Why do the calicheamicins bind to DNA at the minor, rather than the major, groove? I am trying to understand why some drugs bind only to the minor groove and not to the major groove. More specifically, I am interested in calicheamicins.

  They target DNA and cause strand scission. Calicheamicins bind with
  DNA in the minor groove, wherein they then undergo a reaction
  analogous to the Bergman cyclization to generate a diradical species.
  This diradical, 1,4-didehydrobenzene, then abstracts hydrogen atoms
  from the deoxyribose (sugar) backbone of DNA, which ultimately leads
  to strand scission.[7] The specificity of binding of calicheamicin to
  the minor groove of DNA has been demonstrated.

Accommodation in the major or minor groove

I am not in a position to generalize about all drugs that bind to the major groove of DNA, but at least one well-known example, actinomycin D, does so because it intercalates between the base-pairs in the double helix. Although other weak chemical interactions stabilize this binding, much of it is through base stacking with base-pairs. Hence binding requires it be inserted into the major groove in which the base pairs lie (see e.g. PDB 101 Molecule of the Month article).

Binding of calicheamicins, in contrast, involves interaction with two parts of the molecule. The ‘head’ of the molecule makes specific interactions with a TCCT sequence in the DNA (in the case of calicheamicin γ1), which is achieved from the minor groove (intercalation is not necessary) allowing the saccharide ‘tail’ to fit into the minor groove. (Ikemoto et al. 1995).

(Constructed from 3D Structure images on the Protein Data Bank website)

Sequence specificity

A concern of the poster is the fact that the interaction of calicheamicin is sequence specific (there is apparently a preference for d(T-C-C-T).d(A-G-G-A)) whereas access to the bases is restricted in the minor groove. This is addressed in the paper by Ikemoto et al., but without illustration, assuming you are able to visualize the chemical interactions in your mind. I have used Jmol to view the structure 2PIK, have prepared a couple of screen shots to help illustrate the details I shall quote from the text of the paper.

Cleavage of the DNA is performed by the enediyne aglycone (R), which does not make contact with the bases. Two of the regions that do interact with bases are the thio-sugar ring (B) and the aromatic ring (C). These are shown below in the complex of  calicheamicin (coloured yellow) with a deoxy-oligonucleotide duplex, together with a close-up of the interactions of these rings.

In the left-hand frame the DNA has standard cpk colouring, and the phosphates (orange–red) lining the minor groove are evident. The base-pairs are perpendicular to the plane of the image. In the second frame I have tilted the image slightly to allow the rings of the bases to be seen, and coloured the bases (actually the whole nucleoside) red/white/green/blue for A/T/G/C. Quoting from the Ikemoto paper:

  The thio sugar B is positioned edgewise in the minor groove and contacts the A20 residue through van der Waals and hydrogen bonding (B ring hydroxyl to N3 of the base) interactions. The aromatic ring C is positioned between the walls of the minor groove with its iodine and CH3 groups directed toward the floor of the minor groove.… The S-carbonyl linker, which adopts an orthogonal alignment relative to the plane of ring C (favored by the steric demands of the ortho aromatic ring substituents), bridges the minor groove and makes van der Waals contacts with the opposing walls of the groove.

This may not have the clarity of, say, Watson and Crick base-pairing, but neither does the interaction of proteins with particular DNA sequences — one needs to examine the multiple interactions that occur. What I think it does show is that this drug can make specific contact to bases, even though it binds in the minor groove.


What is one Botulinum toxin medical unit? How many Botulinum toxin molecules or grams are contained in one medical unit of Botox?

1 unit is approximately 10 pg

Source

  One unit of MYOBLOC (botulinum toxin type b) corresponds to the calculated median lethal intraperitoneal dose (LD50) in mice. The method for performing the assay is specific to Solstice Neurosciences' manufacture of MYOBLOC (botulinum toxin type b) . Due to differences in specific details such as the vehicle, dilution scheme and laboratory protocols for various mouse LD50 assays, units of biological activity of MYOBLOC (botulinum toxin type b) cannot be compared to or converted into units of any other botulinum toxin or any toxin assessed with any other specific assay method. Therefore, differences in species sensitivities to different botulinum neurotoxin serotypes preclude extrapolation of animal dose-activity relationships to human dose estimates. The specific activity of MYOBLOC (botulinum toxin type b) ranges between 70 to 130 Units/ng.

UPDATE

10 pg of toxin (150 kDa) is 4 x 109 molecules


Identification of species found in fly lab I just found this in my Drosophila lab (within a closed vial) - unfortunately it was dead having been frozen for two weeks. Can anyone help id what it is, and whether it poses a risk to my flies (like mites do)? My inclination is that it is some kind of (moth?) larvae. Note the awesome corkscrew tail...

Found in Uppsala, Sweden, May 2014 in a vial of Drosophila with food (a yeast, sugar, and agar mix). Length is about 3-4mm excl. tail.

I'd guess it's a larva of one of the carpet beetles (Dermestidae), some of which are synanthropic. They probably would be interested not in live flies, but in their food and cadavers.

Its appearance seems to be very characteristic - someone would be able to identify it to generic or even specific level.


Is there an instinct-driven body language for birds? Over the last year or so, I've been observing house sparrows, because they are so prevalent in the northeast US cities. I noticed that a lot of sparrows, even in different cities seem to have very similar body language for communicating. I learned 3 expressions

Here's an example of a sparrow feeding their young. The young bird opens month and flickers its wings in what I can only describe as impatiently.

A sparrow swipes its beak along a surface at its feet - something food related?

A sparrow fluffs its feathers, turning into something like a tennis ball made of feathers.

I'm looking at this video of a sparrow raised in captivity, and it does 2 out of 3 expressions described here.

What interests me is if expressions like these are "local dialects" or universal, thus found across different geographies and times? for example, do sparrows in northeast US use the same expressions as sparrows in Australia? What about sparrows in the United Kingdom in the 1950s?

In general, animal communication contains both "cultural" aspects and genetic components.

As you suggest, the cultural aspects vary more across geographies and times. The genetic components might vary as well, with genetic differences among different populations, but you'd expect them to be more conservative than the cultural aspects. To make the matter even more complex, if the communication behaviors affect mating; they could in turn have an effect on the genetic components!

This article describes birds raised in captivity that had "maladjusted" songs (which would support both genetic and cultural components), and North Carolina cowbirds raised by Texas parents who grew up with a Texas birdsong dialect (evidence for cultural components). Although the piece is mostly focused on song, I imagine the mechanisms would be similar for body language.


how do I find the number of bp in chromosome 3 by knowing number of bp in chromosome 1? If i have a number of bp in chromosome 1 for example(298,295,559 bp) can I use this number to find the number of bp in chromosome 3.

You cannot.  BP numbers vary between the chromosomes.  Chromosomes are numbered by size, so you can always say that 2 is smaller than 1; however, there is no function to determine the exact size of one chromosome based on the exact size of another.


Low copy numbers of plasmids I have a plasmid with the P15A origin which apparently has a low copy number (see here). This would explain why my purification yeilds for subsequent digestion are low (gel shows the plasmid after digestion and clean-up with 5µl being loaded). I am currently growing my E. coli containing plasmid up in 5mls overnight before doing a miniprep. My question is should I grow my 5ml cultures up for longer (2 days) or just give it up and do a larger amount for Midiprep.

