text:
Electron Transport Chain in Mitochondria
I was researching cellular respiration, and this is a rather confusing part. I need help understanding the purpose of Complex II and how the ATP Synthase generates the energy to turn ADP to ATP.

Can you please be more specific and tell us what you don't understand? At the moment this is really too broad.

@Chris is correct. This is a complex topic that is best approached through a suitable text book. You will find a better explanation there than on the web because of the much greater expertise, effort and quality control that goes into a text. 'Suitable' depends on what level you are at and what your background is. For University/College  biochemists try Berg et al.. Be warned, you will need some chemistry to understand this topic.

Okay. I am confused mainly with complex II and the ATP synthase. Thanks!

@JohnDumancic please [edit] your question and explain what you understand, and where exactly you're stuck. Asking for an explanation of the entire workings of Complex II and ATP synthase is still far too broad.

If I'm not misinterpreting your question, I believe your confusion lies in how ATP synthase produces ATP, correct? @JohnDumancic If so, look up chemiosmosis and the electron transport chain on YouTube. Essentially, the buildup of H+ in the inter-membrane space creates a great potential for kinetic energy, and the diffusion of the H+ through ATP synthase releases energy that is paired with the phosphorylation of ADP to ATP.

The good ol'electron transport chain (ETC).
Before beginning let us begin by looking at the structure of a mitochondrion and the purpose of the ETC.

(source: tokresource.org)
Take of note four things:

The intermembrane space
The matrix
The electron transport chain proteins and
ATP Synthase

Now lets talk about the purpose of the ETC, essentially its job is to create a H+ (proton) gradient between the intermembrane space and the matrix it does this by taking protons from the matrix and "pumping" them out to the intermembrane space.
This creates a higher concertation in the intermembrane space and lower concertation in the matrix. This gradient will result in a process called chemiosmosis where these H+ ions (protons) will go through ATP synthase on the inner plasma membrane in order to return to the lower concentration in the matrix.

So the most important thing to note about this is that the flow of protons through the ATP Synthase is what gives it the energy necessary to create ATP.
Alright now that is out of the way lets discuss how the ETC goes about pumping these electrons out of the matrix into the intermembrane as well as how ATP Synthase works.
If you were to zoom into the area that is labeled electron transport chain proteins (that I told you to note) you would see something like this.

(source: cnx.org)
What we see here is that ETC is actually made up of a series of complexes (I, II, III, and IV) and a couple of "electron/reaction" carriers (ubiquinone and cyt c). These complexes and carriers are in charge of moving an electron via a series of redox reaction along resulting in the "pumping" of protons out the matrix at each complex.
*Note, understanding redox reactions help in understanding what is happening here.
The chemistry gets a little intense at this point, so I'm going to quote and link the Wikipedia article on this, which does a wondrous job explaining what occurs complex to complex.

In Complex I, two electrons are removed from NADH [the electron carries from the previous steps] and transferred to a
lipid-soluble carrier, ubiquinone (Q). The reduced product, ubiquinol
(QH2), freely diffuses within the membrane, and Complex I translocates
(pumps) four protons (H+) across the membrane, thus producing a proton
gradient.

Note, that in Complex II no protons are pumped into the intermembrane.

In Complex II additional electrons are delivered into the quinone pool (Q) originating from FAD [Again, electron carriers from previous steps].

Complex III receives the reduced ubiquinones from Complex I and II.

in Complex III, two electrons are removed from QH2 at the QO site and sequentially transferred to two molecules of cytochrome c, a water-soluble electron carrier located within the intermembrane space. The two other electrons sequentially pass across the protein to the Qi site where the quinone part of ubiquinone is reduced to quinol. A proton gradient is formed by one quinol (2H+2e-) oxidations at the Qo site to form one quinol (2H+2e-) at the Qi site. (in total four protons are translocated: two protons reduce quinone to quinol and two protons are released from two ubiquinol molecules).

Finally

In Complex IV, four electrons are removed from four molecules of cytochrome c and transferred to molecular oxygen (O2), producing two molecules of water. At the same time, eight protons are removed from the mitochondrial matrix (although only four are translocated across the membrane), contributing to the proton gradient.

NADH+H+ → Complex I → Q → Complex III → cytochrome c → Complex IV  → O2
Article here
So after all this beautiful chemistry we are left with a proton gradient. This is when ATP Synthase comes into play. Once the proton "flows" through it will bind ADP and inorganic phosphate together to form ATP.
energy + adp + pi → atp

More on how the ATP Synthase works here
This is water down in the actual chemistry portion of it but I feel like it will give you a better grasp on how it all works. If you have anyways especially regarding the series of reactions between complexes feel free to ask!


text:
Why is statistical mechanics relevant to RNA and protein folding?
This is a very naive question. As far as I understand the folding of a molecule is governed by the electromagnetic forces between its atoms and also between its atoms and the atoms in the surrounding environment (so basically a many body problem). So I don't understand how statistical mechanics, such as Boltzmann's law, come to play.
To my knowledge statistical mechanics and thermodynamics exist when we have an ensemble of particle such as in a liquid or a gas. So what is this ensemble for the RNA or protein folding problem?

