I suppose this is a homework, not a genuine curiosity. That being the case, I'm gonna give you two different answers here: the standard one, which is the one I believe your teacher/lecturer expects to see, and a more complicated one in the addendum.

The first thing that draws out attention in the question is the base percentages. Clearly, it doesn't follow the famous Watson-Crick pairing rule (A pairs with T, G pairs with C) and, because of that, we don't see the Chargaff's Rule in this nucleic acid.

Thus, this is not a double-stranded DNA (dsDNA), but a single-stranded DNA (ssDNA).

That being said, the answer to that question can be something along these lines:

  A Type II RE can't cut that nucleic acid because that is a ssDNA.

Addendum:

There is a complication here, which may render the previous answer questionable.

Type II Restriction Enzymes only cleave regular, that is, double-stranded DNAs. So, they cannot cleave ssDNAs, which corroborates the answer we just gave.

But the problem is that ssDNAs can form loop structures, in which there is pairing between bases in the same strand. In those structures, DNA is technically dsDNA and, as such, can be cleaved by Type II RE. For instance, have a look at this paper:
Type II restriction endonucleases cleave single-stranded DNAs in general.

That being said, Type II RE do, in fact, cleave ssDNA (in places where ssDNA form loops and structurally resembles a dsDNA), which makes the question itself meaningless.


Is eradication of the Common Cold possible?

You'd think there would be numbers of papers on this. I have two references but they're not great.  The answer is not really.  Many people carry cold viruses asymptomatically.  This can be either a natural immunity, or that their body has beaten it down but not entirely eliminated it.  Cold viruses do not survive long outside of the body as you stated.  The only way they've made it this far is some survive inside the body until they are spread to other people.  In essence we are the reservoir.  So you could isolate everyone for two weeks, but that won't cause a problem for the viruses that are just tagging along.  There may be other reservoir animals as well for many of the viruses.  But even those that only affect and are carried by humans would survive.

The group of cold viruses is just too varied and different to eliminate them.  Also the cost of such an effort would not really be justifiable given the typically mild symptoms.

Natural Reservoir


What is the function of the Moderator band?

Does it mean it delivers impulses to the anterior papillary muscle faster?

Yes.

  If it does, how does this help?

To facilitate the conduction time thereby allowing coordinated contraction of the anterior papillary muscle.

  and why only the anterior papillary muscle?

This is because its chordae tendineae insert into anterior and posterior tricuspid valve leaflets, so only their contraction before systole would be optimum.

  What makes it special to have a moderator band?

For effective Cardiac Output because it helps in coordinated contraction of ventricular cells. The ventricles must maximize systolic pressure to force blood through the circulation, so all the ventricular cells must work together.


While blood is flowing into the ventricle, it can never be at a higher pressure than where blood is flowing from: if it was, the flow would be going in the other direction. Flow is always from higher to lower pressure, if there is no pressure difference there is no flow.

Before atrial contraction, the ventricle can have no more pressure than the uncontracted atrium, which in turn can have no more pressure than the veins (vena cava or pulmonary depending on which side of the heart we are talking about). When the atrium contracts, it increases the pressure in the atrium, which causes a flow of blood into the ventricle. Whenever a fluid flows, there is a pressure drop that depends on the resistance (very much like voltage in an electrical circuit). However, the AV valve is fairly big and open, so there is little pressure drop from the atrium to ventricle.

  The pressure is equilibrated between two sides of an open valve.

...is mostly true if the valve is large enough. There is still some pressure drop, though: if there wasn't, there wouldn't be flow.

There is no need for the ventricle to be at maximum capacity for pressure to increase. Imagine if you squeeze one side of a balloon: the pressure in the balloon increases, which you can tell because the balloon stretches and expands in the areas you are not squeezing; it need not be at the maximum capacity of the balloon for this to happen. Same for the heart.

As far as the higher pressure in the aorta, I this diagram is slightly exaggerating where the pressure difference starts, but as the ventricle relaxes there is a brief time where you get a small backward flow because the relaxing ventricle ends up having less pressure than the proximal aorta. This pressure drop is what closes the aortic valve (or the pulmonary valve, same process).


Why does the 'Positive-inside Rule' exist?

There are not much explanations available, as far as I can see. The best explanation that I have found is that the positive charge allows the orientation of the protein in the membrane. The orientation for membrane proteins is important as a lot of them are transporters which have a dedicated transportation direction. The same is true for receptors, which transport a signal from the outside to the inside of the cell. Most of the positively charged arginine and lysine residues are found in loop regions which are located between transmembrane regions (often hydrophobic helices).

References:

Topogenic signals in integral membrane proteins.
Positive charge loading at protein termini is due to membrane protein
topology, not a translational ramp
The Positive Inside Rule Is Stronger When Followed by a Transmembrane
Helix
Membrane-protein topology


Decreasing Solubility as Solvent Moves Higher in Paper Chromatography

The solubility of the solutes is the same at all points in the chromatography process. The solutes are clustered together at the beginning (at the solvent front) because none of them has moved very far yet. The reason for the separation of the solutes isn't that they become less soluble, it's that the solutes are moving at different speeds, like cars in an auto race:

  _______
 /____/SF\___
 |_,._____,._)
---`'-----`'--
  _______
 /____/S1\___
 |_,._____,._)
---`'-----`'--
  _______
 /____/S2\___
 |_,._____,._)
---`'-----`'--

At the beginning, both cars (solutes) S1 and S2 are even with the solute front car (SF) because the race (chromatography) has just begun. However, over time, the SF car outpaces S1 and S2 because it is moving faster.

                     _______
                    /____/SF\___
                    |_,._____,._)
                   ---`'-----`'--
         _______
        /____/S1\___
        |_,._____,._)
       ---`'-----`'--
              _______
             /____/S2\___
             |_,._____,._)
             ---`'-----`'--

And at the end, you get great separation:

                                                                _______
                                                               /____/SF\___
                                                               |_,._____,._)
                                                              ---`'-----`'--
                        _______
                       /____/S1\___
                       |_,._____,._)
                      ---`'-----`'--
                                           _______
                                          /____/S2\___
                                          |_,._____,._)
                                         ---`'-----`'--

(Thanks to retrojunkies.com for the ASCII car)


Does hypothalamus regulate posterior pituitary gland?

The difference between secretion of ACTH  and neurohypophysial hormones is that the prior is a two step process, with CRF from hypothalamus stimulating the anterior pituitary. The latter is produced and secreted from the same cell, only in different organs! Magnocellular neurons stretch from the hypothalamus to the posterior pituitary, where they have their neurosecretory endings packed with hormone storing large dense-core vesicles. The same neurons are osmosensitive, regulating their secretion themselves as physiological need arises. Also, they apparently do dendritic secretion as autocrine signalling. Some reading about this: http://www.ncbi.nlm.nih.gov/pubmed/24265070
and
http://www.nature.com/nrn/journal/v7/n2/full/nrn1845.html
Hope it helps.


I cannot find any definite articles on why there would be a reason for this behaviour other than the same ones that you have mentioned in your article. It could be because it wants to mark its territory or the dog wants to hide its scent.

One point that I would also like to add is force of habit. As Charles Darwin (the father of evolutionary biology) had said in his book titled "The expression of emotion in man and animals"

  ‘Certain complex actions are of direct or indirect service under
  certain states of the mind, in order to relieve or gratify certain
  sensations, desires, etc.; and whenever the same state of mind is
  induced, however feebly, there is a tendency through the force of
  habit and association for the same movements to be performed, though
  they may not then be of the least use’ (reference 1 and reference 2).

It is more of a guess that we make when we see them hide their faeces but in the end, there may not be a reason at all but a habit that do not serve much purpose passed on through evolution. It is left upto our own liberty as to guess what the exact reason is.


What is the genetic difference between two cone branches?

I don't understand your hypothesis. But the number of pairwise differences between two cells assuming neutrality ($\pi$) in the two different branches in $\pi = 2 \mu L t$, where $\mu$ is the somatic nucleotide mutation rate (around $10^{-11}$ on average), $L$ is the length of the sequence of interest (eventually the whole genome). $L$ can therefore be of the order of $10^9$. $t$ is the number of cell generation since the two cell lineages split. $t$ depends on the relative positions of the two branches but it could be $10^4$ cell generations. With these very quick approximations, we can estimate the number of pairwise differences as

$$\pi = 2 \mu L t \approx 2 \cdot 10^{-11} \cdot 10^9 \cdot 10^4 = 200$$


According to Amy Rosenfeld, it is about 8 hours eclipse and 18-24 hours until "its done". Not sure if it means until burst or until the latent period is over. These times are in vitro and are cell line dependent. In vivo might be different. Burst size also cell depndent. Source: https://youtu.be/NP56XjzyPfQ?t=1301
In this video https://youtu.be/4S3DXXtRZZg?t=152, it is said, that each cell can produce up to 600k viral particles of SC2, but I'm not sure, what is exactly meant by the number. Later in that video: https://youtu.be/4S3DXXtRZZg?t=187 it is said, that the virus seems not to kill cells for about 5-6 days.


Assay for Beta-galactosidase activity in single cell microscopy

I found this paper.