I am also curious as to what actually controls the plasmid copy number inside cells. An explanation of the regulation of plasmid copy number would be much appreciated.

I am sure you have done it; just a note to others: do a PCR screen to
ascertain that the plasmid is there.
For minipreps you generally do not need a starter culture.
If you have screened your clones and now just want to amplify and keep the plasmid for cloning purposes then go for a maxiprep with 200-400ml cultures.
Do not overgrow the cells, your extraction becomes difficult and you would get even worse yields. Just set up a huge culture and pool the cells before extraction. Always seed and harvest cells that are in exponential growth phase.
If you need to screen the plasmid for clones or something then do a colony PCR, keep the colony inoculated in a small culture (make a temporary glycerol stock if your screening is taking time). If screen is positive then incoulate the starter culture for maxiprep/gigaprep culture with this stock.


Identification of an insect found near Shirdi, Maharashtra I found the insect nside house near Shirdi, Maharashtra. I have captured the image

It's a household centipede whose scientific name is Scutigera coleoptrata.
It's venom doesn't do much harm to humans.

Sources:
Picture 1 and   Picture 2


RNA-seq Data on domestic animal with different environment I want to find the RNAseq data available on domestic animals in different environments. If microarray data is available, it would be more useful. If you know I would appreciate to inform me.

There is something called GEO, which is maintained by the NIH and is a massive collection of data obtained from RNA seq, microarray, etc. experiments. One thing you can do is search for a paper that has done what you are looking for. The paper may have a GEO accession number, and you can use that number at the GEO website to find the data you want. You may also search GEO directly but Im not too familiar with it. It may just be easier to find a paper with a GEO accession number.


Can someone identify this ant? This is one of seven ant queens I just collected yesterday morning (2015-09-21 9AM) around home.

I live in Hong Kong, at a hillside facing south. The weather was as follows (Hong Kong Observatory Daily Weather Summary, Hong Kong Observatory Daily Extract):

Mean Pressure (hPa): 1008.6
Max temp in my district: 24.2C
Min temp in my district: 28.0C
Mean dew point: 23.8C
Relative humidity: 66% - 95%
Rainfall: 16.9mm

Judging by the ridged head and the large mandibles, I'm guessing this is one of the Tetramoriums (Wikipedia, AntWeb).

The colour is dark brown. The total length from the tip of the mandibles to the tip of the abdomen is about 17mm. The length of the large wing is also 17mm. I don't know what habitat it lives in and I also don't know how the workers or soldiers look like, as I have never seen where these ant queens emerge from.

If anybody is fairly confident in identifying this species, I would also appreciate some tips about keeping it and starting a colony. I have a make-shift ant farm made out of two plastic bottles, one nested inside the other like a Russian doll. Out of the seven queens that I collected, three are already dying. A fourth one already show signs that she won't make it either.

More info

When I picked them up, they were not exactly "outdoors". The short but heavy rain was mostly over and these queens were "taking shelter" in the stairwell of my building, which is usually dim, slightly damper and cooler than outside.

Here are more pictures; these should be better because I just took these in natural daylight:

Somebody at The Ant Farm and Myrmecology Forum suggests that this is in the genus Carebara (previously Pheidologeton). After some more Google search of my own, and image comparing, I believe that this is indeed a Carebara affinis, which has previously been spotted in Hong Kong. Could somebody confirm?

In my opinion you are pretty close to the exact identification.

I think it is Marauder Ant, which could be Pheidologeton diversus, but probably Carebara affinis as well.

The main feature I can gother from your pictures is Venation of wings which matches with Pheidologeton diversus venation (it would probably match with affinis as well, but I failed to find the picture):

Venation match: the combo picture of the wing from the post and the wing from the reference:

This ant is known as Hong Kong inhabitant -


Are low-intensity radio-waves carcinogenic? A recent review article, Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation reached a surprising conclusion

  our analysis demonstrates that low-intensity RFR [Radio Frequency Radiation] is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.

They suggest the oxidative stress can cause cancer and non-cancer pathologies.

This study has received next to no media coverage. With RFR impacting so many people it makes me wonder, is this study valid? I would expect this to be front page news given the large number of studies reviewed.

Are low-intensity radio-waves carcinogenic?

This study has received next to no media coverage. With RFR impacting so many people it makes me wonder, is this study valid?

Well first of all, lets be clear: that is not a study.  Its a review article, basically a paper that summarizes a series of studies published.  The review itself isn't valid or invalid necessarily, it simply takes a series of papers (which may or may not be correct or relevant) and then summarizes them.
As for validity, that is a summary of a lot of obscure papers on mechanisms by which RF fields could interact with cells, rats or in a few cases plants.  Its hard to say if the conclusions are valid, but selecting a few papers at random, they are mostly very obscure journals and many report very specialized measurements that are far removed from demonstrating carcinogenic effects in humans.  Its difficult to draw conclusions that are relevant to human health from that, although it does seem plausible that low frequency fields could have a measureable effect on cells or even rats.

Are low-intensity radio-waves carcinogenic?

Assuming you mean in people, that is a hard question to answer, and not the right question given a review article that does not address effects in people.  A better place to look may be this review article:
Carcinogenicity of radiofrequency electromagnetic fields
published in The Lancet and addressing evidence of carcinogenicity in humans.  To summarize:

The Working Group concluded that there is “limited evidence in humans” for the carcinogenicity of RF-EMF, based on positive associations between glioma and acoustic neuroma and exposure to RF-EMF from wireless phones. A few members of the Working Group considered the current evidence in humans “inadequate”. In their opinion there was inconsistency between the two case-control studies and a lack of an exposure-response relationship in the INTERPHONE study results; no increase in rates of glioma or acoustic neuroma was seen in the Danish cohort study,4 and up to now, reported time trends in incidence rates of glioma have not shown a parallel to temporal trends in mobile phone use.
The Working Group reviewed more than 40 studies that assessed the carcinogenicity of RF-EMF in rodents, including seven 2-year cancer bioassays. Exposures included 2450 MHz RF-EMF and various RF-EMF that simulated emissions from mobile phones. None of the chronic bioassays showed an increased incidence of any tumour type in tissues or organs of animals exposed to RF-EMF for 2 years. An increased total number of malignant tumours was found in RF-EMF-exposed animals in one of the seven chronic bioassays. Increased cancer incidence in exposed animals was noted in two of 12 studies with tumour-prone animals12 and 13 and in one of 18 studies using initiation-promotion protocols.14 Four of six co-carcinogenesis studies showed increased cancer incidence after exposure to RF-EMF in combination with a known carcinogen; however, the predictive value of this type of study for human cancer is unknown. Overall, the Working Group concluded that there is “limited evidence” in experimental animals for the carcinogenicity of RF-EMF.

Note that cancers that people theorize to be associated with exposure to nonionizing EM fields tend to be extremely rare, meaning that studying them is very difficult.  This leads to a lot of uncertainty, because one must try to correlate very rare events with environmental effects. Therefore "limited evidence" does not mean "no", it just means that the effect is hard to measure and may or may not be significant given what we know.