There are too many possiblities. And it still would need supercomputers to calculate how a protein is folded. As well as it is still unkown how the complete mechanisms are working.... therefore statistics are necessary...

Consider a polypeptide, newly synthesized, prior to folding up into its 3-dimensional shape, or structure.  Each substituent amino acid, contributes to the unique sequence of the polymer, and each affects, in some small way, the number of different states that the polymer could be found in, at any given moment.  Given the constraints imposed by the length and geometry of the chemical bonds, there are some states the polymer cannot adopt, but there are many, many states that are potentially available, and each has a unique energy. Over time you can plot these energies yielding a distribution.

I’m no physicist, but your statement “To my knowledge statistical mechanics and thermodynamics exist when we have an ensemble of particle such as in a liquid or a gas” is surely incorrect. The problem of protein folding is one of thermodynamics — finding the structure of lowest free energy, and the path by which it is reached from a random coil.
One of the difficulties relating to the path is that of getting ‘stuck’ in a position in the energy landscape from which the protein cannot escape. This is called ‘frustration’ and there is apparently a quantitative treatment of ‘minimal frustration’ using the statistical mechanics of spin gasses. This is mentioned in a review by Onuchic and Wolynes, available on-line, which you will probably be able to understand better than I can.

If you want to relate statistical mechanics to RNA and protein folding, you're on the right track with ensembles. Macromolecules are very dynamic and exist in many physical states. These macrostates are what are described by David on an energy landscape. The macrostates can be further broken down into microstates which are closely related movements of the macrostates. It depends how specific you want to get when describing your system. Statistics come into play when describing the populations of the macromolecule in its different macrostates. Typically, the macrostate with the most favorable energy conformation is the most populated.

You seem to have confused two different ways of discussing a thing with two different things. Electromechanics always applies, whether talking about liquids or gases or what have you. All molecules are subject to electromagnetic forces. And all matter has populations of molecules, which we can talk about with statistical mechanics. In statistical mechanics we abstract away some of the details of electromechanics and treat them statistically, just like how in economics we abstract away some of the details of individual psychology. So both apply, in every case. The problem is that RNA folding is a particularly tricky physical system, so abstracting it away is with statistical mechanics is far harder than it would be for say, a noble gas.

Indeed, statistical mechanics is applicable to the systems with many degrees of freedom (typically of the order of the Avogadro constant, $N_A\sim 10^{23}$). Gases, liquids, and solids routinely fill this definition, as they consist of huge numbers of atoms or molecules, each of which has at least three degrees of freedom (for molecules we also need incorporate their rotation and elastic movement).
There are two ways how statistical mechanics can be applied to proteins (see, e.g., the discussion in the book by Doi):

one may consider a solution containing a macroscopic (i.e. $\sim N_A$) number of polymer molecules
one may consider a single polymer molecule as a statistical ensemble, because a polimer with many links can adopt huge number of configurations and therefore satisfies most of the criteria necessary for applying statistical phsyics. This is specially true for polymers with $10^5-10^6$ links, but provides useful guidelines for relatively short protein molecules, with typical lengths of a few hundreds od amino-acids.

As an example we may consider protein folding (see, e.g., this question): a protein would fold spontaneously even in a vacuum, and even if the forces between its parts were non-existent. The reason is entropy: a chain of molecules can adopt billions of configurations in space, of which the stretched configurations would form only a small fraction. Statistical physics tells us that all these configurations are equiprobable, and we therefore are likely (what practically amounts to certainty) to find protein in a folded configuration. (This equiprobable state is referred to as maximal entropy or maximum of an appropriate thermodynamic potential, if we are not dealing with a closed system.)
Adding interactions between protein links and between the protein and the solvent molecules makes the problem even more amenable to statistical physics analysis (although now one may have to deal with folding-unfolding phase transition).

References

M. Doi, Introduction to polymer physics
K. Huang, Lectures on statistical physics and protein folding

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
Are there evolutionary advantages for the bee sting to kill the bee?
The question title says it all: are there advantages for the sting of a bee to kill the bee? It seems to me getting rid of this would have only advantages, and might've been selected for if a mutation like that occurred.

The bees you are most likely to be stung by, do not participate in reproduction.

The ones that do participate in reproduction do not die if they sting you.

@Aron That's an interesting piece of info, if you'd like credit for it, please post it as an answer.

@Aron, I believe that bees capable of reproduction do not have stingers. Male bees either get a reproduction organ (drones) or a stinger (workers). Never both.

@Octopus Queens do not have barbed stingers. In some cases Queens (often related) will fight to the death over a hive.

@Aron, Queens also are not male.

@Octopus, firstly. Worker done bees are female. Secondly what I said was carefully chosen. I might have implied that all bees that participate in repro can sting, I never did. I merely stated that those bees who do sting you would not likely die from stinging you.