Zhang GJ et al. (2009) In vivo optical imaging of LacZ expression using lacZ transgenic mice. Assay Drug Dev Technol.7:391-9. doi: 10.1089/adt.2009.0195.
Abstract
beta-Galactosidase (beta-gal) (encoded by the lacZ gene) has been widely used as a transgene reporter enzyme. The ability to image lacZ expression in living transgenic animals would further extend the use of this reporter. It has been reported that 7-hydroxy-9H-(1,3-dichloro-9,9-dimethylacridin-2-one)-beta-d-galactopyranoside (DDAOG), a conjugate of beta-galactose and 7-hydroxy-9H-(1,3-dichloro-9,9-dimethylacridin-2-one), is not only a chromogenic lacZ substrate but that the cleavage product has far-red fluorescence properties detectable by in vivo imaging. In an attempt to noninvasively image lacZ expression in vivo, we applied fluorescence imaging to a G protein-coupled receptor (GPR56), knockout (KO) mouse model, in which the lacZ gene is introduced in the GPR56 locus. Compared to wild-type (WT) mice, GPR56KO/LacZ mice showed three- to fourfold higher fluorescence intensity in the head area 5 min after tail-vein injection of DDAOG. beta-Gal staining in sections of whole brain showed strong lacZ expression in homozygotes, but not in WT mice, consistent with lacZ activity detected by in vivo imaging. The kidneys were also visualized with fluorescence imaging both in vivo and ex vivo, consistent with beta-gal staining findings. Our results demonstrate that fluorescence imaging can be used for in vivo real-time detection of lacZ activity by fluorescence imaging in lacZ transgenic mice. Thus, this technology can potentially be used to noninvasively image changes of certain endogenous molecules and/or molecular pathways in transgenic animals.

The work in the paper is cited in a more recent paper which reports beta-gal-based chemiluminescent imaging in mice.
It's unclear if any of this would be successful at a single bacterial cell level.


What is the function of the RNA primer in DNA replication?

DNA polymerases need a primer oligonucleotide (RNA or DNA) - their substrates are an existing 3'-OH group and a dNTP. The primase however is a typical RNA polymerase, capable of initiating polynucleotide synthesis de novo by positioning a complementary ribonucleoside 5'-triphosphate opposite its complementary DNA base. The primase makes an RNA primer that the DNA polymerase can then use for chain extension. The RNA primer is ultimately degraded and replaced by a DNA polymerase.

The rationale for this difference is that DNA polymerases have an active site that is geared towards proofreading and that primerless initiation would be an error-prone process. By having the primers 'tagged' by virtue of them being RNA, it is possible for the replication machinery to use them but then replace them with a high fidelity DNA copy of the template strand.

Edit in response to OP comment:
Synthesis of the leading strand consists of extending an existing DNA. However the leading strand is also originally initiated, at the ori element, with an RNA primer. Once that first initiation event has taken place the synthesis of the leading strand is simply a process of extending that original primer.

Some viruses employ ingenious variations on this theme such as using tRNA primers , or proteins - see Wikipedia.


What is the brightest color a light source that only emits blue frequency light can achieve?

The color that human vision perceives for a specific frequency of light (prior to saturation of any cones) is derived from the relative responses of different cones.  For example, at about 480nm, the response of S and M cones are roughly equal.  However, the human eye is not able to distinguish pure colors (single wavelengths) from combinations of wavelengths which produce the same response in each of the three cone types.

It is possible that a blue light source could appear white to the human eye, because the cones which inform our perception of color are not strictly monochromatic.  Rather, they have a range of sensitivity across the spectrum, and all cones are at least somewhat sensitive to blue light.  (See this diagram.)
If the blue light is so intense that it saturates all cones, S (blue), M (green), and L (red), then it will be perceived as white light.  However, in order to saturate the low-sensitivity M and L cones, the intensity of the light would be blindingly high.  Prior to this point, but after saturating the S cones, the apparent color of the light would shift toward green before eventually appearing white.  For intensities that are not saturating to any cones, the hue of the color blue will remain constant, while it's value (or lightness) may change.


What is the actual size of a nucleotide?

If you want experimental papers, we should be precise about what we're measuring. "The dimension of a nucleotide" is rather imprecise, as a nucleotide is a rather oblong, knobbly thing.

0.34 nm is a relevant measurement related to nucleotides, but it's specifically the distance between consecutive bases in a standard B-form DNA helix - that is, what's the spacing between the "rungs" on a DNA ladder.

This measurement can be confirmed by several experiments, primarily those involving X-ray or neutron crystallography or scattering. For example, both the Wilkins and Franklin papers that were published back-to-back with the famous Watson & Crick DNA structure paper referrence the strong 0.34 nm reflections from X-ray fiber diffraction which Watson & Crick reference as the spacing of the bases in their model of DNA structure. Other papers have confirmed the measurement. This 1983 Biomed Biochim Acta paper uses wide-angle X-ray scattering to find it. Additionally, there are a large number of structures in the Protein Databank which contain DNA structures - these have been determined by a number of different approaches (X-ray crystallography, neutron diffraction, NMR, electron microscopy, etc.) and all of which are consistent with the 0.34 nm average spacing of base pairs. (Modulo minor structure-to-structure variations.)


As you correctly say, tendons are made up of collagen fibers. Collagen is one of the most important proteins (or, to be more specific, family of proteins, as there are many types of collagen) forming connective tissue in the body.

Collagen molecules have a particular structure that allows them to form long fibers, composed by three different strands that form a triple helix. This is a schema of a collagen helix (each ball represents one aminoacid):

(source: Wikipedia)

These helices can then be bound together to form a collagen fiber, through the action of an enzyme called lysyl oxidase which binds two lysine residues from two different helices together (lysine is one of the aminoacids that makes up collagen).

Here is a scanning electron microscope of a collagen fiber:

(source: Science photo library)

Collagen is secreted out of the cells that produce it so, although there may be cells around the collagen molecules, it is important to understand that it is part of what is called the extracellular matrix, the extracellular structure that supports the cells in our body.

As for the photo you linked, it is an hematoxylin and eosin (H&E) stain of a tendon. Hematoxylin colours cell nuclei in dark blue, so the dark spots are definitely cells.
The pink "waves" are indeed collagen fibers, the cells are probably the tenocytes, the specialized fibroblasts of the tendon, which produce the collagen.


What is the difference between Integrin to Cadherin?

Cadherins look like chains, that are stretched out only when bound to Ca++. They contribute to cell adhesion through adherens-junctions and desmosomes (cell-cell adhesion). They bind weakly by themselves, but function sort of like velcro, in that they make a strong junction when they are many.

Integrins can be of alpha and one beta type. Both types are used in a junction, and they sort of "claw" around the ECM. They also depent on Ca++ (and also Mg++) for correct binding. They join the cell to the extracellular matrix through aktin-linked cell-matrix juntions and hemidesmosomes. There's one alpha and one beta integrin per junction (i think) and they sort of "grip" the ECM by one of them going in the front and the other in the back of the ECM unit.

Both integrins and cadherins are transmembrane proteins, that also need adaptor proteins on the intracellular side.

For clarification:
Adherens junctions transfer the force of aktin filaments from one cell to another, using classical cadherins between the cells.
Desmosomes connect intermediate filaments between neighbouring cells.
Aktin-linked cell-matrix junctions link aktin filaments to the ECM.
Hemidesmosomes link intermediate filaments to the ECM.

Source: lectures at the university of Tromsø, Norway. Also my textbook.


Why do crocodiles have a high concentration of lactic acid in their blood?

As far as I can tell from a brief literature search, the explanation for the high concentration of lactic acid in the blood of crocadilians is two-fold:

The lactic acid is generated from the anaerobic muscular activity involved in capturing their prey.

In a gloss from Science Daily a journalist writes:

  Concealed below the water's surface, crocodilians stealthily approach animals that have come to drink, spring upon their prey, and drag them into the water and drown them. This powerful burst of activity generates an extraordinary amount of lactic acid in their muscles…

It is maintained at a relatively high concentration in blood so it can be used to acidify the stomach for the digestion of its meal.

I am less sure about this. Certainly the crocodile needs to acidify the stomach, and the scientific article glossed by the Science Daily shows how the lungs are bypassed to allow carbon dioxide to reach the stomach:

  During this period of digestion crocodilians divert blood through a special vessel that bypasses the lung, named the left aorta… …when crocodilians are digesting a meal, they chose to shunt and direct CO2-rich blood straight to the stomach where glands make use of the CO2 to form gastric acid and bicarbonate. Consequently this shunt enables crocodilians to secrete gastric acid at a rate that is approximately 10 times the highest rates measured in mammals.

My supposition is that lactic acid also contributes to the acidity, but I may be wrong on this point. If anyone has information about this, I shall be happy to add it to my answer.


What is the difference between the mitotic spindle and microtubules?

Short answer
The spindle is made up of microtubules

Background
From Nature:

  Spindle fibers form a protein structure that divides the genetic
  material in a cell. [...] At the beginning of nuclear division, two
  wheel-shaped protein structures called centrioles position themselves
  at opposite ends of the cell forming cell poles. Long protein fibers
  called microtubules extend from the centrioles in all possible
  directions, forming what is called a spindle. Some of the
  microtubules attach the poles to the chromosomes by connecting to
  protein complexes called kinetochores. Kinetochores are protein
  formations that develop on each chromosome around the centromere,
  which is a region located near the middle of a chromosome. Other
  microtubules bind to the chromosome arms or extend to the opposite end
  of the cell. During the cell division phase called metaphase, the
  microtubules pull the chromosomes back and forth until they align in a
  plane along the equator of the cell, which is called the equatorial
  plane.


Is there a protocol for freezing and thawing Bacillus subtilis cells?

While I have never done bacterial stock cultures from spores, I don't think it is necessary, as the standard procedure for making bacterial stocks should work without problems.

For that you grow your bacteria in liquid culture until you reach the late log phase (so you have a lot of bacteria in your media), take 1 ml of the culture, mix it with 100% glycerol to reach a final glycerol concentration of 50% and then freeze it a -80°C. At this you can store it for long times (probably not indefinitely but for years is possible).

When you want bring your cultures back to life, take the tube and either use an inocculation loop or a pipette tip to scrape a bit of the frozen culture and plate it on an appropriate agar plate. If you want to scale up, pick one colony from the plate into liquid media.

Since glycerol is a pain to pipette (and can also have sterility problems), I have switched over to DMSO as a cryo-protective agent for bacterial cultures as well. Simply add 15% (end concentration) DMSO into the cryo vials (so 150ul DMSO to 850 of culture), mix and then freeze the cells. In my experience this works as good as glycerol.