Suggestions for self-studying experimental techniques I would appreciate any suggestion regarding self-studying experimental techniques used in biology for a theoretical scientist (candidate).

Maybe I should be more specific. I'm a biology major, but took as little experimental courses as possible, and I didn't paid much attention to those I took. (shame on me, right). Then I got a MS in applied math. When I revisit my molecular biology/genetics and biochemistry textbooks, I realized that they are mostly descriptive.

An experiment/technique oriented textbook would be very helpful for me, especially if it will also provide an overview of the methods.

My purpose is not the make up for the lost undergrad years, change my research orientation or master experimental skills. I'm aware that this is not achievable by reading some texts. My sole purpose is to not get lost on theory/experiment interface. When someone asks how something could be proven experimentally, I want to know what options are there in the field.

I cannot more highly recommend Molecular Cloning 4 ed.. It is a really comprehensive text which covers numerous molecular biology experimental techniques including different types of PCR.

EDIT: Also, there are some great suggestions for other books and websites that also cover molecular biology techniques in the answers to this question: Short, concise, practical manual for doing experimental biology


Are single-celled organisms capable of learning? I've read that the amoeba is capable of learning.  Since these protists have no nervous system, it's safe to assume that even highly simplified learning mechanisms of the Aplysia are miles off in the evolutionary distance.

How does this species learn?  I would presume that there is a complicated chain of receptor mediated transcription regulation, but what are the specifics?  What types of receptors does an amoeba have to sense its environs?

I'd like to know what is the reference for amoebic learning. I cannot comment directly on this, but there is some evidence for  "adaptive anticipation" in both prokaryotes and single-celled Eukaryotes which do not have a nervous system.

In the case of E. coli, it has been shown that the bacteria can anticipate the environment it is about to enter.  E. coli in the digestive tracts of mammals will typically be exposed to initially a lactose, and then later to a maltose environment as the bacteria pass down through the animal tract. This suggests that upon encountering a lactose environment, maltose operons are induced. I.e., upon encountering lactose, maltose is anticipated. This suggests a "genetic memory" of the sequence of sugar types where lactose is always encountered before maltose.

Further cultures (500 generations) of E. coli in the absence of maltose but in the presence of lactose reduced the maltose operon activity to negligible levels, suggesting that this is an adaptive prediction of environmental changes.

Mitchell, A et al., Adaptive Prediction of environmental changes by microorganisms, 2009, 460, 1038


How does ANF increase GFR? ANF as we know reduce the Na+ uptake and K+ removal in the distal tubules and it also functions as a Vasodialator (?) But again it says that ANF increases the Glomerular filtrate ? But if it is acting has a Vasoldialator (ie, antagonistic to Vasopressin) how is it increasing the GFR ? Shouldnt it lower the GFR ?

ANF - Atrial Natriuretic Factor also called Atrial Natriuretic Peptide

GFR - Glomerular Filtration Rate

ANF (Atrial Natriuretic Factor more commonly known as ANP - atrial natriuretic peptide) squeezes (vasoconstricts) the efferent arteriole. This means the pressure in the glomerulus is higher (like if you squeeze the end of a hose) and so more fluid is squeezed out i.e. the glomerular filtration rate (GFR) is higher. It also dilates the afferent which means more fluid is going in, further increasing GFR (Marin-Grez et al.)


Biological Calculations (a) At the moment of fertilization a female egg is about 100μm in diameter. Assuming that each lipid molecule in the plasma membrane has a surface area of 10-14 cm2 , how many lipid molecules are there in the egg plasma membrane if 25% of the surface is protein?

(b) Each fertilized egg cell (zygote) divides 30 times to produce all the eggs that a female child will need in her lifetime. One of these eggs will be fertilized giving rise to a new generation. If lipid molecules are never degraded, how many lipid molecules have you inherited that were synthesized in your grandmother? Assume for calculation purposes that the lipid molecules synthesized by your grandmother is equally divided between the daughter cells at each cell division.

My answer:
 (a)  Given, a female egg is about 100μm in diameter.  Radius = 50μm
           Each lipid molecule in the plasma membrane has a surface area of 10-14 cm2.
           25% of the egg surface is protein and 75% of the surface is lipids.
           Therefore, Surface area of egg is = 4π(radius)2
                                                                                =  4*3.14*2500*10-12
                                                                      =  3.14*10-8 m2
                                Area for the presence of lipid molecules = 3.14*10-8 *3 / 4
                                                                                = 2.355*10-8 m2 = 2.355*10-8 * 104 cm2
        Number of lipid molecules in egg plasma membrane = 2.355*10-4/10-14 = 2.355*1010 molecules

(b) Each fertilized egg cell divides 30 times into 2,4,8……230 cells. Assuming that the lipid molecules     synthesized by our grandmother is equally divided between daughter cells at each cell division.
•   After 30 divisions we have 230  cells synthesized in grandmother
                      Initially the zygote has 2.355*1010 lipid molecules from above calculations.
                      Therefore, each cell has 2.355*1010/230 = 21.93 molecules.
•   After mother takes birth, she inherits lipid molecules present in zygote, that is a single cell

Number of lipid molecules that is inherited from grandmother by mother is 21.93 molecules.

This zygote undergoes division for 30 times.
Thus, each cell inherits = 21.93/230
                                          = 2.0424*10-8 lipid molecules from zygote

•   Finally, a single cell in mother undergoes the zygote formation that leads to our birth.

Hence, we have 2.0424*10-8  lipid molecules inherited from our grandmother.

Can anyone please confirm it?

I think almost everything is correct except for the last part.
The reason one may easily overlook that part is that we inherit the complete 22 molecules from our mother who inherited the whole 2.35 * 10^10 molecules from her grandmother zygote. Grandma gave the whole thing to her daughter and that that number was distributed in all the cells in mom's body, which is 22 per cell. These 22 lipid molecules would be inherited by us from our mom, so the answer seems to be 22 logically.
This can be understood easily as given below:
2.35*10^10 -> From granny to mommy
22 -> From mommy to us
Hope this made sense... Thanks!


Can you explain the behavior of this snake? I just saw this video in which a snake is swallowing grapes.
 ("Whip snake eating grapes").
In the video, the snake just doesn't eat but goes on to swallow 2-3 grapes.
I did some research on the internet and in "bio stack exchange" but only to find that "snakes are obligate carnivores", which simply means they don't have the body mechanism to digest a vegetarian diet.
My guess is that it mistook the grapes for a prey due to the smell coming from the grapes, which may be left there by a rodent or any other organism the snake feeds on.
Can you provide a possible explanation for this snake's behavior? Regards

You're right, snakes rely on scent to capture their prey. The fact that snakes are carnivores may be the one constant among all snake species; absolutely none feed even partially on plant matter. So if plant matter is found in their feces, it must have gotten there accidentally.