Fitness of the colony vs fitness of a single worker
Bees have a division of reproductive labour (they are eusocial). Only a queen reproduce (and the males called drones) while the workers dedicate their existence to ensure the survival of the colony. If committing suicide will be of any help to the colony then one would expect a bee to do so. What I just said is an oversimplification of the structure and mating systems of bee colonies.
You should have a look at the field of social evolution to have a better understanding of what's going on with bees!
What is the cost?
Above I argued why nobody really cares much if a single worker dies. This being said, if the bee survived to stinging, then it could eventually keep protecting the colony as it was doing before stinging. So why does it has to die? Clearly, there must have a cost to not die. It seems very plausible to me (but cannot offer an evidence for it) that there would be a strong physiological cost to create a stung that that would not kill its carrier. Such physiological cost (even if mild) can by large outweigh the cost of losing a single worker for the colony.

Re "Only a queen reproduce(s)", surely the drones play a part as well, no?  But I think the key here is looking at the survival/fitness of the hive, not individual bees.

Well sure. The drones aren't really part of the colony though and they are just fed as larvae and then fly away (although it may vary among species). In some species (of ants at least), workers sometimes take over colonies or reproduce secretly. I'll fix the eventual confusion but we'll keep my answer as simple as it currently is. Thanks for your comment.

"Clearly, there must have a cost to not die" I disagree. Evolution is not about optimization. Its about "good enough". A barbed stinger increased the effectiveness of the stinger at the cost of the bee's life. Losing the bee is "good enough".

My answer is an oversimplification as I did not want to dig into the details of kin selection theory for such a simple question. I don't understand how your metaphors of "what evolution is about" mean. If there was no cost to being able to stung without dying than one would expect variants that do not die to increase frequency. Sure, it is possible that there is a phylogenetic constraint or something similar going on.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Does evolution head to some optimum?
Currently we have many species which are "good enough" for current environment, some species emerge, another die. So let's say that they could be close to some local optima. Does the evolution head to some optimum that in future we will have only one species which will be superior to all other extinct form of life?

The environment is highly variable thus it is unlikely (I'm going to say impossible) that a single species would be the best in all possible environments. Species do often exist close to a "local optima" - see fisher's geometric model of adaptation - there's a recent paper showing that it seems to be a good model for real world adaptation

The question is unclear in many ways. First, you seem to be assuming that all species are evolving in the same fitness landscape, when all species (and populations) exist in their own fitness landscape. Second (assuming that a global optima really exists), why would this imply that all species but one should go extinct? Third, other species (the entire foodweb) constitutes "the environment" for a particular species, which means that the environment is never stable (since all species evolve).

Fisher's Adaptive Hypersphere model proposes a single adaptive peak with a range of genetic configurations that could bring the population closer to optimum.

According to Orr (1998), the inclusion of drift in the model adjusts the expected sizes of mutations that become fixed. Early in adaptation, fixed mutations are predicted to be larger on average than those fixed later.
Tenaillon (2014) discussed simulations of adaptive walks within the geometric model, w/ the dynamics of adaptation and the phenotypic effect of mutations.
An increase in E. coli fitness over 10,000 generations was documented by Lenski & Travisano (1994) indicates "yes" to your question

An issue in the question that I will ignore
You say

Does the evolution head to some optimum that in future we will have only one species which will be superior to all other extinct form of life?

Firstly, it is a little bit weirdly phrased. By "superior" I suppose you would refer to a species that could outcompete all the other. This sounds very impossible to me firstly for simple ecological reasons. However, it would be a long answer to fully address this point and I don't feel like addressing (I might not be very much able to) in addition to the other questions.
Evolution vs Natural Selection
Just for a start. Evolution is way more than just Natural selection. There are plenty of other absolutely essential processes such as mutation and drift that are important to understand.
What is Natural Selection?
Natural selection is the process by which most fit individuals end up being at higher frequency in the population as a result of reproducing more and surviving better. Natural selection does not necessarily diminish the probability of a species to get extinct. It will not necessarily increase the ability of a species to compete another. It will not necessarily increase the rate of increase in the number of individuals in the species.
local vs global optima
Reading you post you seem to understand the concept of local vs global optimum (from algorithmic maybe). If selection alone was acting in the population and if mutations were feeding genetic variation to this population at a low enough rate, then population will ultimately reach a local optimum and will get stuck there forever. They would never reach a potential higher local optimum somewhere else. Drift may allow for such switch though, it is refer to "shifting balance theory".
Envrionmental change
The environment changes much faster at a local scale that you seem to think. When talking about environmental change for a lineage, we are not only talking about important ice age or current days global warming but we are talking about more subtle and more frequent changes. Imagine a species of unicellular living in a 50 cubic centimeter puddle. For them environmental change are drastic and frequent. So do population really have time to achieve any equilibrium. It is here a general question that comes in many field of evolutionary biology and also outside biology. Are the system that we study expected to be at equilibrium (in regards at some variables at least) in nature or are they never given the time to reach any equilibrium?
Mutations and drift
Mutation and drift are stochastic processes in evolutionary biology (among others). Mutations is the ultimate production of genetic variation. Most mutations are deleterious but not all are. The exact mutation (and mutational effects) and number of mutations that will occur in a population in a given amount of time is a stochastic process. Genetic drift refers to the random sampling of individuals that are chosen to survive. Drift is inversely proportional to the population size and you may want to have a look at this post to get some intuition for why this is the case.
How much fitness is lost du to ever occurring mutations?
As mutations are always occuring we might wonder how far is a population from its optimum due to these deleterious mutations.
Let's consider a very simple model.
Let $p$ be the frequency of the wild-type (not mutant) allele, $s$ be the deleterious effect of the mutation in the homozygote mutant and $h\cdot s$ be the deleterious effect in the heterozygote. The mean relative fitness in the population is
$$\bar w =  1 - 2 p (1-p) h s - (1-p)^2s$$
Let's define the mutation load $L$ as $1-\bar w$. As a consequence
$$L = 2 p (1-p) h s - (1-p)^2s$$
At selection-drift equilibrium the expected frequency of $p$ is $p=\frac{\mu}{hs}$, where $\mu$ is the mutation rate. As a consequence the
$$L = 2\mu$$
and
$$\bar w = 1- 2\mu$$
Let's assume that fitness effect at different loci are multiplicative (no epistasis). As a consequence an individual carrying $n$ deleterious mutations has a fitness of
$$\prod_{i=1}^n 1-s_i $$.
Let's further assume that all mutations have the same deleterious effect on fitness, that is $s_1=s_2=...=s_n=s$. Let $l$ be the number of nucleotides on which deleterious mutations can occur. Coming back to $w=1-2\mu$, we can say that over all loci in the genome the fitness is
$$\bar w = \prod (1-2\mu) ≈ e^{-\sum_{i=0}^l 2 \mu} = e^{-2\mu l} = e^{-U}$$
, where $U=2\mu l$ is the genome-wide deleterious mutation rate. According to best estimates, in humans $U≈2.2$ and therefore our load is $L = 1-e^{-2.2} ≈ 0.9$.
From this simple model, we would expect that 90% of the mean fitness of a population is lost due to ever recurring deleterious mutations. This sounds pretty big and suggest that we'll always be pretty far way from an actual optimum.