Can anyone explain the idea of anodic nerve stimulation?

Short answer
Both anodic and cathodic current pulses can evoke neural activity, as shown in your image.

Background
You have to be aware that the current direction is arbitrary and the 'convention' you mention depends on your discipline. In electrophysiology, the anode is generally considered to be the positive electrode, the cathode is generally the negative electrode and the anode the positive. In physics however, current is assumed to be positive (due to historical reasons) and therefore the definition of anode and cathode is opposite.

Secondly, there is no reason to assume that nerves under the cathode are stimulated (and not under the anode), as is shown in your picture - in both cases a neural response is elicited. For example in cochlear implants, biphasic current pulses are used, because these are safer than simple anodic or cathodic pulses. Biphasic pulses are charge balanced and consist of an anodic phase and an opposite cathodic phase. (Cochlear implants are arrays of electroides implanted in the inner ear that stimulate the auditory nerve directly and are used to treat sensorineural deafness).

In animals and humans, both anodic and cathodic pulses can evoke neural responses. In human cochlear implant users, the anodic phase is more effective than the cathodic phase. In contrast, in animals usually the opposite is observed. The reason for this discrepancy is unclear (Machery & Cazals, 2016).

Whatever the exact reason of their differing effectivity in evoking neural activation - both anodic and cathodic current pulses can evoke neural activity.

Reference
- Machery & Cazals, Adv Exp Med Biol (2016); 894:133-42


This is by far too long for a comment, so as an answer: I spend now quite a while using Pubmed and other search tools, to find more information. The most recent article I found over and over again was the one from Juneja and colleagues: "Sequence divergence within the sperm-specific polypeptide TCTE1 is correlated with species-specific differences in sperm binding to zona-intact eggs." (which you probably also found). This article has only been cited two times, which is a bad sign for an article making so important connections. My guess is that no further research in this area either happened or has at least not been published. So beyond this I am afraid that there is no other information available (I am happy to change this, if there is any other information available).


Do cells communicate only in binary levels?

Binary responses are associated with switches, which in turn are associated with bifurcations in the steady states of the biological system in question. Varying some system's parameter (such as a cell's signalling strength) cells can switch from 'on' to 'off' (or viceversa) states. As an example, check out Gardner's toggle switch
(https://www.nature.com/articles/35002131), in which this property is exploited in a synthetic system.

However, cell-cell interactions can be much more complicated, allowing behaviours other than binary responses, such as multistability or oscillations. Thus, upon varying a parameter, a cell's state can, for example, go from a particular 'off' state, chango to an oscillating state and then change again to an 'on' state. Thus not only binary responses operate in cell communications, but many intermediate responses are also possible. For a review in multistability in biological systems, check out: http://m.pnas.org/content/101/7/1822.long

Hope it helps!


What is the meaning of a reported OD600 value?

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

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

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

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


The fight/flight situation, through activation of the sympathetic part of the autonomous nerve system, leads to secretion of catechol amines, i.e. adrenaline and noradrenaline. The effects of these hormones, if excreted continously or without real resting time, are thought to be bad for your health. If you recall the possible effects of those two substances (which are both similar to amphetamine, by the way), and look at what big studies have found about the impact of high blood pressure then you know the most important negative effect of stress, IMHO.

http://en.wikipedia.org/wiki/Sympathetic_nervous_system


Why People have skin color between fair and dark?

Mendel's laws were very basic to aid in the comprehension of genetics.  You think of Mendel's genes as an +- pair where + is dominant and - is recessive, making our +- gene produce offspring with the + trait but still being a carrier of the - trait.

However, when it comes skin colour, eye colour, hair colour, height, tendency to muscle growth, and a thousand other things, the gene is more like a series of ++-++-+++-, + is more recessive than -, but some of + will still show up over -.

In short, the colour of a person's skin is not a simple +- gene of dark and fair; everyone carries a certain amount of pigment genes and certain number of non-pigment genes.  The amount that one carries of each of the genes will determine his skin colour and his/her ability to pass on the dark/light characteristic.


How do researchers know that a species is at risk of extinction?

The to assess the extinction risk of a species, Researchers first study the ecology and global populations of the species.

Then mathematical models are applied to  simulate the population dynamics and estimate extinction risk.

The results are collected in the IUCNs Red list.

https://www.iucnredlist.org/


Identify this bug (which looks like a cross between a beetle and a bed bug)

That is a weevil. Coleoptera, Curculionidae. Weevils have distinctive snouts, and elbowed antennae. They can be crop pests, and eat seeds, but do not spread diseases to humans. I suspect these have just found their way into your home by mistake. https://bugguide.net/node/view/1126677


If you are not getting amplification, there are multiple things to visit before you want to design internal primers. You should try troubleshooting your PCR reactions before designing and ordering internal primers. If you are doing the PCRs wrong, it is likely you will run into the same problems again with internal primers.

There are excellent guides to trouble shooting PCRs - Just a google search "Trouble-shooting PCRs" should give you a lot of material to go through. This is from NEB, but there are several others, each manufacturer having their own, so you could refer to one of whose reagents you are using.

Primers generally give good reads from the 5' end for about 600-700 bp and after that the quality of base calling deteriorates, so if your target amplicon is above 1500bp or so, you would need internal primers because the 'external' primers would give you good sequences for only 1400 bp or so (600-700 bp from both directions, for fwd and rev primers). So internal primers can be used to sequence the regions that cannot be reached by the main (external) forward and reverse primers. The published papers from where you are using the external primers will most likely have the internal primers if CO1 is long enough to require internal primers.

Otherwise, you would need to align the existing sequences from the other populations, and look through regions of the alignment that are conserved which could act as potential priming sites. There are other issues to be taken care of before you can consider a 'conserved region' a 'priming site' and go ahead and order primers. Again there are excellent primer design tutorials available, just a google search away.

Let me know if any parts of the answer are not clear, or sound like jargon and I will do my best to simplify it for you. However, I would strongly suggest troubleshooting the PCR first - for e.g. trying a gradient PCR to find the optimal annealing temperature.


How potent is the venom from the Australian platypus?

The Internet says that platypus venom can kill small animals, but I haven't come up with a definitive source for this.

There is an informative Wikipedia page about the venom here. Basically the venom contains a number of toxic peptides including a family of C-type natriuretic peptides, some defensin-like peptides and nerve growth factor. Defensins are very widely-distributed in nature but typically are used by cells as antimicrobials. Natriuretic peptides have a range of effects upon fluid balance and blood pressure control - these are the best-characterized components of platypus venom.

These peptides are all genetically-encoded, so they are made as segments of precursor polypeptides. Intriguingly some of the the C-type natriuretic peptides contain a D-Leu residue. (All of the amino acids used in protein synthesis are the L stereoisomeric forms.) The presence of a D-amino acid in a peptide derived from a genetically-encoded molecule suggest that there must be a specific isomerase present, and evidence for this isomerase in the venom has indeed been found as reported in Torres et al. (2006) Mammalian L-to-D-amino-acid-residue isomerase from platypus venom. FEBS Lett.580:1587–1591. The introduction to this article states:

  Platypus venom contains many non-protein and protein components...whose roles are yet to be established.


What is the minimum caloric intake for a truly starving adult

A better example is the stories of tibetan monks who wrote accounts of their experience to survive for months or years on faith alone, and watch their hair and nails fall out in the search for wisdom. they could tell you how fast a coma arrives from eating just 300 calories per day.

There isn't a minimum amount though, because it's all subjective for time until, temperature, survival chores, time until coma, time until difficulty moving... you can probably keep someone in an emaciated coma with intravenous injections, or someone could stay awake with high exposure risk to illness, hair loss, nail loss. The question is vague, and there are 100 scientific studies about calorie restriction, so you are hoping someone will read 10-20 pages until they find some information for you.

It also depends how many watts the human needs to use in that situation to stay alive.

In 30'C you probably need 30 watts to stay warm, and 20 degrees about 60 watts, so the value can double based on temperature, you must change your question a bit.

60 watts basal metabolic rate body temperature would use 70 calories per hour, about a slice of bread, so 1400 calories per day without bedcovers. It depends a lot on ambient temperature and exercise, for example 1 mile of walking uses 100 calories. At less than 1000 calories per day, exercise becomes difficult and the person gets thin. Jogging uses about 250 watts. Extreme athletes and triathletes peak at about 650 watts for sprinting.

There are 100ds of citations on caloric defficiency and restriction, with values around 350 - 700 per day, which change metabolism considerably:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014770/

https://www.ncbi.nlm.nih.gov/pubmed/2718912


So we know that NK cells work by receiving activating signals through receptors, and then degranulate such that cytotoxic molecules enter the target cell, and induce apoptosis. NKG2D is such a receptor, and cells that are becoming transformatively stressed by mutations and the like upregulate expression of NKG2D ligands on their surface for elimination. This is one example, and NK cells have different subsets of activating receptors, such as NCRs. NKp30 and NKp44 are examples of NCRs and activate NK cells through detection of heparan sulfate compounds on the surface of tumor cells. The question, then, is what happens to cancer cells that can: (1) downregulate NK cell receptor ligands on their surface, or (2) abrogate NK cell receptor function in their vicinity?

In an earlier study, it was shown that mesenchymal stem cells broadly inhibit NK cell activity through activity of prostaglandin E2 and indoleamine-2,3-dioxygenase, which downregulates each of the three aforementioned NK cell surface receptors. A later study using melanoma cocultured with NK cells again came to the conclusion that the same cancer cell secretions would inhibit NK cell activation in their vicinity.

By the same token, if we consider a cancerous cell that upregulates MIC expression, NKG2D receptors will recognize this and activate the NK cells. A cancerous cell with a truncated MIC that lacks an extracellular domain will fail to activate surrounding NK cells through that pathway. Keep in mind: many mutations go into making a cell cancerous, and many more go into giving it enough fitness to avoid getting killed from the start. These are just examples of critical pathways that result in immunoevasion.