Here, check out this post, which answers your question perfectly:

  In most instances, these have been attributed to accidental ingestion, perhaps eaten with a prey item or mistaken for prey by scent...One interesting case was discovered by Harvey Lillywhite in a study published in the journal BioScience in 2008. Studying the scavenging behavior of pitvipers in the intertidal zone, Lillywhite observed cottomouth droppings that were composed almost entirely of seaweed. This was too much plant material to have been eaten secondarily or by accident, and he suspected that there was some other cause for the snakes to be eating it (it certainly wasn't for energy as the seaweed was passing through completely undigested. Lillywhite wondered if it was possible the snakes were feeding on seaweed simply because it smelled like fish. An interesting laboratory experiment proved their hypothesis correct; they offered various plants to cottonmouths, some with fish and others without. The plants without fish were investigated by the snakes, but ultimately left uneaten. Those that did contain fish were quickly devoured. Even when the fish was removed, the snakes ate the remaining seaweed simply because it smelled like their prey!


Can someone identify this mushroom? I found this monster on my lawn in New Hampshire USA, with a pileus that measures about 8.5 inches across. My mother has threatened to eat it unless I can demonstrate that it's poisonous, so any help identifying it would be greatly appreciated. I should mention that the mushroom is a slightly richer more brown than the fluorescent lighting suggests.

My best guess so far is an armillaria of sorts.

Cheers!

This is most likely a member of the genus Amanita, judging by the vellum traces on the cap, remains of a ring (2nd photo, under your thumb), free white gills.

What we are missing for a better id is the base: is there a volva, a bulbous end...? Please dig out your mushrooms instead of cutting them off.

Also, the colour is significant: are there pinkish tinges (-> A. rubescens?) or is it just brown?


What is this strange worm-like creature? Hi! While I was in my front yard this morning, I happened to look down and see this little guy wiggling thru the grass. He isn't like anything I've seen before.

He is about 2 1/2 inches long. He has a small horn coming out of his back near what appears to be his behind. His belly is a light green color. Also, he starts to flick around when I touch him (To catch him, I scooped him up in a small pot.)

I live in north west Mississippi in the hills near the delta. I am also surrounded by a large forest with all kinds of both pine and normal trees, if it helps.

Thank you in advance!

I believe this is some sort of Cranefly larvae, see here:  I've found these guys both directly in streams and along the banks of rivers, but also underneath rocks far away from major sources of water. There are different types of cranefly larvae, but they all have the same characteristics, (bulbous bodies, worm like, not easily noticeable arms, alien encephilization)

It may also be deer fly larvae ( a type of horsefly ) but they typically are more "spiky" on the sides.


Why does evolution only involve heritable traits? If natural selection favors a certain behavior that is learnt, then wouldn’t that behavior be found more often among a population (as more offspring will learn that behavior from their parents or their peers)? Since the behavior is not encoded in the genes, it is not heritable, but it is transmitted through other means and will thus accumulate in the population. This, to me, seems a lot like the effects of evolution, yet this is not a heritable trait. So my question is why does evolution concern only heritable traits and not those that can be reproduced by learning?

There is a lot to say to address this question fully. I will be brief and a little messy to try to introduce you to some concepts and that will hopefully push you to learn more by yourself.

Heritability in genetics

In genetics, heritability is a statistic that describe the fraction of the phenotypic variation that which is caused by underlying genetic variation. Please have a look at this post to understand the concept of heritability as used in genetics. Note that there are two such statistics, named heritability in the broad sense $h_B^2$ and heritability in the narrow sense $h_N^2$.

Basics of non-genetic inheritance

Here, I will refer to "heritability in the broad" as the passation of trait value (such as behaviour for example) and environment characteristic to another organism. One must not confound what I call here "heritability in the broad" and heritability in the broad sense as defined in genetics ($h_B^2$).

Sure, a lot of things can be inherited from one organism to another. Any such heritable (in the broad sense) trait is susceptible to show interesting variation in the frequency at which trait values are found in a population. If, in addition to that, this trait is susceptible to spontaneous changes (the equivalent of mutations in genetics), then this trait can show interesting evolutionary patterns. If in addition to that, different trait values have different aptitude to replicate (the equivalent of natural selection in genetics), then such trait can evolve in an "even more interesting way".

What can be non-genetically inherited?

Two things can be inherited without the use of any sort of genetic information (I also exclude epigenetic information incl. DNA methylation or protein concentration in the yolk).

Environment (Ecological inheritance)
Meme

See more on Ecological inheritance and memes below.

Ecological inheritance

This is probably the first type of inheritance one would think of when not thinking about biology. In humans, it is not uncommon for offspring to inherit "stuff" from their parents when they die. Similarly, beavers can inherit a dam that has been built by their parents. This type of inheritance in generally called Ecological inheritance.

This type of inheritance might eventually be important to evolutionary processes (see literature on niche construction).

Inheritance of a meme

Definition

A meme has been named by the analogy to a gene. A meme is any idea, behaviour, thought or tradition (piece of culture) that can be inherited. The concept of an internet meme is now quite popular, but a meme is more than just an internet meme. While genetics is the study of genes (and much more actually), memetics is the study of memes. Memetics is a very interdisciplinary field of study that attract biologists, philosophers, mathematicians, linguists and archeologists among others. The hypotheses built in the field of memetics rarely offer predictions that can be easily tested, and therefore a good part of the work in this field remains very uncertain.

Analogy to genes

A meme could be a joke for example. If the joke is funny it will replicate easily and enter in new brains. This meme could be said to have high fitness. The joke may come into spontaneous changes (mutations). Be careful with analogies and they may show nothing but similarity. For example the nature of memetic mutation seem to be quite different than from the nature of genetic mutation.

Example

In humans, the examples are very easy to find. As I am writing this answer, I am currently trying to pass on a meme which has been given to me by some other authors. Hopefully I won't mutate this meme too harshly.

Lots of monkeys and apes are transmitting traditions, foraging methods and other memes to their offspring, sometimes through active teaching but often through imitation (or emulation). A classic example is the one reported in Rhythms of Vision in 1975 (I could not find the original peer-reviewed paper). A female monkey, one day had the good idea of washing a sweet potato. This behaviour has since increased in frequency throughout the population so that most monkeys now wash their sweet potatoes.

Pitman and Durban (2011) (and others before them) report that some population of orcas use cooperative hunting while some other population does not. Variation for this trait seems not to be caused by genetic variation.

How does inheritance work?

Inheritance can be "vertical" (parent to offspring) or "horizontal" (between individuals of the same or different species). This holds true for both genetic (consider transduction) and non-genetic inheritance (teaching to offspring or to the neighbors).

In addition to that the passation of a meme can be active (teaching) or passive.


How do taenia form a species? I know that there are many hermaphrodite animals and plants. But many of them seem to still exchange genes by mating with another member of their species.

I now happened to read the Wikipedia article on Beef tapeworm, and it turns out that there normally is one worm per host, and it self-fertilizes. Which makes some sense - if I were a large internal parasite, I wouldn't want to wait around for my host to pick up a second member of my species before I can reproduce.

But this means that there is no gene exchange when taenia reproduce. Does it mean that they are all clones of each other, barring spontaneous mutations? How does evolution function in taenia when they don't mate? How comes there are different taenia species if they can't evolutionary adapt to new environments by producing offspring with mixed-up genes?