The short answer is NO.
Here, very briefly (since it would take to much to properly analyze all the aspects of this topic), is why:
First of all, the environment is constantly changing so there will be no such thing like 'the end of evolution'. Even if you try to stabilize the environment artificially (a lab setup) the organisms will continue to interact each other, mutations will occur, new stuff will evolve anyway. (here one example https://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment)
Moreover, each environment is made up by sub-environments (niches) that can be colonized by different organisms each of them will tend over time to adapt to their niche while competing with all the other organisms in the nearby environments but no organism will ever be the fittest for all those niches.
Zooming into molecular evolution, there are some enzymes that have reached "perfection" in the sense that they can catalyze a certain reaction at the maximum speed possible (https://en.wikipedia.org/wiki/Diffusion_limited_enzyme). However, even in these cases, such enzymes are well fit to their local environment (the specific cell type) and they will not work as well (or at all) in different conditions. So, even if they may perform a reaction perfectly, they may always evolve. For example, they may change substrate specificity of temperature stability or they can evolve different reaction mechanism.


text:
Do all prokaryotes have ATP synthases and an electron transport chain?
I was looking this up and I'm wondering if so far I'm correct about the following:

For the most part eukaryotes do aerobic respiration, which involves glycolysis, the Krebs cycle and oxidative phosphorylation involving ATP synthase and an ETC
Prokaryotes can either do aerobic respiration, anaerobic respiration or fermentation, the first two of which require an ETC and ATP synthases, which would be located in the plasma membrane of the prokaryote

If that is the case, I was wondering if there are prokaryotes that only do fermentation, and if so do they have ATP synthases and an ETC? In other words, are there any organisms without ATP synthases and an ETC (which would force them to survive on fermentation alone, unless there is some other method of energy production in prokaryotes that doesn't use ATP synthases and an ETC that I'm missing)?
Thanks

This is an interesting question (I really mean this — see below), for which a straight answer is remarkably difficult to find on the web. When I googled for it I got pages with statements that obligate anaerobic bacteria still had the electron transport chain (ETC) and ATP synthase as there were different electron acceptors other than oxygen. Yes, we know that things are different in thermal vents and hot springs, but what about gas gangrene? I am not a microbiologist, but I did play with the metabolism of some bacteria for a biochemical bioinformatics lab some years ago, so I can give two instances where anaerobic bacteria appear to lack either the ETC or both the ETC and ATP synthase.
Clostridium perfringens
This is the anaerobic fermenting bacterium that leads to gas gangrene in infected wounds and was a major cause of limb loss and mortality in the First World War. The DNA sequence of Clostridium perfringens has been determined. I quote at length from the paper as it describes the fermentation, but italicise the key statement for those who wish to skip this:

We could not find any genes coding for tricarboxylic acid (TCA) cycle- or respiratory-chain-related proteins, in contrast to C. acetobutylicum, which has incomplete TCA cycle enzymes. Similar to C. acetobutylicum, we could construct a pathway map for anaerobic fermentation resulting in the production of lactate, alcohol, acetate, and butyrate, all of which have been commonly detected in C. perfringens cultures. In the fermentation pathway, pyruvate is converted into acetyl-CoA by pyruvate-ferredoxin oxidoreductase (CPE2061), producing CO2 gas and reduced ferredoxin. Electrons from the reduced ferredoxin are transferred to protons by hydrogenase (CPE2346), resulting in the formation of hydrogen molecules (H2) that are released from the cell together with CO2.