As for why are small masses more immunoevasive than single cells? This goes into a sort of power in numbers logic. A single tumor cell doesn't produce as much inhibitor compounds as a mass of tumor cells. This is an interesting concept because in the hunt for pro-angiogenic compounds, a problem for a while was you would remove a large mass, and a smaller unknown mass would quickly begin to grow. They found that although large masses secreted more pro-angiogenic compound, the tumor cells also secreted so much inhibiting compounds that smaller tumors in the vicinity were effectively inhibited. Once the large mass was removed, this inhibition got lifted.


Is human face more resistant to cold than other body parts?

In response to cold your body causes blood supply to the skin to drop in the whole body. This is to conserve heat, but results in us feeling really cold. Exercising reverses this, resulting in an increased blood supply to the skin in order to remove excess heat and in this case we feel hot.

As mentioned, the head receives a large blood supply, and continues to do so despite other tissues being restricted. This is particularly as a result of the brain requiring a lot of oxygen and glucose. This keeps our head warm.

This phenomenon is why hats keep us warm and are important in cold weather, we lose a lot of heat from our head.

It is also likely that the skin on our head contains less cold receptors, as these aren't likely to be required. However the other parts of our body, particularly the soles of our feet and anterior surface of our hands have many sensory receptors. They are likely to make first contact with anything that may be harmfully cold.


I don't know, which technique you worked on, but there are the so-called 'Next Generation Sequencing' methods. I think the oldest of that is a pyrosequencing technique called 454 sequencing (I think it is provided by Roche). However, this method is too expensive compared to even newer methods and the support will be stopped within the next months, as far as I know.

Furthermore, there are the Illumina and the ion torrent technique. Finally, there is SMRT sequencing of which some people say that this is even third generation sequencing. I think, this paper provides a nice overview. And if you're interested in further reading, yet you know what to search for.


First, there are three ketone bodies: Acetone (top), acetoacetic acid (middle), and beta-hydroxybutyric acid (bottom), see the illustration from the Wikipedia:

The second and the third are taken up by heart and brain cells and then converted into Acetyl-CoA which is fed into the citric acid cycle where it is further metabolized. Acetone is mostly excreted. See here for some more information.

Aceto acetic acid is either converted into acetone and removed from the body or enzymatically converted into beta-hydroxybutyric acid by the beta-hydroxybutyrate dehydrogenase.
The third possibility is that it is converted into Acetyl-CoA. See the figure for the scheme:

For a more detailed explanation of this process (both, the generation and the metabolization of the ketone bodies) see here.


Does the genetic material the sperm carries affect its physical properties

I think there is a strong driving force for sperm to be free living haploid versions of human beings.  Since they are a product of meiosis sperm are the product of recombination of both the male chromosome sets.

While I'm sure that if we look closely enough, the germline cells that produce the sperm are contributing some protein and structure to the sperm, the life cycle of the sperm is mostly the result of the genome that it contains within itself.  Sperm are prone to defects.  On the average in human beings about half of sperm are non-motile: simply unable to form the flagellum or power its motion adequately for motility. That's a pretty strong selective force in the life of our other, 'half genome' selves.

Sperm selection - the sorting of which sperm from a single male achieves fertilization is pretty rigorous.  It can take 30 minutes to days.  Once in contact with the ovum, the sperm executes a critical set of transformations and biochemical activations to get past the various layers of the cell.

Sperm are from the man, but they are each living creatures on their own which we hope will deliver themselves up to the ovum to create another human being.  They vary in their genetic quality and effectiveness and this is highly related to their genetic make up.

Because each sperm is the product of two stages of Meiosis, they can be full of genetic defects, most of which would be fatal in a diploid human being.  The functions of the sperm as it goes through its short but competitive life weed out genetic abberations and help assure that the next generation of diploid human beings is as healthy as they can.

So they are not DNA boxes that swim.  I'd be hard pressed to think of a passive role for a cell in biology - they are all working pretty hard... I'd be interested in a comment with suggestions of something that is not under selective pressure in biology.

It sort of reminds me of the old argument about passive mating in females. Behavioral biologists used to think that female animals had little or no active role in mating.   That myth was retired about 30 years ago now.  That link points to an introduction to an entire volume reviewing that whole discussion of active female roles in reproduction in case anyone reading is interested.

BTW I'm not an expert on gametes, but I'd be surprised if the ova also didn't have a complimentary but quite different selective process they had to get through to become a fully presented candidate for fertilization.

Just to add a note about how the functioning sperm genes affect the diploid organism: This is one of the most important things that sperm does.  The genes that function in the living spermatazoan are the same genes the diploid organism uses, or at least a substantial number of them.  Further, these genes are scattered across all the chromosomes and so major chromosomal defects and important genes are functional if fertilization is completed.  As an example here's a cool blog post about how mosquito sperm have been shown to use odorant receptors to orient themselves in the fertilziation process. Those same receptors and the signalling genes that link that signal to the sperm behavior are probably quite useful to the adult mosquito.  I'd be surprised if human sperm also did not use similar pathways to function.

Not to beat a dead horse, but the recent nature has a report of small RNAs in mouse sperm as being an epigenetic carrier for stress.


Structure of fitness landscapes in the NK model

Very little is known about the structure of fitness landscapes.
H.A. Orr (2005; also Whitlock et al., 1995; Kryazhimskiy et al., 2009) explains that most experimental results do not actually attempt to measure the fitness landscape, but instead report just the average fitness versus time and average number of acquired adaptations versus time. This can't be used to discern epistatic interactions, or any combinatorial structure of the landscape. In general, the theory of adaptive walks has developed without reference to real data and even the most refined theories can only correspond in vague qualitative ways (see Kryazhimskiy et al., 2009 for the best example I know).
Szendro et al. (2013) surveyed the few recent experiments that conducted a methodical examination of all mutations in a subset of loci of model organisms, but most studies (6 out of 12) were able to empirically realize only small fitness landscapes of just 4 to 5 loci (so 16 to 32 vertexes), with the largest full fitness landscape having length 6 with all 64 vertexes examined (Hall et al., 2010), and the largest number of vertexes in a single study being 418 out of the possible 512 in a length 9 landscape (O’Maille et al., 2008). These are extremely small landscapes, and thus don't have much power in distinguishing proposed theoretical models.
After extensive searching, I have not been able to find examples of theorists doing worst case analysis of fitness landscapes. The closest to worst-case analysis is Orr-Gillespie theory (Gillespie, 1991; Orr, 2002; 2006; Kryazhimskiy et al., 2009) that assumes that the wild-type is still very fit after an environmental change, and so beneficial mutations are extremely rate. This allows the authors to introduce extreme value theory and consider just the asymptotic properties of distribution tails thus allowing a more general treatment with fewer parameters; in some cases leading to a full classification of adaptive trajectories (Kryazhimskiy et al., 2009). This approach is easier to relate to experiment, but unfortunately completely ignores the combinatorial structure (beyond first-order) of the fitness landscape and always just samples the next potential mutant from the tail of a distribution without taking into account how it is progressing in the landscape. Although Orr (2006) introduced the basics of fitness landscape structure, the structure was much simpler than the NK model; he used Perelson & Macken's (1995) block model with each block as completely unstructured beyond first-order.

References
Gillespie, J.H. (1991). The causes of molecular evolution. Oxford University Press.
Hall, D. W., Agan, M., & Pope, S. C. (2010). Fitness epistasis among 6 biosynthetic loci in the budding yeast Saccharomyces cerevisiae. Journal of Heredity, 101: S75-S84.
Kryazhimskiy, S., Tkacik, G., & Plotkin, J.B. (2009). The dynamics of adaptation on correlated fitness landscapes. Proc. Natl. Acad. Sci. USA 106(44): 18638-18643.
O’Maille, P. E., Malone, A., Dellas, N., Hess, B. A., Smentek, L., Sheehan, I., Greenhagen, B.T., Chappell, J., Manning, G., & Noel, J.P. (2008). Quantitative exploration of the catalytic landscape separating divergent plant sesquiterpene synthases. Nature Chemical Biology, 4(10): 617-623.
Orr, H.A. (2002). The population genetics of adaptation: the adaptation of DNA sequences. Evilution 56: 1317-1330.
Orr, H.A. (2005). The genetic theory of adaptation: a brief history. Nature Reviews Genetics 6(2): 119-127.
Orr, H.A. (2006). The population genetics of adaptation on correlated fitness landscapes: the block model. Evolution 60(6): 1113-1124.
Perelson, A.S., & Macken, C.A. (1995). Protein evolution of partially correlated landscapes. Proc. Natl. Acad. Sci. USA 92:9657-9661.
Szendro, I. G., Schenk, M. F., Franke, J., Krug, J., & de Visser, J. A. G. (2013). Quantitative analyses of empirical fitness landscapes. Journal of Statistical Mechanics: Theory and Experiment 2013(01): P01005.
Whitlock, M.C., Phillips, P.C., Moore, F.B.-G., & Tonsor, S.J. (1995). Multiple fitness peaks and epistasis. Annu. Rev. Ecol. Syst. 26: 601-629.


Is it possible to still grow taller after growth plates have been closed?

No, because growth only occurs at the epiphyseal plate or growth plate. In the picture here, the epiphyseal plates are the two horizontal lines in the tibia and fibula, and bone growth occurs in the upward direction, or toward the middle (shaft) of the bone. Once the epiphyseal plates close, the bones can no longer elongate.

It's possible to have a second "growth spurt," but it's only because the epiphyseal plates haven't closed. David Robinson, the basketball player, was 6'7" as a senior in high school, but ended up being 7'1". The "growth spurt" is caused by the sex hormones, which is why a significant amount of growth occurs during puberty.


Type of Tree With Somewhat Squarish Fruit

That looks like a persimmon — your first image is of immature fruit.

Compare with:

UC Davis — Fruit and Nut Education

Google Image link


How many mRNA strands are in a single dose of the COVID-19 vaccines?