This question has a related issue that should be addressed first: what is a species? To some extent, if you want to understand how speciation can occur, then you have to consider how you are going to define a species. There is no species concept that applies to all species, past or present. The most widely applied concept is the biological species concept (Mayr 1942), which applies (imperfectly) to sexually reproducing species. Of course, Taenia does not always reproduce sexually. I think the discussion of species concepts is beyond this question but I encourage those that are interested to check out references [2-4] as well as a series of papers published in Systematic Zoology in the mid-70s. Here, I'll focus on genetic differentiation with a subtext of reproductive isolation.

Genetic differences can accumulate between populations$^1$ of Taenia in two different ways. The first is non-adaptive evolution via genetic drift. Drift is when allele frequencies change by random processes. For example, just by chance, tapeworms in a particular host may not live very long because the host was killed in a mudslide. Those tapeworms don't produce as many proglottids over their interrupted life so they don't leave as many copies of their alleles. Tapeworms in a host that lives a long time produces lots of proglottids and therefore produce many more copies of their alleles.  The key point here is that the process of genetic drift is random. Allele frequency changes in one population of Taenia will be different from allele frequency changes in another population. Thus, over time, different populations of Taenia can become genetically different solely by chance. It's called non-adaptive evolution because natural selection is not evolved.

Adaptive evolution by natural selection can still occur on individuals that are asexually reproducing. Genetic differences will accumulate in a population over time to due mutations. Some mutations may be beneficial, some may not. Selection can increase the frequency of beneficial mutations and decrease the frequency of very mutations. Note that non-lethal but harmful mutations can accumulate in asexually reproducing species (see Muller's Ratchet) but I am assuming survivorship is decreased by harmful mutations for this example. If we assume that Taenia in different populations are subject to different selective pressures, then genetic differences can accumulate, leading to speciation. Note that drift will also affect the allele frequencies of both beneficial and harmful alleles because drift is random.

That brings us to the "mixed-up genes". I assume you mean the new genetic combinations that occur via sexual reproduction. Even if a host typically has only one individual of Taenia (not always the case), I suspect the opportunities for sexual reproduction in a population of Taenia are frequent, especially over evolutionary time. Consider places where tapeworm infestation of humans is high. Such places often have poor sanitary conditions so the opportunity for mixing of fecal material from different human hosts is high, and therefore the opportunity for mating among different individuals of Taenia is also high. If you have many humans living in squalor over long periods of time, then you have conditions very favorable for sexual reproduction of Taenia. Remember too that Taenia produce lots of proglottids, each with the chance for reproduction. Each reproductive opportunity creates new genetic combinations potentially subject to natural selection.

The final point to consider is population size. If the population size of Taenia is small (relatively few individuals) then genetic differences can accumulate fairly rapidly by genetic drift but the accumulation of beneficial mutations in the population will be low. If the population size is large then new mutations including beneficial ones can occur relatively often, increasing the rate of adaptive evolution among different populations.

Footnote

I'm assuming some sexual reproduction among individuals of the same population and individuals from different populations do not interbreed. Without sexual reproduction, we have to think about the individual as the species and that makes my head hurt.

References

Mayr, E. 1942. Systematics and the origin of speceis from the
viewpoint of a zoologist. Columbia University Press, New York, USA.
Howard, D.J. and S.H. Berlocher (eds.). 1998. Endless forms:
Species and speciation. Oxford University Press, Oxford, England.
Wheeler, Q.D. and Meier, R. (eds.). 2000. Species concepts and
phylogenetic theory: A debate.  Columbia University Press, New
York, USA.
Coyne, J.A. and H.A. Orr. 2004. Speciation. Sinauer Associates,
Inc., Sunderland, Massachusetts, USA.


Limit on the Number of Facial Phenotype Individuals of each species all have unique facial structure variations (shape of nose, position of chin etc) from humans to birds and fish etc. We humans don't seem to be reaching mathematical limit of uniqueness easily (maybe till the end of the world) considering huge variation and all possible combinations that define our facial structure/traits. However some animal populations are way more larger than humans and each year they reproduce in large amounts.  Considering their huge populations, is it possible for some species to reach their mathematical limit of having unique facial structure variations therefore start repeating the same facial structures?  For example can individuals of some fish species (sardines, sea breams etc) be already sharing exact same facial structure/geometry as a result of reaching all posible facial structure  variation limit?

Okay, theoretically possible, but only in theory.  Practically, it's totally impossible.  Let's start by defining why it would theoretically be possible.
Theoretically, there are only so many possible arrangements of proteins in the face, which would represent a limited number of possible facial appearances.  However, as you probably guessed, there are zillions of proteins being expressed in each body organ, such as an eye.  So just from the perspective of the number of different possibilities, it would be impossible.
One might think that since the facial features are controlled by genetic variation, eventually these features will begin to repeat themselves, but such is not the case, for two reasons:

There are way to many genes - and alleles - that control facial features.  We're talking thousands if not millions.  When you raise that number of alleles to each others' powers, you start to see the impossibility of repeating the exact same combination, especially since every new generation is introducing new alleles from a new blood line.

Genetic code is not the only thing that changes how you look.  A whole branch of genetics, epigenetics, is devoted to the changes of gene expression unrelated to DNA sequence.  The expression can be changed by environmental factors, even as early as when the embryo is forming the placenta.  This is why identical twins (who have identical DNA) do not actually look exactly the same, or even have identical fingerprints.

Bottom line, totally impossible.

Sources:

Face shape is in the genes, PLOS, 2016
Epigenetics, Wikapedia, 2017
Why do identical twins have physical differences?, Anonymous, 2005
Introduction to epigenetics, University of Leicester, 2013
How many Proteins exist in human body?, Innovateus, 2013


What percentage of a cell's volume is occupied by protein? I was looking at one of David Goodsell's illustrations of a cell:

And it seems to suggest a very crowded picture of the intracellular environment. Just how crowded are cytoplasms? What percentage of the volume is typically taken up by protein, water, and other major species?

The tricky part is to define what is the volume of a biomolecule as it is a folded chain full of bumps and holes. Water is all around and in the folded structure and is actually important to keep the conformation of at least some of the proteins/RNA/DNA.

At the same time we know that 60% of your body in mass is water. Let's visualize that. Bio molecules have roughly the same weight per volume than water. Now add into the equation that a good third of the filled actually is water due to the structure holes, adsorption etc. You now have roughly:

  % empty space = 60%-(40%/3)= 47%

To help think about it imagine a grid with roughly one cell out of two being filled. That looks pretty crowded to me. Then you of course have variations with blood and secretions on one side and bones on the other but you have the big picture.

For an example look at an electron microscopy picture of a striated muscle cell: http://histology.med.umich.edu/sites/default/files/muscleQ4.jpg. It looks pretty much like the half filled grid isn't it? Of course seeing individual molecules is hard but the white space correspond to mostly empty space with a couple of actine fibers. The dark corresponds to actine+myosine fibers: an extremely tight space. And we have roughly half of each :-)


Can spider silk be synthesized to be used for 3D printing? With the recent rise in 3D printing, I keep hearing about more novel ways to use the technology: cell 3D printing, liquid aluminum or plastic 3D printing. For example,   this Ted talk deals with printing a human kidney. What interests me is if the current technology can be adapted to print with spider silk. The silk has some amazing properties, and apparently there are multiple types of silk that spiders use.