The related bacterium, Clostridium acetobutylicum, mentioned in the extract, is also an obligate anaerobe. (It ferments a variety of plant mono- and poly-saccharides to acetone, butanol and ethanol — used to produce explosives in the First World War.) Although it has some enzymes of the TCA-cycle, it is unable to use the cycle oxidatively, and, like Clostridium perifringens, lacks the enzymes of the electron transport chain and an ATP synthase.
Ureaplasma urealyticum (Ureaplasma parvum)
This micro-organism is a micoplasma (Mollicute) rather than a bacterium — i.e. it lacks a cell wall. It infects the human urogenital tract. It lacks the components of an electron transport chain but does possess a functional ATP synthase. It generates a hydrogen ion gradient, not by increasing the hydrogen ion concentration within the inter-membrane space by the oxidation of NADH in the ETC, but by reducing the intracellular hydrogen ion concentration by generating ammonia from urea (plentiful in its habitat) in a reaction catalysed by the urease it encodes. The sequence of the organism and references to previous work on its urease activity can be found here.
Evolutionary considerations
The reason I find this question interesting is that anaerobic organisms preceded aerobic organisms, so the question arises whether there are any contemporary anaerobic bacteria that have evolved from these primaeval anaerobes and have never possessed an electron transport system — or are all contemporary anaerobic organisms lacking an ETC derived from organisms with an ETC (aerobic or using some other electron acceptor) and have just lost these functions through non-use (as is most likely in the examples above)? This question must surely have been considered by those in the field.

Very nice! These organisms are super interesting.

Yes. I find them fascinating too.

Yes there are, though I had to dig a lot to find them. They are called strictly fermentative bacteria.
Lactic acid bacteria (Lactobacillales (Firmicutes)) ferment glucose through pyruvate to lactate using the glycolytic pathway, and include the genera Streptococcus, Lactococcus, Lactobacillus, and Leuconostoc.
From Madigan et al. 2014 Brock biology of microorganisms, 14th edition (PDF):
p. 66.

"Microbial eukaryotes that contain hydrogenosomes carry out a strictly
  fermentative metabolism. Examples include the human parasite
  Trichomonas (Sections 17.3 and 32.4) and various protists that
  inhabit the rumen of ruminant animals (Sections 1.5 and 22.7) or
  anoxic muds and lake sediments."

p.93.

"Reversibility of the ATPase explains why strictly fermentative
  bacteria that lack electron transport chains and are unable to carry
  out oxidative phosphorylation still contain ATPases. Many important
  reactions in the cell, such as flagellar rotation and some forms of
  transport, are coupled to energy from the pmf rather than directly
  from ATP. Thus, the ATPase of organisms incapable of respiration, such
  as the strictly fermentative lactic acid bacteria, functions
  unidirectionally to generate this required pmf from ATP formed during
  substrate-level phosphorylation in fermentation."

Trichomonas (Excavata) is an eukaryote.

I'm no expert, but looking at the English, The statement "" strictly fermentative bacteria that lack electron transport chains"   <--  doesn't state that all strictly fermentative bacteria lack an electron transport chain, and doesn't state that strictly fermentative bacteria lack an electron transport chain.   If I say "birds that have long legs", it suggests there may be birds that don't have long legs.

That said, I can see how perhaps strictly fermentative bacteria don't have an ETC(perhaps it'd mean they had an ETC but couldn't ever use it, which would perhaps be strange). But anyhow, while it may well be that they don't have one,  that quoted text doesn't say that they don't have one.

This is a very late answer, but many Mycoplasmas lack most major metabolic pathways beyond glycolysis; so no electron transport chain, and no tricarboxylic cycle (refer Pollack et a. 2002).


text:
Does mechanotransduction of cells play a role in the biocompatibility of titanium?
What exactly is mechanotransduction as the information varies between sources. Some sources indicate that mechanotransduction is the underlying principle where cells pull on the surface they grow on to test their stiffness, so they can stretch and facilitate cell growth and differentiation. Other sources indicate that mechanotransduction is how cells detect mechanical stimuli and turn them into chemical signals.
Is this the main reason titanium is biocompatible to replace bones because it has a low surface resistance and cells on stretch on it?

Welcome to BiologySE... since this is a homework question you should see the site's help section...http://biology.stackexchange.com/help/homework

You have 2 questions, one in each paragraphe, and it would have been better to ask separately. For the 1st one, the two statements are not antagonistic: the second is the general definition of mechanotransduction. The 1st one is one of the phenomena that arise via mechanotransduction: a mechanical stimulus (resistance of substrate when exerting force on it = its stifness) is turned into signals that lead to a specific behaviour (spreading, differentiation)

First off, AOZ has a wonderful page about titanium alloy uses in medical applications you should read and that most of my info is coming from:

Suitability of Titanium for Implant Purposes

I think you're having a couple of easy to correct misconceptions. First, titanium alloys are used for medical implants and replacements because they're lightweight, stronger by tensile strength than steel and judged to be completely inert and immune to corrosion by all body fluids and tissue, and is thus wholly biocompatible. It's also non-magnetic, meaning you can even go through an MRI machine with it! The range of alloys that we're able to produce is also key to the widespread use of titanium in medical applications as different alloys can serve their purpose as anything from hip joints to jaw reconstruction bases to spinal fusion devices based on their composition.
But cells don't exactly "stretch on it" and in fact in many operations additional material is used to ensure that the host body is able to function with the implant. This includes the use of polymethyl methacrylate bone cement to ensure that implant joints stay in place, and the use of roughened bioactive surfaces (hydroxyapatite) to stimulate the integration of the bone and surrounding tissue onto the implant.
As far as mechanotransduction goes, the problem is that it covers an extremely wide range of topics so ascribing it only one definition can quickly cause issues between studies. I usually go off of Nature's definitions for these kinds of things, which in this case says that "Mechanotransduction refers to the processes through which cells sense and respond to mechanical stimuli by converting them to biochemical signals that elicit specific cellular responses" (1). If you peek at the studies highlighted on google scholar for mechanotransduction you can see that the range of work is extreme and that's why ascribing the term one specific meaning at this point is unrealistic.


text:
Where to go next with clustered C elegans neuronal time series
I'm doing some independent research with the C Elegans nervous system (with the OpenWorm project) and was looking for some guidance as to where I should go next.
Right now, I'm dealing with calcium fluorescence imaging time series datasets for a subset of neurons in C Elegans. Here are my five time series clustered by similarity:

and here are correlation matrices for the neurons across the datasets:

There are obvious patterns here.
I have many vague ideas of where to go next, but I'm wondering if anyone with more expertise can provide some guidance as to what approaches I can take to:

Look at this data in the context of known C Elegans neuronal connectivity
Trying to reconstruct connectivity from functional data (develop an algorithm for this, not a simple task)
Understand why certain correlations exist
Look at computations occurring among neurons in these datasets and isolate computational building blocks
Developing a minimal network model for C Elegans.
Understanding information flow

I'm overwhelmed by all of these ideas and need some guidance/a concrete starting point.

What is your worm background? For example, you mention constructing a connectivity network (or something like that), but the synaptic connections of all of these neurons has been known since 1986, based on serial electron micrographs. It seems like the names of the neurons is the same in all five datasets, their order in the figures is changing between

I'm aware we have a connectome and I have read lots of literature analyzing the static connectome. I'm interested in looking at functional data in the context of the connectome. One approach I had in mind is trying to develop an algorithm for reconstructing connectivity from functional data with the intention of attempting to develop a theory relating the two or to just get insight relating static graph characteristics to dynamics.2)The reason the neuron names change order between figures is because neurons are clustered differently in the different datasets, leading to different orderings.

Yes, it wouldn't let me edit my typo. What is the difference between the five datasets, in other words, what are the worms doing, crawling, eating, defecating, egg-laying, etc.? How any animals are being assayed in each dataset? Have you tried making a figure for each neuron, to compare how each one behaves in all five conditions?

This data was obtained from Saul Kato for his paper "Global Brain Dynamics Embed Motor Command Sequence of C Elegans". I'm able to infer movement patterns based on his results in the paper. Nevertheless, I don't have access currently to actual behavioral data.


text:
What is the closest possible analogue to human cells?
For an experiment, I need a specific number of cells. I will grow these cells in an incubator, and then measure the number of cells which have decayed due to the induced radiation. I am using a standard cell counting chamber (Hemocytometer) to count the number of cells.
The research question is to find the best armour for radiation; low-level really.
I was wondering which cell is the closest substitute to a standard human cell. People are telling me about yeast, but doesn't that grow from budding?
Any help and/or suggestion is appreciated.

The best analogue for human cells are human cells. There is nothing like a "standard human cell", since there are too many cell types. But since you probably want to study a specific cell type, you can culture these.

Sadly I don't have the equipments to culture human cells. However, any idea as to how will I go about culturing human cells, and which ones are the easiest to harvest?
If not, any bacteria/fungi which can be used as an alternative? Say I want to study skin and blood cells. I can use my own blood, maybe a drop or so. However, is there any chance of harvesting a sample of bacteria and use them?

Is there any chance that you collaborate with a research institute in your area about this? They often have programs for projects like this.

@Chris, I am in the process of asking a couple of research institutions for help. My parents have a facility like this, but that's unavailable due to the fact that there is an on-going IVF batch. There is a 99% chance that they'll say yes. Any ideas for the E. Coli strain?

They will most likely not let you in a cell lab with bacteria.

What about Escherichia coli? Every undergraduate lab has easy access to plenty of E.coli culture methods and its stupid easy to culture. There are always HeLa cells as well if you really want the perfect analogue to human cells because, well, they are human cells. Other options would include:
a) HEK 293 cells (Human Embryonic Kidney 293 cells), which are nice for what you're looking at as they don't replicate out of control, but are still extremely easy to grow. However, they're generally used as hosts for gene expression and they're finicky when it comes to contamination and they don't really act like normal cells that would be hit by low level radiation (ie tissues that are closer to the skin's surface)
b) 3T3 cells which would be nice for you as they are contact inhibited cells, meaning they functionally keep growing into a layer one cell thick (a monolayer) which could be nice for you, especially if the low level rad you're testing is alpha emitting in which case you need a homogeneously thick cell layer.