Well, we can work this out empirically.
We know that the average molecular mass of a base of a RNA is 339.5 g/mol.
However to calculate the approximate molecular mass of a single-stranded RNA molecule, you multiply the number of bases by 320.5 and add 159 (same source). This means for a single-stranded molecule of 1000 bases, it will have a molecular mass of 320,659 g/mol. The Pfizer vaccine has a sequence of 4284 bases.
4.284 * 320659 = 1373703.156 g/mol.
The Pfizer vaccine has 30 ug/shot (PDF, see page 27 under "Description") or 30x10-6 grams
number of moles = mass/molar mass.
n= 30 x 10-6 grams/137370.156 g/mol
n= 2.18 x 10-11
number of molecules = n (above) x Avogadro constant (6.022 x 1023)
Number of molecules = 1.3 x 1013
Now this is a ball-park figure because the RNA isn't actually RNA it has had some special additions to the uridines that make it less susceptible to immune regulation, replacing the uridines with  1-methyl-3'-pseudouridylyl (see Wikipedia link to structure above). However, I believe this alteration to the mass, will not alter the number substantially; it'll still be in the 10 trillion range.


Why are Chromosome Territories important?

First, this idea was discredited or ignored during several decades, some studies suggest that CT is random in some eukaryotes that isn't necessary the truth. It is not easy at all to determine is CT are random or not
Second, not all eukaryotic organism are the same. Plants and Fungi have cell walls, animals do not. Fungi can have a dikaryotic cell or even undergo somatic hybridisation.
Third, "chromosomes are more unfolded in lower eukaryotes such as yeast."Chromosome Territories: The Arrangement of Chromosomes in the Nucleus
This article does not mention that S. cerevisiae is an exception, on the contrary "and may even hold for single-cell eukaryotes, such as budding and fission yeast".
Thank you for the question, I learnt a lot while searching for an answer


There are some inhibitors in the cell, which have specific effects on signal transduction. These are mostly second messengers (like cAMP, cGMP, calcium ions,  inositol 1,4,5-trisphosphate and others), which are then able to diffuse relative fast to other proteins. There they can either amplify a signal or cause inhibiting processes to start which then terminate the activation of the signal transduction cascade.
The problem is that these inhibitors that they work unspecific in their inhibition and termination. Signal transduction is tightly controlled as they directly influence the expression of various genes.

A lot of the proteins in these cascades are kinases which are activated upon phosphorylation and then carry on by phosphorylating the next step of the cascade. The activity is stopped by phosphatases which remove the phosphorylations from the kinases and thus inactivate them until the next signal is passed down the cascade. It works like in this figure (from here):

Specific inhibitors for single proteins in the signalling cascades are available as drugs against cancer. Since these signalling cascades regulate gene expression including cell cycle control, they are important targets for dysregulation in cancer. A numer of kinases in the MAP kinase pathway for example are mutated there and constantly active. The so called small molecule inhibitors bind to the protein and inhibit the kinase activity, preventing a permanent signal. See this article for more information:

Targeting cancer with small molecule kinase inhibitors


What kind of memory is "keyboard/keypad memory"?

Short answer
Motor memory

Background
A striking personal example of your account pictured in the question was my experience where I had to type in my PIN at the bank counter on a keypad. It turned out I entered it incorrectly several times in a row, despite the fact that I had used that PIN a zillion times on ATM machines. Luckily, the bank employee had seen this phenomenon many times before, and she explained to me that the standard computer keypads have a different numerical layout than ATM machines. So to type in my PIN correctly I had to do it under visual guidance - an awkward experience. It showed quite strikingly that I had been entering my bank PIN using motor memory.

Much of our motor behavior is learned - think of learning to walk, cycle or ice skate. To achieve motor learning, the central nervous system is believed to use internal models that predict the mechanical dynamics necessary to execute a task. In theory, the internal model is an association from a desired trajectory for the hand to a pattern of muscle movements. This map is basically unique for the objects that we have learned to interact with. Because we routinely use our hands to interact with a remarkably diverse variety of mechanical systems, the ability to learn and recall internal memories is thought to be a fundamental property of the motor system (Shadmehr & Brashers-Krug, 1997).

Reference
Shadmehr & Brashers-Krug, J Neurosci (1997); 17(1): 409-19


Why are red blood cells preferred to study the structure of plasma membrane?

Human RBCs are relatively simple in structure compared to the other cells in question; they contain no cell organelles (so far I knew; please correct me if there is any new theory) and therefore contain only one membrane.

RBCs do not have significant amount of extracellular matrix making them very easy to work only with the cell membrane. RBCs float in a fluidy medium (blood-plasma), so easy to collect, distribute in containers, keep into various solution. no need of maceration. Human RBCs are very uniform in shape and size, and do not divide. That makes it useful for various experiments like demonstrating plasmolysis and deplasmolysis as well as quantitative experiments on membrane biomolecules.

One classic example is Edwin Gorter and F. Grendel that first showed that cell membrane is bilayer; that is upon observation on RBC. They took known number of RBC, denatured the membrane, extracted the lipids and spread that as a lipid monolayer on water-air interface. They found that the monolayer is twice bigger than total surface area of taken RBC ! *

  Source:  * The Cell/ Cooper/ 4th Edition/ASM-Press and Sinauer publication.

However this is not a reference-based answer, but these are the features more than enough to make me so lazy that I would choose only RBC and flyaway from any-other option.


What is the scientific name of this parrot?

Looks like a male plum-headed parakeet (Psittacula cyanocephala)

wiki: the plum-headed parakeet


Why does regular exercise increase brain volume?

Well, Erickson et al (2011) attribute the increase in brain volume in the aerobic exercise group to brain-derived neurotrophic factor (BDNF).

Specifically (p. 3020):

  In fact, we found here that changes in serum BDNF levels were
  associated with changes in anterior hippocampal volume; an important
  link because the hippocampus is rich in BDNF, and BDNF levels increase
  with exercise treatments in both rodents and humans. BDNF is a
  putative mediator of neurogenesis and contributes to dendritic
  expansion and is also critical in memory formation. Our results suggest that
  cell proliferation or increased dendritic branching might explain increased
  hippocampal volume and improvements in memory after exercise

with the caveat:

  however, increased vascularization (15, 16, 33) and dendritic
  complexity (34) may also be contributing to increased volume


How many generations are required for a specific neutral mutation to reach fixation?

Kimura and Ohta (1968) showed that the expected time for a neutral allele to reach fixation is

$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$

where $p_0$ is the initial frequency and $N$ is the population size. The model assumes a Wright-Fisher population (panmixia, constant population size, exclusively sexually reproducing hermaphroditic individuals, ...) and negligible mutation rate at the locus of interest.

  how do i calculate po in terms of known quantities, such as mutation rate?

You can compute the expected allele frequency at mutation - drift balance (e.g. see here or any decent intro textbook to population genetics). In short, let $\theta = 4N\mu$, where $\mu$ is the mutation rate, the expected heterozygosity is

$$H = \frac{\theta}{\theta + 1}$$

From that you can compute the allele frequencies $p$ and $q=1-p$ by solving $H = 2pq$.

If needed, you can get the entire distribution of allele frequency given $N$ and $\mu$ (and even $s$ and $h$ if needed) in Wright (1937).


Intelligence is something which has to have a definition, and there are many, but I would cautiously say no.

The reason that I say this is because swarming behavior can be largely reproduced by a simple set of rules - matching distance to your neighbors and direction and speed as well.  To me this really removes any intention or even conscious element to swarm behavior although its clear individuals do make decisions, they don't have to be more intelligent than a mouse looking for food or other kinds of animal behavior.

That being said, others have literally built definitions of intelligence inspired by swarming - a decentralized sort of mind which makes decisions based on the interactions of component individuals.  You could argue that our own brains are a similar sort of ensemble, and therefore no more different than our own intelligence if we look closely enough.

So take your pick really.


Your friend is incorrect. From Wikipedia:

  The word organism may broadly be defined as an assembly of molecules functioning as a more or less stable whole that exhibits the properties of life.

(Viruses are specifically excluded, as they depend on a host cell to fulfill all the functions of life.)

While cells extracted from a multicellular organism like a plant or a person may be able to be cultured in vitro for a time, they cannot survive independently - they require the intervention of humans (or very well-trained monkeys) to obtain nutrients and oxygen, and process/remove waste. A unicellular organism like a bacterium, for example, can handle these functions on its own - it can either synthesize or find a source for its own nutrients, and can reproduce on its own to create more organisms.

The key difference is being self-sustaining. An organism needs to be able to feed itself, take care of its waste, reproduce a full version of itself, respond to stimuli, etc. (see the "properties of life" link above). A single cell from a multicellular organism cannot do all that without assistance (kind of like a virus, actually), while a true unicellular organism can.


Is there any size limit to the amount of information a human (or other) brain can hold

Yes, there is a limit:

  Despite the impressive complexity and processing power of the human brain, it is severely capacity limited [1].

Human brain has 78.82– 95.40 billion neurons [2] and about $3.6 \cdot 10^{14}$ synapses in the cortex [3]. We shouldn't worry about running out of space, because neurons connect with each other to exponentially increase brain capacity to about 2.5 million gigabytes as Paul Reber, professor of psychology at Northwestern University claims for Scientific American [4]:

  Each neuron forms about 1,000 connections to other neurons, amounting to more than a trillion connections. If each neuron could only help store a single memory, running out of space would be a problem. You might have only a few gigabytes of storage space, similar to the space in an iPod or a USB flash drive. Yet neurons combine so that each one helps with many memories at a time, exponentially increasing the brain’s memory storage capacity to something closer to around 2.5 petabytes (or a million gigabytes).