I found this project: Spiderbot 3D printer.  Can spider silk actually be synthesized in large enough amounts to enable 3D printing?

The "...in large enough amounts to enable 3D printing?" part of your question is, I think, still unknown, but spider silk has been being synthesized in transgenic goat milk for quite a long time already, and I suspect that it's now just a matter of time before the answer to your question is an unqualified "yes."

See Macromolecules, 2011, 44 (5), pp 1166–1176, doi:10.1021/ma102291m


Are There Exceptions to Animal Cells not Having Cell Walls? In the January Issue of SciAm (discussing Haemophilia):

  When damage occurs to blood vessels, exposure of the blood to collagen in the cell walls and material released by the cells triggers the activation of clotting factors.

I read the original in print, but it is available online here.

This seems to imply that animal cells (in this example, those of humans) have cell walls.  I sometimes see similar implications in other resources.  However, in elementary biology, one is taught that animal cells never have cell walls.

Therefore, my question: Are references to animal cell cell walls (such as the above, for human animal cells) simple mistakes--or are they exceptions to a generalization?

Humans, as well as the rest of the metazoans (i.e. animals), absolutely do not have cell walls. What humans do have is extracellular matrix (ECM), which is the sort of fibrous, sort of gel-like material in which cells in many of the tissues are embedded. Collagen is a major component of ECM.
From the old copy of Alberts that is hosted on the NCBI website:

Tissues are not made up solely of cells. A substantial part of their volume is extracellular space, which is largely filled by an intricate network of macromolecules constituting the extracellular matrix (Figure 19-33). This matrix is composed of a variety of proteins and polysaccharides that are secreted locally and assembled into an organized meshwork in close association with the surface of the cell that produced them...
Two main classes of extracellular macromolecules make up the matrix: (1) polysaccharide chains of the class called glycosaminoglycans (GAGs), which are usually found covalently linked to protein in the form of proteoglycans, and (2) fibrous proteins, including collagen, elastin, fibronectin, and laminin, which have both structural and adhesive functions.


How to identify genes required for biofilm formation This is just a homework question:

Q: Let’s assume that there is an unknown set of E. coli genes that are required for biofilm formation. Describe a genetic experiment you could perform to try to identify those genes.

The one idea that I can think of is:

Compare strains that produce biofilm against strains that do not produce biofilm. Sequence genes, find differences, interrupt genes in biofilm producing strains and confirm biofilm ability is impaired.

Is there a better approach than this?

You could do different things: First you could, as you say yourself, sequence the complete genomes of the strains from a biofilm and compare these with some, which do not form biofilms. This may give you an idea which genes are involved when they are present in the "biofilm genome" but not in the other. The proof would be to disrupt these genes either by removing or mutating them or by gene silencing techniques and see what the outcome is.

It is also possible that only a mutation in a gene which exists in the sample and the control genome makes the difference. Then site-directed mutagenesis would help to identify the important genes.

The second possibility is that there is no real difference in the sample and the control genome and the difference for developing a biofilm "simply" lies in the difference of gene expression. Then the isolation of RNA (either total or mRNA only) would help to find involved genes. If the environment makes the difference for the development of a biofilm, then the biofilm and the control cells should have show no (or almost no) difference in their gene expression profiles when they are cultivated under identical conditions. You then need to test the gene expression for different environmental conditions (including those that favor the development of biofilms) to find genes which are involved.

This comparison of the different conditions will then deliver genes which are uniquely or more highly expressed in the biofilm group, a lot of genes which are comparable in expression to the control sample, and some genes which have a lower expression than the control. It is now worth looking at the higher (or unique) and lower expressed genes, find out their function and then start mutating them to check their function for the formation of a biofilm.

Additionally there is the chance that the gene(s) which is necessary for the biofilm formation is located on an extra-chromosomal plasmid. I would also check the plasmids present in the biofilm and the control sample, sequence them (if present) and see which genes they express. The function for the biofilm formation can easily be tested with a simple transformation.


Why denatured proteins can't fold back in their native form I was wondering why a denatured protein isn't able to fold back into it's native form again.
Because a polypeptide before it's folded has a enthalphy and entropy drive to do so. What does the denaturation process do whith this favouring force to fold into the native structure.
In my opinion I can't see the differences between the unfolded protein (direct after translation) and the denaturated protein.

In short: the unfolded state is a high-energy state of the protein, which will move towards lower-energy states. Some of these states are the folded protein, while others states are denatured protein (forming "wrong" interactions with itself or other proteins). Energy barriers between these states keep the protein in the denatured state even though the folded state might me more favorable.

Or in other words: it's trapped in the denatured state because of kinetics, even though thermodynamics would favor the folded state.

A nice figure to illustrate this: http://www.ghrnet.org/index.php/jbmbr/article/viewFile/1027/1397/6798

If you go into a little bit more detail, you will find that a lot of proteins (especially larger ones) are usually folded by chaperones. These helper proteins will bind to the emerging protein chain to prevent it from aggregating. In a sense they guide the protein to a folded state. In a similar way, chaperones can help proteins overcome the energy bariers that normally prevent it from going from an aggregated state to a folded state.

This review in Science  is very complete, but also contains some nice figures that give you an idea of what happens:
http://science.sciencemag.org/content/353/6294/aac4354.long /

If you're a pirate: http://science.sciencemag.org.sci-hub.bz/content/353/6294/aac4354.long


Where can I find the tissue-specific protein expression levels for hTERT (telomerase subunit)? I find a number of contradictory sources regarding the tissues in which hTERT - the protein - is expressed. Does anybody know some resource that authoritatively (as authoritative or widely-accepted as is possible) lists the various tissues and hTERT's protein expression levels?

Any similar resource for gene expression of hTERT?

I have found that biogps.org has all expression data I need:

https://biogps.org

https://biogps.org/#goto=genereport&id=7015


Reduction of size in diatoms due to asexual reproduction From this we can see that diatoms reduce their size after asexual reproduction.

This would ultimately lead to nonviable small size. Is there any mechanism to avoid this ?

The ability to reproduce sexually is closely associated with cell size
  of the diatom. It is the most prevalent method of restoring cell size,
  and it is often triggered when the size of a cell is less than a
  critical level (usually smaller than half of the original size for
  most species).

Source : Sexual reproduction in diatoms


Change solvent of bacterial solution I have to perform an RNA extraction that should start with 900 uL of 2%SDS bacterial solution. The problem is that the sample is in 900 uL of PBS.

I thought about centrifugation of the sample at 5ºC, remove PBS and then add the 2%SDS.

DO you think bacterial RNA quantities will vary?

Thanks!

I'm assuming that you have a solution of bacteria in your buffer directly after growing them for some time, and without performing a lysis step yet. The 2% SDS step looks like it is for lysis of your cells.

In that case, centrifuging the bacteria and resuspending them in lysis buffer is a very common step in many protocols. Separating whole bacteria from medium or buffer by centrifugation is pretty easy and should just work. But if at any of your previous steps you already lysed your bacteria, this won't work because the cells aren't intact anymore.