I was thinking of E. Coli in the beginning. However, I am in a school: grade 12. Sadly, I don't have access to a fancy incubator which can grow these cells. However, I presume I can get it kicking by asking others for an incubator.
I don't really have a biology background. Is there any protocol specification available to grow these cells?
Lastly, thanks a lot for this! It really helps! :)

Hm... Well, I guess reading this is a decent start as it outlines what is necessary to have and the basic principles behind cell cultures Basics of Cell
Culture. But at the end of the day there's many reasons why cell cultures are done in university and lab settings, and doing so without the resources provided by those settings will be expensive and difficult. I would advise talking to your teacher, or your contacting your local university's biology department I think they would be more than willing to help you!

Last question, and I will be out of your hair. Which strain of E. Coli should I use? Most of them seem toxic. Will E. Coli K-12 be the one?

No worries! There's two common strains of E.coli that are most used in labs: K-12 and B strain. Which ever one of these two that you can get from a supplier/teacher/university professor is the one you should use as for your purposes it should not matter.  If you are interested though here is a good starting point for some of the more common strains.

I think yeast is a great idea. They are safe and cheap to grow, easy to obtain, and easy to see in the hemocytometer. Human cells are not something you grow in a school; you'll probably need licenses, you cannot buy a cell line in the supermarket and the medium (what they grow on) is ridiculously expensive.
Of course yeast doesn't really resemble human cells, but they will die from radiation all the same. What kind of radiation are you using? UV seems the most appropriate (still be careful that you don't burn yourself / your eyes / other people), any kinds of radiation you can use in school (if any) is probably not strong enough to kill a significant number of cells. You might be better of using a Geiger-counter or something like that to measure it directly.

You don't need special licences unless you want to modify cells genetically. And standard media come between 3 and 10$ per bottle.

@Chris One bottle gets finished too fast :P Plus you need flasks and FBS too. And a CO₂ incubator and a very clean room :P


text:
Would it be possible to eat things from another planet
Although at first glance my question is perhaps better suited for a space exploration or sci-fi forum I looked  and felt this forum was more appropriate.
What makes plants and animals edible and allows us to gain nutrition from them? If life evolved separately from life on earth would any of it be edible to us or to any other creature that evolved on this planet.
My question is not about stuff being toxic, its about if anything other than life on earth, would be digestible? Do we need to evolve side by side with our food? I know of convergent evolution, that may make things look similar, but is there something at a cellular level that makes things edible. Does everything edible have DNA?
I don't have an academic background in biology so apologies if this question sounds silly. It's been bugging me for ages. My gut feeling tells me that nothing will be edible but I don't have any science to back that up.
I'm a vegetarian so I'm not just thinking about hunting and eating aliens either!
Thanks.

Given that we have pretty much no idea what life on other planets may be like it is nearly impossible to answer this question in a non-opinion based way

Amino acid chains are found in carbon rich meteorites so that gives a clue.

Short Answer- No, chances are negligible.
Long Answer- Digestion is a chemical process which is mediated by enzymes. Enzymes are highly choosy molecules so that they only perform the work they're made for. In digestion, enzymes like proteases (for breaking down proteins), lipases (for breaking down lipids), amylases (for breaking down starch), DNAses (for breaking down DNA), etc. are involved. For example, amylase is specialized to break down polysaccharides (carbohydrate polymers) into mono/di/tri/oligo-saccharides. See this from wikipedia:

The α-amylases are calcium metalloenzymes, completely unable to function in the absence of calcium. By acting at random locations along the starch chain, α-amylase breaks down long-chain carbohydrates, ultimately yielding maltotriose and maltose from amylose, or maltose, glucose and "limit dextrin" from amylopectin.

And this image from here:

Lets forget the "completely unable to function in absence of calcium" part as it is out of the scope of this question. But it is necessary to know how specialized enzymes are to answer your question. They are so specialized that amylase can break starch, but not cellulose. See this image:

Source
You must have noticed, in the diagram above, the minute difference between starch, cellulose and glycogen (BTW glycogen is another polysaccharide), but even that difference is enough for enzymes to tear apart one and pass on the other molecule.
The above explanation was necessary to tell why the answer is no. If we eat something, enzymes are needed to break it down. But if enzymes cannot recognize something, then they can simply not work on it. So, if you even want to eat space grass, forget about being able to digest it. Because even if we confirm that life on earth came from space through meteorites billions of years ago, then also during this time period of billions of years both that life of space and this life on earth would have evolved so much that they might not match, even chemically!
Hope this helps. Tell me if you want any more details :)

Absolutely! The only limitation animals face on eating substances or objects is the size of the opening to their oral cavity, so if there is something on another planet that will fit in your mouth then you can definitely eat it.
Whether one would be able to derive energy from the exo-material is an entirely different question.


text:
Is there a formal definition of `nature` in Biology?
I've been discussing with a friend about Earth Day and at a certain point came out the question

What do you call "nature"?

He said that he considers "nature" basically all matter, including plastics and all kind of man-made materials.
I said that as far as I understand, "nature" is the ensemble of all Earth's ecosystems, thus if something is not part of an ecosystem, it is not "nature".
Is there an official definition of what is considered to be "nature"?
If yes, what is it? If no, is there a reason?