References:

Marois R, Ivanoff J. Capacity limits of information processing in the brain. Trends Cogn. Sci. (Regul. Ed.). 2005 Jun;9(6):296-305. doi: 10.1016/j.tics.2005.04.010. PubMed PMID: 15925809. Full text available on http://www.psy.vanderbilt.edu/faculty/marois/Publications/Marois_Ivanoff-2005.pdf
Azevedo FA, Carvalho LR, Grinberg LT, Farfel JM, Ferretti RE, Leite RE, Jacob Filho W, Lent R, Herculano-Houzel S. Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. J Comp Neurol. 2009 Apr 10 513(5):532-41. p.535 right column top sentence. Via Bionumbers http://bionumbers.hms.harvard.edu//bionumber.aspx?id=106322&ver=4
Roth G, Dicke U. Evolution of the brain and intelligence. Trends Cogn Sci. 2005 May9(5):250-7. p.253 right column 1st paragraph. Via Bionumbers http://bionumbers.hms.harvard.edu//bionumber.aspx?id=106138&ver=2
Paul Reber. What Is the Memory Capacity of the Human Brain? Scientific American. Apr 2010. Available from http://www.scientificamerican.com/article/what-is-the-memory-capacity/. Accessed 12.07.2014


Alternative to distilled water for pH test

Rainwater might not be the best option.

Rain water is naturally acidic due to the reaction of CO2 forming some weak carbonic acid [see here for explanation].

 Source: Wikipedia

As a result, pH of "pure" rainwater is usually between 5-6; usually around pH 5.6. See here.

  Most rainwater has a pH of 5.6 to 5.8, simply due to the pressence of carbonic acid (H2CO3).

Presence of any sulfur or nitrogen oxides in the air (perhaps from burning coal plants or city traffic from 100s of km away) would lead to rain becoming even more acidic. From environment.co.za:

  Sulphur dioxide reacts with water vapour and sunlight to form sulphuric acid. Likewise NOX form nitric acid in the air. These reactions takes hours, or even days, during which polluted air may move hundreds of kilometres. Thus acid rain can fall far from the source of pollution.


What kind of spider is this? Brown with white spots

Sub-adult tropical orb weaver spider.  "Its range is largely circum-Caribbean, occurring in Florida, Louisiana, and Texas along the Gulf Coast of the United States."

Harmless to humans and considered beneficial.

  Bites of this species are not known to cause serious effects to humans. ... The web probably catches many moths and other night flying insects; these spiders may be particularly beneficial along woodland borders of field agroecosystems and within orchards.


Are there constraints on where intron/exon boundaries occur with respect to the triplet codons of the reading frame?

As pointed out by others this is not true. I just verified this for humans (annotations from gencode21).
Methodology:

Obtained the start points of the CDS for all genes
For each exon of each gene, calculated the distance between the CDS start and exon end
Obtained the remainder after dividing this value  by 3 (modulo)

Commands:

Command-1:
    awk 'BEGIN{FS="\t|;";OFS="\t"} $3=="CDS"{print $4,$9}' gencode.v21.annotation.gtf > cdsstart.txt

Command-2:
    awk 'BEGIN{FS="\t|;";OFS="\t"} NR==FNR{a[$2]=$1;next} ($3=="exon" && $9 in a){if($4>a[$9]) q[($5-a[$9])%3]++} END{for(i in q) print i,q[i]}' cdsstart.txt gencode.v21.annotation.gtf

Result:

position | # cases
_______________________
   -2    | 101191
   -1    | 100954
    0    | 99499

As you can see the exons do not necessarily terminate at the third position of the codon.


How to batch convert gene names to protein IDs in Uniprot?

ID mapping

This is called ID mapping. It used to be a headache as programmatic sequence comparisons were the only real way, but it is pretty trivial these days.

As mentioned in the comments, by far the most popular and easy method is to use Uniprot's list uploader for mapping. The corresponding publication can be found here.

Example

Programmatic access

The web user interface will work for thousands of IDs, but is like to result in errors for queries exceeding 10,000 IDs. In that case programmatic queries are probably better. I've slightly modified this from the Uniprot docs so that the IDs are queried 1 at a time to avoid any errors in exceeding query size. The python code would be:

import urllib,urllib2

list_to_convert = ["b0014", "b0015"]
url = 'http://www.uniprot.org/mapping/'

print "From To"
for genename_id in list_to_convert:
    params = {
    'from':'GENENAME',
    'to':'ACC',
    'format':'tab',
    'query':genename_id
    }

    data = urllib.urlencode(params)
    request = urllib2.Request(url, data)
    contact = "" # Please set your email address here.
    request.add_header('User-Agent', 'Python %s' % contact)
    response = urllib2.urlopen(request)
    page = response.read(200000)
    print page.splitlines()[1] #Ignores the header line returned by uniprot

The output from this looks like:

From    To
b0014   P0A6Y8
b0015   P08622

Web GUI

b0014 and b0015 aren't actually STRING IDs. They are IDs referred to as gene names and are used across a variety of databases including Uniprot.

The mapper:

Note in section 2 of the ID mapping that I have set the left option to "gene name". "STRING" won't work.

The result is below:


Could anyone please identify this Indian bug?

The species from the photo is almost definitely a Catamiarus brevipennis.

The bulged and striped abdomen
The non-striped legs
The unique pattern on the wings
The antenna thick at the beginning and becomes thinner towards the end.
The protonum also has a unique granular structure unique to Catamiarus brevipennis.

Source : India Biodiversity Portal


Explanation of "differential transcript usage" (DTU)

No, it is a completely different thing, which has to do with splicing and alternative splicing.
I refer you to some genetics text for details on splicing and alternative splicing, but I will give here a very brief and incomplete explanation fo what they are and how they fint into DTU.
Genes are composed of introns and exons. Exons are the only parts of genes that are usually composing the mature transcript (intron retention is possible, but we are not interested in that).
Splicing is the mechanism by which in a eukaryotic gene, introns are removed, and the mature transcript is assembled only using exons.
During splicing, not all exons are necessarily retained. Imagine a gene with exons 1, 2 and 3. It is possible that the main form (called isoform) is the one consisting of exons 1, 2 and 3. Let's call that Isoform 1. However, due to a phenomenon called alternative splicing, other isoforms, can be generated, for example one isoform composed by exons 1 and 3. Let's call that Isoform 2.
On average, we may imagin that the abundance of Isoform 1 compared to Isoform 2 is rather constant. However, some treatments or some changes in environmental stimuli, can give rise to a Differential Transcript Usage by which the relative abundance of the two isoforms changes.


What is the mechanism by which lamins regulate gene expression?

So my answer was deleted because it "didn't answer your question."  Except that it did.  The article linked here, Gene expression, chromosome position and lamin A/C mutations, is an entire paper devoted to what we knew as of 2011 about lamins and gene expression, with references.  Your question was not a simple question, and article details how lamins are involved in gene expression.
I shall quote it here in order to "answer your question", and perhaps the moderators will see fit to not delete the post this time.  If said moderators think I should write a review of a review to facilitate your understanding, then I obviously have not understood the meaning for this board.
I don't have enough rep to leave a comment on anything other than my own answer, which seems to have been the appropriate way to link to the paper.  I figured an answer to your question would still be useful.
I would recommend reading the entire article as it is very useful in understanding additional indirect hypotheses for lamins controlling gene expression.

The Lamina as a Regulator of Gene Expression
In most cells, a dense heterochromatin network is visualized as electron dense material adjacent to the inner nuclear membrane and the nuclear lamina. The dense network is typically considered to reflect the association of transcriptionally inactive genes with the nuclear lamina. Specifically, this heterochromatin is thought to reflect a repressed gene state and suggests that the nuclear membrane and lamina may play an active role in gene repression.5 Lamin A/C and its binding partners can interact with DNA, histones, transcription factors and chromatin.6 Lamin-associated domains (LADs) are cis-acting sequences thought to range in size from ∼0.1–10 Mb, and these domains are thought to regulate the interaction of chromatin with the nuclear lamina; generally LADs are considered to be transcriptionally repressive.7 The precise sequences that define LADs have been elusive but nonetheless the LAD concept implies that the lamina and the genome interact in a specific manner. Therefore, it follows that one mechanism by which LMNA mutations may confer pathology is by altering the interaction between the lamina and chromatin. Consistent with this, LMNA mutant cells have altered chromosome territories.4 Meaburn and colleagues first examined chromosome localization in proliferating LMNA mutant fibroblasts and found that it resembled the chromosome organization associated with quiescent or senescent fibroblasts. They suggested that mutations in LMNA produced structural disruption to the lamina inducing a chromatin organization that may resemble an inappropriate cell cycle state. The presence of LADs and the fact that mutations in LMNA associate with altered nuclear architecture suggest that the nuclear lamina plays a vital role in both scaffolding chromatin and regulating chromatin organization. In this model, it is possible that distinct LMNA mutations may alter distinct regions of the genome leading to mutation specific profiles of altered gene expression.


Is there a link between autoimmune diseases and X-chromosome inactivation?

Yes, here is an article on it: "The role of X-chromosome inactivation in female predisposition to autoimmunity"

Below see the method and results summarised.

  Using a DNA methylation assay, we have examined the X-chromosome
  inactivation patterns in peripheral blood from normal females (n =
  30), female patients with a variety of autoimmune diseases (n = 167).
  No differences between patients and controls were observed. However,
  locally skewed X-chromsome inactivation may exist in the thymus, and
  therefore the underlying hypothesis remains to be disproved.


Is viral protein expression important for peptide vaccine?

To find candidate proteins which can be used as peptide vaccine, these need to fulfill some criteria:

The most important is that the peptide (or protein) used for
vaccination shall not have a closely relate sequence in the organism
in which the vaccination shall occur. Otherwise either no reaction
(due to immunologic tolerance to self) or an autoimmune reaction
might happen.
The peptide/protein need to be expressed on the surface of the
microbe (either virus or bacteria) since otherwise it will not be
recognized by the immune system. Also domains of a potential vaccine
candidate which are inside of membrane are not useful.
The epitope needs to be stable enough to be used as a vaccine and
also be present on the microbe (otherwise there is no immune
reaction).