Do toxin producing strains of E. coli constantly produce toxin or only under certain conditions? Background

E. coli is prevalent everywhere but only some strains produce toxins harmful to humans, such as E. coli O157:H7.

Questions

1) Would anyone know if these strains are always producing this toxin or is it only under certain conditions?

2) Is it the toxin itself that makes people sick and not the presence of the bacteria?

1) That depends on the fact, if the protein in the bacterium is regulated somehow or it is constantly expressed. That could be different for different toxins and even for the same toxins in different strains, so there is no  plain answer for all strains and toxins.

2) That, I guess, also depends on the toxin. There are some that are basically toxins, but do not make people sick. Sometimes, the toxin is produced by the bacterium, but never secreted. Sometimes it is secreted, but has no influence on the host. Sometimes the host does react to a toxin. But the human immune system can also react to the bacteria before they start producing toxin (if it is somehow regulated) or before the toxin concentration secreted by the bacteria starts to be harmful.

In the case of E. coli O157:H7, this paper states it produces two different Shigatoxins (that were supposedly causing its pathogeny), but also some other toxins/toxin-like proteins.

I have studied some E.coli genomes previously, some non-pathogenic had several toxin-related genes, some pathogenic had actually none at all (at least none that could be annotated).


How well supported is the hypothesis that aging is mainly caused by the number of mutations in tissues? I heard the hypothesis, that the (main) reason of aging is the increasing number of mutations in body tissues. The higher the number of mutations is, the older tissue is.

Is this true? And how well supported is the idea?

Have somebody measured the numbers of mutations in different tissues at different ages, and if so, where I can get these numbers?

I think telomere shortening largely accounts for the replicative cell aging.
http://www.ncbi.nlm.nih.gov/pubmed/22901253
The increase in no. of mutations with age surely does affect the tissue/organism survival too. There's a recent study that I'd like to share here. It is quite interesting and informative.
http://www.iflscience.com/health-and-medicine/mutations-found-115-year-old-womans-blood-could-help-unlock-secrets-aging


Why do glial cells of the retina become more abundant the closer they are to the optic nerve? I am doing a project on expression of GFAP in the zebrafish retina. GFAP is a marker for glial cells.
I have found that the glial cells are more abundant the closer they are to the optic nerve at the middle of the eye. This may just be because the cells are more tightly compacted here than at the edges of the eye...
But I am wondering if it may have something to do with the glial cells being involved with neuornal processes, and the optic nerve being the transmitter of signals from the eye to the brain?

Any particular glial cell you're noticing this with?

I know that Astrocytes modify Calcium concentrations in the synaptic cleft. Perhaps at places where there are more synapses, more Astrocytes must exist to regulate such thing? Here's an interesting paper on a possible role of Astrocytes on associative networks:

http://www.antanitus.com/


Does a bird know it's different? I live in Northern Virginia, USA. As I am sitting here there is a large flock of small (blackish) birds in a tree. They are quite prevalent here. For the sake of brevity I will call these birds "sparrows." I don't believe it matters what they really are.

There are also several medium-sized blackish birds perched on the eaves of the townhouses. Again, I'll call these birds "crows". (We have a committee of large vultures (yes, really) in the neighborhood as well, which is why I call the crows medium-sized.)

The crows (tend to) lay their eggs in the sparrow's nests. Little crow hatchlings are then "raised by" the sparrow parents, along side thier smaller "siblings".

Does the now adult crow think it's just an oversized sparrow? (IOW, do all of the crows I see have identity issues and feelings of inadequacy due to their extreme gigantism? :) )

Crows don't lay their eggs in sparrows' nests - they lay them in crows' nests. What you're describing, though, here is brood parasitism. This relieves the parasitic parent of the responsibility of rearing young, building nests, protecting the eggs, etc.

Brood parasitism is seen in a number of duck species, with females laying their eggs in the nests of others. One example is the goldeneye, Bucephala clangula. Interspecific brood-parasites include the most cuckoos and cowbirds, black-headed ducks, and indigobirds, whydahs, and honeyguides. About 1% of all known bird species are obligate brood parasites (never make nests, need a host).

Here is a picture of a reed warbler feeding a cuckoo which was a parasite, its egg having been laid in the warbler's nest.

Parasite nestlings suffer a relatively high mortality, either from rejection by the host (host bird will not feed the parasite) or rejection before fledgling (once nestling graduates to tree branch, the hosts stop feeding it). However, clearly since cowbirds and cuckoos are still alive and well, enough of them do survive.

Do they think they are of the host species? There was no literature I could find on this. While the parasite messes up the host parents and 'siblings' (when there are surviving 'siblings'), there is much less follow-up done on the behavior of the parasite once fledged. Common sense will therefore need to come into play.

If a cowbird thought it was an indigo bunting, it would not be able to reproduce, as it would try to attract a bunting mate and fail. Since the hosts continue to experience parasitism over many generations, and the population of parasites does not necessarily decline in a given area over several generations (in some areas, it is the host population that declines), I would have to say, yes, the bird 'knows' it's different (probably only on an instinctual - not cognitive - level); the parasite bird feels nothing about its bad behavior, and does not learn their own behavior from their host parents. Instinct takes over; they mate with their own kind, and continue to parasitize the host birds' nests.

Brood parasite
Host–parasite coevolution beyond the nestling stage? Mimicry of host fledglings by the specialist screaming cowbird
Brood parasitism by cowbirds: risks and effects on reproductive success and survival in indigo bunting
Brood parasite


Very frequent multiple births in humans 18th century Feodor Vassilyev is said to have had children by two wives, each of whom only ever had twins, triplets or quadruplets. His first wife has 16 sets of twins, 7 of triplets and 4 of quads; his second had 6 sets of twins and 2 of triplets. Is there any known plausible biological explanation for this, or do we have to dismiss it as a fabrication?

I could understand a woman's body being unusually susceptible to multiple births. I can't find information on whether these women tended to have monozygotic or polyzygotic offspring, but neither option seems unviable to me. However, since it's unlikely two of Feodor's sexual partners would share such a trait, one would think to attribute it to him. Presumably there would have to be a mechanism by which paternal DNA can trigger embryo fissions, in which case I imagine the offspring would be polyzygotic.

Risk factors for dizygotic twinning are related to multiple follicular development, and include maternal family history, ethnicity, geography, maternal parity, maternal age, and, of course, use of assisted reproductive technology. There may be a genetic component to monozygotic twinning as well, but that rate is fairly consistent across populations. Other risk factors, such as diet and supplementation, have been proposed, but the data are less robust. There are some interesting studies demonstrating geographic clusters of twinning, but these tend to be demographic clusters that are associated with other risk factors.

Though a higher risk of twinning can be transmitted from a father to his daughters, the father's family history of twinning is not a significant risk factor (for his own children to be twins). To clarify -- if a man has a family history of multiple births, his children are no more likely to be twins than the general population, but his daughers are more likely to give birth to twins. This study is one example of the studies that have shown a significant independent association between maternal family history and twinning, with no significant independent association with paternal family history.

As far as the case of Feodor Vassilyev is concerned, many people have lived on this earth, making very unlikely events in a single instance more likely to have ever occurred. I would say this case is either a hoax or a rare chance event. There is no modern data I'm aware of that would support a paternal genetic reason that this particular man produced so many multiples.


Why do our bodies maintain blood pressure but not the flow rate? This might be a silly question but i'm not not clear

I'm always told that blood pressure is homeostatic parameter and can't not be changed but isn't what important is the flow rate to the organs? why not maintain flow rate

Doesn't having enough blood flow to the organ already satisfy our bodies to function properly or do pressure play any role? what happens if blood flow is constant but blood pressure drop below normal

there's some case when one have blood lost , pressure drop and our bodies respond by constricting artery and that results in decreased cardiac output.Isn't that worst? decrease cardiac output just to maintain blood pressure

Forgive my little understanding out this I know my thought is kind of logically wrong but please help me understand. thank you

A constant blood-flow would not be advantageous to organisms with a varying activity level. The blood supplies (mainly) oxygen to the tissues and the supply of course needs to match the requirements. Organisms rely on a number of mechanisms to ensure this match, one of these is to increase the blood-flow (heart-beat). But flow through a (blood) vessel relates directly to the pressure and inversely to the cross-sectional area of the vessel, so if the flow is increased, the organism must accept either a higher blood pressure or expand  the blood-vessels. Of course, it is in reality a compromise of both mechanisms.


Using punnett squares to express sex/gene linkage and recombination frequency I have been using punnett squares to visualize mating experiments. I am looking at a pairing which is known to have a crossover event occur. I know from empirically collected data the recombination frequency is ~3%. Can punnett squares be used to express the results bearing the recombination frequency in mind or should I consider a different visualisation technique?
The end result of what I want to achieve is the expected genotypic/phenotypic outcomes taking recombination into account.
In addition the pairing has a sex-linked mutation which further complicates things e.g. aB/Ab x Ab/Y
Here is an example punnett square:
 a-B/A-b x A-b/Y
 -------------------------
 | x   | A-b     | Y     |
 -------------------------
 | a-B | A-b/a-B | a-B/Y |
 -------------------------
 | A-b | A-b/A-b | A-b/Y |
 -------------------------

If a want to represent a recombination event in the punnett square (e.g. to produce a-b/A-b and a-b/Y does this mean I would  need to add a-b as an additional trait to the punnett square like so?
a-B/A-b/a-b x A-b/Y
 -------------------------
 | x   | A-b     | Y     |
 -------------------------
 | a-B | A-b/a-B | a-B/Y |
 -------------------------
 | A-b | A-b/A-b | A-b/Y |
 -------------------------
 | a-b | A-b/a-b | a-b/Y |
 -------------------------

If that is the case, that would give me a frequency of 16.666666% for each.

The Punnett squares are a general way to visualize the product of any two polynomials; for example, you know that the result of (a + b)(c + d) is the sum of the four terms ab, ac, bc, bd. You may put it this way:
  | a   b
----------
c | ac  bc
d | ad  bd

Suppose that the female sex gametes are of two types, X1 and X2, which are transmitted with probabilities 0.9 and 0.1; suppose that males form three types of gametes, X1, X2, and Y, with probabilities 0.45, 0.05 and 0.5. Then, you may visualize the outcome of a general population mating this way:
    |Fem   X1   X2
    |      .9  .1
--------------------
Male|
X1  |     X1X1  X1X2
.45 |     .405  .045
    |
X2  |     X1X2  X2X2
.05 |     .045  .005
    |
Y   |     X1 Y  X2 Y
.5  |     .45   .05

(You may note that this situation roughly depicts the population genetics of color blindness)


Do viruses pickup new genetic sequences from the host cell? Virus replication does not involve meiosis so the virus genome does not gain diversity from having two parents , so other than from mutation, do viruses obtain new genetic sequences from the host cell ?
Do virus genomes show evidence of containing base pair sequences which originated from host cell ?

Yes.  See for example this article, which describes how some viruses can pick up bits of human DNA.  Here's a quote from the article:

...researchers have shown that a large group of viruses, including the influenza viruses and other serious pathogens, steal genetic signals from their hosts to expand their own genomes.


Is there any kind of immortality in plants? I asked a question about immortality of hydra and learned good things about senescence. Now I would like to know about immortality in plants, if there is some kind of immortality in plants and how this occurs - how does it protect itself from senescence?

I can find no examples of immortal plants, but then again immortality is rather hard to prove, it's rather like trying to prove that space will never turn in to a pony - as long as time exists it could still occur, only if you go beyond the end of all time would you be able to say that it has or has not happened but then time would no longer exist and nor would space/the pony.

However, for examples of long lived plants it is perhaps best to look at trees - there are some species that live a long time and they can easily be aged. Here is a list of oldest known trees. It is difficult to tell how old these trees can become, and thus whether they are "immortal", because anything that lives that long is likely to encounter sources of extrinsic mortality during it's lifetime - predation, deforestation, extreme weather, erosion, natural disasters, contaminants, humans, disease, parasites etc. (rather than intrinsic dying of old age).

A lot of plants go through some kind of apoptosis, where cells are programmed to die. Plants such as annuals, biennials etc. die after a few months or years in a programmed way. It is difficult to say whether long lived species of trees would do the same after a few thousand years of life, because we just don't get to see many reach that stage of life, or if the mechanisms causing it have been suppressed (which could explain their long life).

Luke has posted a very thorough answer on the cellular and genetic aging of plants here. And to quote him:

  "...it seems to me likely that plants may also have enhanced maintenance
  against other cellular stresses than DNA damage, such as build-ups of
  aberrant proteins. It therefore appears that in a protected
  environment some plants could live indefinitely"

Wikipedia has some very good pages on the evolution of senescence & aging. This article has also a good section on plant aging and I hope you can access it.

and finally, if you want to have a laugh, take a look at this entry on plant immortality and aging from creationwiki.org...

  "Plants are actually or potentially immortal organisms that will live
  indefinitely provided their environmental requirements are met. In
  striking contrast to plants, humans and animals have a maximum life
  expectancy regardless of whether their needs are fulfilled. Although
  it is true that some plants grow as annuals, all plants are actually
  perennials by nature, and have adapted to a programmed life cycle in
  some instances to match growing seasons. Otherwise, plants only die
  because of biochemical starvation or disease. If their physical
  requirements are met, plants will grow indefinitely."

Some great clear science there, well done creationists... but it's just plain wrong.


Why exactly are the reflections of sunlight in this dragonfly's eye hexagonal? I photographed a rather cooperative, large dragonfly today and after getting back to my desk and looking closer at the images I realized that the reflection of the Sun in its eyes produced large hexagonal bright spots that are:

much larger/wider than if the eye surface were smooth specular reflector
relatively uniform in brightness all the way to the edge
have very sharp edges, transition from bright to dull red is very abrupt.

I'm aware that the components of compound eyes are usually at least roughly hexagonally packed, but what is happening here is something more than that.
What is it about a dragonfly's compound eye that can account for all three of these characteristics of reflected sunlight?
Presumably this is the same red dragonfly species as is seen in Identify these two large, colorful dragonflies in Taiwan? It's the same area and time of year.

Two more taken at different angles relative to the Sun. (click for larger)

Here is the image in comments. The direction of the sun can be seen from the shadow of the left antenna. I just sketched this image to note some observations, it's the best answer that I can find at this time.

source