If you want to read further on this topic, there is an interesting Paper from the WHO available, which gives a nice introduction:

Guidelines for the production and quality control of synthetic
peptide vaccines

To answer your question: No, these proteins cannot be used for this purpose, as they are relatively closely related to the same proteins in the human body. This will probably lead to no immunologic reaction at all. Additionally, these proteins are located inside of cells and thus not exposed to the immune system.


When we're thinking about cells that get infected with viruses, we have a two of subgroups to consider, often denoted susceptible or permissive. In essence, a cell which a virus is meant to successfully infect must not only possess a receptor to that virus for adhesion, but also the ability to replicate the virus (so it needs the machinery!). So these cells must be susceptible and permissive!

After adhesion you end up with an entry phase, this differs by virus, but you can essentially break it down into endocytosis, membrane fusion, or injection. You can get an idea of injection from something like lambda phage, outlined here. Enveloped viruses can fuse with the host membranes because these envelopes are often derived from ER, golgi network, or another plasma membrane. (Remember, viruses are essentially coding 3 basic sets of genes: for structure, replication and binding. It can't just code for everything it needs, either, so viruses hijack the host cell machinery to replicate.) Naked viruses, those that are just a protein coat and nucleic acid in essence, enter the cell through endocytosis and end up uncoating in a vesicle. And to stress it again, if the cell didn't have a receptor for the virus, it probably didn't get it. Portal of entry does make a difference, but I'm trying to keep it simple for our purposes!

Being said, when we're considering most viruses, membrane fusion and endocytosis aren't really using any energy but the host cell's, right? And then when the virus gets in there, they continue to use the host's resources becauase they really didn't bring a lot of baggage, either!

On the matter of "knowing" what they're doing, viral particles really don't do anything themselves. What I'd argue is that they've evolved methods of becoming particularly good at being viruses, many of which make it seem like they're making conscious choices, but suppose the following: Most of the time, viruses are probably just reproducing in such great numbers that it's just faster to get lucky and produce a strain with a better overall fitness.

Mind you, this whole time your body is attempting to fight off the virus, as in HIV, for example, eukaryotic cells have methods at each stage of attempting to protect themselves,

Source: Cellular Self-Defense: How Cell-Autonomous Immunity Protects Against Pathogens

You also have NK cells and macrophages responding to IFN produced by cells distressed by viruses, and eventually the presentation of viral antigens which result in effector T cells and antibodies unique to the virus in question. Another article here shows some methods by which some inhibitors of HIV infection can be evaded by the virus, as well, and just as likely, you also see that HIV has mechanisms of evading innate/active immunity as well! For example, if your antibodies recognize a viral capsid protein, what do they have to bind to if there's a lipid membrane in the way, as in HIV? What if the receptor composition changes?

In closing, viruses are obligate intracellular parasites. They need you to survive, but their objective is to replicate, so sometimes they do end up killing their host, but they aren't really communicating with each other in a fashion like: "I wonder how those other viruses are doing?" They really don't have a means of responding like that, so the end goal? Just keep moving from host to host and keep replicating, in the most basic sense.


Bird brain-eating Mantis - how does it crack the skull?

The mantis doesn't need to crack the skull to eat the brain. It can get to the cranial cavity through an easier way: the eye socket.

Have a look at this image of the ruby throathed hummingbird (Archilochus colubris) skull:

Source: http://wildlife.ohiodnr.gov/species-and-habitats/species-guide-index/birds/ruby-throated-hummingbird

You can see the huge eye sockets. This image (not a real skull, but a plastic cast) shows that even more clearly (also Archilochus colubris):

Source: http://www.boneroom.com/uploads/4/8/1/1/48118243/s521972503441136676_p1061_i1_w640.jpeg

According to the original paper of the research, which was linked by the NY Times article and by your very question (Nyffeler, Maxwell and Remsen, 2017):

  Bigas et al. (2006:237) described the feeding behavior of the mantids in the mist-nets:

  “The modus operandi of the mantis seems to be to approach the bird,
  which is always hanging downwards, and then enter the cranial cavity
  via one of the eyes, feeding on the brain tissues.” (emphasis mine)

If you look at the image you shared you can see that the mantis' mouthparts are positioned at the side of the hummingbird's head, which corroborates the claim that the mantis uses the eye socket to get to the brain tissue.

Sources:

Nyffeler, M., Maxwell, M. and Remsen, J. (2017). Bird Predation By Praying Mantises: A Global Perspective. The Wilson Journal of Ornithology, 129(2), pp.331-344.
Bigas, D., J. Piccardo, And J. L. Copete. 2006. Praying mantis killing passerines in mistnets. Dutch Birding 28:237–238.


How does coffee cause calcium loss in our body?

Caffeine and coffee do not seem to have any significant adverse effect on calcium metabolism. The supposed mechanisms are inhibition of calcium absorption in the intestine and stimulation of calcium excretion in the kidneys.

Effects of caffeine on bone and the calcium economy (Food and Chemical Toxicology, Journal, 2002):

  Caffeine-containing beverage consumption has been reported to be
  associated with reduced bone mass and increased fracture risk in some,
  but not most, observational studies. Human physiological studies and
  controlled balance studies show a clear but only a very small
  depressant effect of caffeine itself on intestinal calcium absorption,
  and no effect on total 24-h urinary calcium excretion. The
  epidemiologic studies showing a negative effect may be explained in
  part by an inverse relationship between consumption of milk and
  caffeine-containing beverages. Low calcium intake is clearly linked
  to skeletal fragility, and it is likely that a high caffeine intake is
  often a marker for a low calcium intake. The negative effect of
  caffeine on calcium absorption is small enough to be fully offset by
  as little as 1-2 tablespoons of milk. All of the observations
  implicating caffeine-containing beverages as a risk factor for
  osteoporosis have been made in populations consuming substantially
  less than optimal calcium intakes. There is no evidence that
  caffeine has any harmful effect on bone status or on the calcium
  economy in individuals who ingest the currently recommended daily
  allowances of calcium.

The Association between Coffee Consumption and Bone Status in Young Adult Males according to Calcium Intake Level (Clinical Nutrition Research, 2016):

  This study analyzed and compared the BMD [bone mineral density] and
  bone metabolism markers according to coffee intake in Korean young
  adult men aged 19-26 years. No significant associations were found
  between current coffee consumption level in Korean young men, and bone
  status and metabolism according to the calcium intake levels.


Duplicity Vs. Singularity of Mammals Organs

It's just how we evolved. At some point in the past, a distant ancestor of ours had two lungs, two kidneys, one liver etc.( maybe then there was a pretty good reason for this). We evolved following that pattern and now we ourselves have two lungs, two kidneys, one liver etc.

Snakes, for example, have just one functional lung because their elongated form doesn't cope well with having two full-grown lungs. Humans on the other hand have a body shape that works very well with two lungs, so we didn't have to sacrifice one lung.

There are other examples of different organ distribution, like the octopus which has 3 hearts. Usually the more different the internal symmetry, the more distant the common ancestor.


Can the dead be brought back to life by viruses?

You must tell facts from fiction; viruses need living cells to replicate because they do not have the molecular machinery at hand to generate energy and construct building blocks essential to life. So no, viruses cannot bring back the dead or revitalize dead cells.

One thing that comes close to it are the so-called zombie ants. These ants have been infected by a parasitic fungus that can take over the ant's nervous system (Fig. 1).

Fig. 1. Zombie ant found in Brazil, infested with the fungus Ophyocordiceps. Source: National Geopgrahic.

These fungi eventually kill their hosts, but before doing so they temporarily take over their nervous system. In the case of Ophyocordiceps unilateralis (Evans, 2011), the spores lodge themselves into the ant's head through an exposed part of the ant’s exoskeleton. The fungus then infiltrates and targets the ant’s brain, taking control of the ant. Then it makes the ant leave its colony and head for a leaf that provides the ideal conditions for the fungus to grow. The ant crawls under the leaf and goes into a “death grip”—biting down hard on the leaf's major veins. This allows the fungus to slowly feed on it. When the fungus finishes growing, it eventually kills the ant and releases its spores (Source: Smithsonian).

The interesting thing is that the zombie ant not only provides shade and humidity when hanging under the leaf, it is also positioned directly on top of the ant’s colony, so when the spores burst out they fall on other ants and begin the cycle all over again. There are hundreds of mind-controlling fungi like this one, but the chances of this type of parasitoid fungus evolving to target humans as hosts are unlikely (Source: Smithsonian).

Reference
- Evans, Commun Integr Biol (2011); 4(5): 598–602


What are the relative roles of coding DNA versus regulatory DNA thought to be in evolution?

Yes, a simple google search reveals millions of academic citations talking about "regulatory evolution".
But it's a little over-simplistic to divide coding vs. regulatory DNA. Indeed, some coding DNA is in fact also regulatory at the level of determining gene expression in cis (a well-known example of this would be codon usage).
It is moreover incorrect to think that coding DNA products don't do gene regulation. This was recognized very early on in the ideas of "structural gene" vs. "regulatory gene". These days we would call the latter transcription factors, we don't really use the structural/regulatory terminology anymore. Transcription factors do most of the actual active work of gene regulation in trans, in collaboration of course with regulatory DNA.
So in conclusion, yes it's important and there are tons of studies that you can google if you want to investigate these problems. I would suggest reading more about cis-regulatory and trans-regulatory elements. Of course, there isn't an exact mapping of coding<-->trans and noncoding<-->cis, it's just a helpful simplification.


When did the mammalian outer ear evolve?

Yes, it is believed to be linked to the mammalian inner ear bones. Since they act as amplifiers, the faint sounds gathered by the outer ear have a greater benefit. But really early mammals show many adaptations that they were relying very little on sight and a great deal on hearing. External ears just might not be beneficial enough unless you are really relying on hearing. The only other vertebrates that rely that much on hearing, the owls, also have external structures to help gather sound.

The fact that both developed at the same stage is circumstantial evidence that they may be linked as well.


Fainting, passing out, and blacking out are all common terms for the same thing, a sudden loss of consciousness of short duration.  The medical term for this is syncope. It is caused by a decrease in blood flow to the brain, limiting the the availability of oxygen and nutrients to the brain cells.  Brain cells have high energy requirements, so this causes them to stop functioning, causing loss of consciousness and muscle tone.

There are many causes of syncope.  In the situation mentioned, a likely possibility is a pressure change in the carotid sinus which is located at the side of the neck. When sensed by a nerve, this can cause primitive parts of the nervous system to change the dilation of blood vessels and the beating of the heart in a manner that brings on syncope.

Dreaming during syncope is not uncommon and that fact may be useful in distinguishing syncope from epileptic seizures according to research by Chiesa et al..


Short version

The paper has nothing to do with punctuated equilibrum vs. gradualism (see also here), which was published a few years earlier. This debate is much different (but equally important, I think).

The authors of the Spandrels paper criticized evolutionary biologists of taking a very narrow view of the evolutionary process. They claiming (wrongly) that evolutionary biologists believed that every single trait on an organism was an adaptation that resulted from natural selection. The trait would not be present unless it was an adaptation. The authors claimed (rightly) that traits could not be considered independently. Instead, the traits had to be considered in light of the evolutionary history and developmental biology of the organism. To your specific questions:

The architectural metaphor was wrong. Does it make their entire argument wrong? No. They did not understand architecture. That does not mean they did not understand evolutionary biology.
Are some of their claims wrong? I think yes and no, but the full answer requires more nuance than can really be given here so read the long answer below if interested. I don't know of a single reference that supports/rebuts the Spandrels paper but consider Why Evolution is True by Jerry Coyne, The Greatest Show in Earth by Richard Dawkins, and Endless Forms Most Beautiful by Sean Carroll. None of these address directly the charges lodged by the Spandrels paper but they do show how evolutionary biology is integrative of many ideas instead of isolating each trait without considering the biology of the entire organism. (I have no commerical interest in any of these books. I simply support the ideas presented.)

Long version from my perspective.

In 1979, Stephen J. Gould and Richard C. Lewontin (hereafter, G&L) published a paper, "The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme", in the Proceedings of the Royal Society of London, Series B.  The title of the paper mixes two metaphors. The first is the character Dr. Pangloss from Voltaire's "Candide." Dr. Pangloss is a bit of an optimist, who says,

  It is demonstrable ... that things cannot be otherwise than as they are; for as all things have been created for some end, they must necessarily be created for the best end. Observe, for instance, the nose is formed for spectacles, therefore we wear spectacles. The legs are visibly designed for stockings, accordingly we wear stockings. ... [A]nd they, who assert that everything is right, do not express themselves correctly; they should say that everything is best." - Dr. Pangloss

Dr. Pangloss is saying that everything has a purpose, and each thing is designed specifically for that purpose. G&L extend this metaphor to evolutionary biologists.  G&L claim that evolutionary biologists (at least to the time of their publication) tended to make claims similar to Dr. Pangloss: every trait that could be found on an organism results from natural selection and adaptation.  G&L write,

  An adaptationist programme has dominated evolutionary thought in England and the United States during the past forty years. It is based on faith in the power of natural selection as an optimizing agent. It proceeds by breaking an organism into unitary "traits" and proposing an adaptive story for each considered separately. - G&L

Hence, the Panglossian paradigm. Every trait has an adaptive purpose and is necessarily the "best" that it can be. G&L then argue that evolutionary biologists of the time failed to consider the entire organism when assigning adaptive value to each trait separately.

  We criticize this approach and attempt to reassert a competing notion ... that organisms must be analyzed as integrated wholes, with bauplane so constrained by phyletic heritage, pathways of development, and general architecture that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. - G&L

G&L are saying that the many organismal traits are functions of evolutionary history, developmental pathways, and other structural contraints.  G&L argue that most evolutionary biologists of the time did not consider the entire organism when ascribing adaptive value to any one trait. In G&L Panglossian metaphoric terms, evolutionary biologists had decided that the adaptive value of the nose was to support glasses, but they had failed to consider that the nose may have evolved for other reasons (e.g., smell) and that the supportive value of the nose was an evolutionar by-product instead of an evolutionary cause.

This brings us to the second metaphor, the architectural spandrels. Spandrels are triangular spaces that form when two arches meet, or when an arch meets a rectangle.  According to G&L, spandrels are a necessary by-product of the architectural joining of the two shapes. The spandrel itself serves no purpose. In evolutionary terms, spandrels have no adaptive significance that resulted from natural selection. Instead, they are an evolutionary by-product that resulted from selection on other traits (arches and rectangles).

While the architectural metaphor apparently fails, their primary argument does not change.  Traits cannot be considered individually. Traits of an organisms must be evaluated as one part of the entire organism, together with it's developmental biology and its evolutionary history.

Here are two examples to represent their argument, written for a general audience. The first example is based on the human hand.  Our hand has five fingers. Each finger except the thumb has three bones (called phalanges), which you can see easily when you curl your finger. The thumb has only two phalanges. What is the adaptive value of having four fingers with three bones each, and a thumb with two bones? You might say that such a structure imparts excellent manual dexterity, from grasping to manipulating objects. But, would we not have that same dexterity if we had four fingers, or six? Why does the thumb have only two bones and not three? How could that be adaptive? These specific traits may not be the direct result of natural selection.

The structure of our hand is explained by our evolutionary history. Our primate ancestors had five fingers. So did our earliest mammalian ancestors, as did our earliest reptilian ancestors. However, some of the earliest amphibian ancestors, such as Acanthostega, had more than five digits (toes, fingers). Somewhere in early amphibian evolutionary history, our ancestral lineage converged on five digits, and most descendant vertebrates retain that five digit pattern. Even those vertebrates today without five digits usually display five digits during development, such as the ostrich (scroll down to image of blue-stained bones). If we assigned an adaptive purpose to the  human hand independently of its evolutionary history, we might very well be wrong.  Science doesn't like wrong.

Think about the five toes of your foot. Each toe has three bones except for the big toe, which has two bones. Manual dexterity? No. Evolutionary history? Yes.

The second example is the groove in your upper lip below your nose. This groove is called the philtrum. Can you think of an adaptive function for the philtrum? You might think that it helps to direct odors towards our nostrils, or hypothesize some other adaptive purpose. However, it appears that the philtrum is a by-product of the development of our embryonic face (YouTube video). The trait of our philtrum may not have adaptive significance. It is a by-product our face formation when the two sides meet in the middle.

G&L's publication produced quite an uproar. It's easy to find criticisms of the paper. Some have criticized the architectural metaphor. A bad metaphor does not necessarily make a bad scientific argument. Others have criticized the scientific rigor of their arugments. This blog entry, associated with the respected ecology journal Oikos, dislikes the paper and identifies several problems. The Oikos blog also links to several other sites that either support or dislike the G&L article. Most evolutionary biologists disliked the claim that they did not see the "whole organism."

Rightfully so, I think. I do not know of one evolutionary biologist (myself included) that has ever considered a particular trait without considering the broader evolutionary history of an organism. Indeed, considerable effort is spent by evolutionary biologists to determine how the evolutionary history of an organism influences its trait. The same applies for evolutionary developmental biology and other biological processes. For example, Martin et al. (1993) related evolutionary rate to body size, metabolic rate, and generation time of various animals, a very integrative (not isolating) approach.

To be fair, I think the G&L paper needs to be considered in the context of its time. Remember that i was published in 1979. Reread the first G&L quote above. They say, "during the past forty years."  The G&L paper was published in 1979. Forty years before this paper was published was during the "modern evolutionary synthesis." Without going into details (ask another question on Biology.SE!) the modern evolutionary synthesis provided the genetic mechanism (and so much more) that explaiend how Darwin's concept of natural selection could actually work. Once the relationship between Mendelian genetic inheritance and natural selection was proposed, many evolutionary biologists tested this connection. It is not surprising to me that G&L perceived this strong "bias" towards a selectionist (Panglossian) paradigm because many biologists of the time were trying to understand how Mendelian genetics contributed to natural selection.

At the time of the modern synthesis, the structure of DNA was not yet known.  The structure was finally realized by Watson and Crick (and Franklin!) in 1953, only 26 years before G&L's paper. Today we think nothing about the DNA structure but molecular genetics has advanced so much since G&L's publication that we have a much greater understanding of evolution and natural selection at the genetic level. Today, you can't study the evolution of a trait without considering its underlying genetic architecture.

In my opinion, one of the most, and perhaps the most, important development in the field of evolutionary biology is the field of evolutionary developmental biology (evo-devo). This field did not really mature as a discipline until about 2000, when the Proceedings of the National Academy of Sciences in the US devoted an entire issue to the topic. Developmental biology was a discpline that G&L had argued was important to consider. I'd bet that even they had no idea how important the evo-devo discipline would become to understanding evolutionary change. Still, recognition of the relationship between evolution and development was recognized as long ago as the mid-1800s by Ernst Haeckel. Evolutionary biologists were not necessarily considering traits in isolation from evolutionary history or developmental biology.

In the end, G&L used broad brush strokes to paint evolutionary biologists into a small canvas, claiming that biologists had a narrow evolutionary viewpoint. The evolutionary biologists responded (then and now) that their perspective was wide, even when focused on a particular trait.

The G&L paper continues to prompt considerable debate, which I think is the value of their paper. Every young graduate student should be required to read the paper. Even jaded scientists need a refreshing jolt to an established way of thinking. Our thought processes will alway benefit when we are reminded that evolutionary biology is a broad discipline that must embrace many other disciplines to arrive at a full understanding of the history of life on Earth.


Reference request: neocortex creating 11 dimensional structures

I finally found the work. It was in the sources of the sources of the article that I gave as an example.