Why was the question downvoted? Please leave a comment. I personally think it is a good question

@Remi.b I guess we'll never know, but I have seens on several SEs people that think a question to be "unanswerable" and downvote without thinking too much about it.

Is there a definition of "nature"?
I don't think there is any commonly accepted definition of "nature" in biology. To my experience, the term "nature" is actually relatively rarely used in conferences or peer-reviewed papers.
Why is there no formal definition of nature?
The concept of "nature" has been developed outside the field of science or philosophy. As often concepts in the popular culture are used without a proper, complete definition. Even if there is an vague intuition that correspond to a concept, it does not mean that there is any way to make an objective definition of this concept. I think the absence of formal definition of nature mainly come from the fact that nature as used in the population culture does not mean much.
Is the term "nature" used in Biology and with which definition?
I just did a quick review of the use of the term "nature" in peer-reviewed articles. It seems that the term "nature" is rarely used or only in the abstract r in the first two paragraphs of the introduction to convey very general (and somewhat inaccurate) ideas.
Often, the term "nature" holds for "essence", "origin" or "intrinsic characteristic" rather than referring to "outside the lab", "landscape" or "ecosystems". Here are some examples of where I found the term nature
"Nature" as "Essence"
From the abstract of Gibson and Dworkin 2004

[..] we highlight recent progress in determining the nature and identity of genes that underlie cryptic genetic effects [..]

From the first paragraph of Woolhouse et al. 2002

Failure to recognize the dynamic nature of the interaction could result in misinterpretation [..]

"Nature" as "outside the lab"
First sentence of the second paragraph of Elena and Lenski 2003

Since Darwin’s day, many examples of evolution in action have been studied in nature [..]

Note btw that there is no good (objective) definition of life either. One might want to have a look at Why isn't a virus alive? for a discussion on the definition of life.

The meaning of words depends on how people use them. However it would appear that your friend is in a minority applying the word ‘Nature’ to man-made things. Thus,
The OED definition includes:

The phenomena of the physical world collectively, including plants, animals, the landscape, and other features and products of the earth, as opposed to humans or human creations

and Merriam-Webster:

the physical world and everything in it (such as plants, animals, mountains, oceans, stars, etc.) that is not made by people


text:
What is wrong with this flower?

Today morning I was surprised to see this flower as it has four normal pale orange coloured petals and one bright red one. This is a flower of Hibiscus and all the flowers of this plant have the normal pale orange coloured petals, while this one has a bright red one.
What can cause this?

Maybe just a rare mutation?

Then why should only one flower show it? If it was a rare mutation I guess all the flowers would have one red petal. But this plant gives the same coloured flowers everyday.

Maybe an insect or fungus that affected the bud?

Could be a rare mutation next to the flower which only affects the flower... maybe sth which was induced... mutations do not necessarily have to occur in seed state etc.


text:
Is it possible to feel pain in some part of a body, but the pain "feeling" is introduced somewhere else?
Is it possible to feel pain in some part of a body, but that the cause of the pain is situated elsewhere in the body? For example, somebody feels pain in his toe, but it turns out that this pain is not signaled by nerves in his toe, but caused by a damaged nerve in the spinal cord, or somewhere in the brain.

Yes, this is pretty common.  Examples include

sciatica, pain felt down the back of a leg to the foot, from irritation to components of the sciatic nerve but commonly at the level of the sciatic nerve roots
angina pectoris, pain from myocardial ischaemia felt in the throat (Latin angina "infection of the throat"), arms, chest etc
shoulder tip pain from a subphrenic abscess

The clearest possible example of this is phantom limb pain, where pain is perceived to be arising from an amputated limb indicating that the pain is arising from central mechanisms.

As a side note, transferred pain is actually pretty critical to know about as a ski patroller. To use your example of myocardial ischemia (and, for that matter, infarction) one of the big symptoms in males is pain radiating down the left arm and up into the throat, in some cases reaching as far as the hand, which is pretty far from the heart.

Referred pain* whoops. I haven't had to use the generic term… ever, that I remember.

An example of pain evoked by distant sites in the body is referred pain.  It's defined as pain perceived at a location other than the site of the painful stimulus. An example is the case of angina pectoris (chest pain), caused  by myocardial ischemia (decreased oxygen supply to the heart due to a narrowing or complete blockage of the coronary arteries). Angina often results in pain felt in the neck, shoulders, and back rather than in the thorax (chest), which is the actual the site of the injury.
A massage-related field of therapy has evolved around this - trigger point therapy, where trigger points are defined as the cause of pain elsewhere in the body. From personal experience I can add my gratitude to this field of therapy; it's been good to me.

Trigger points. source: Trigger Point Therapy

Another common medical condition that causes pain elsewhere is the spinal disc herniation. The disc pushes against the nerves in the spinal and causes pain, usually in the leg, foot or arm. https://en.m.wikipedia.org/wiki/Spinal_disc_herniation
Sometimes the pain disappears with rest, sometimes surgery is necessary and sometimes the pain partly remains even after surgery.

When I went to a doctor years ago because of pain in my arm that had lasted months, he diagnosed it as tendonitis. It wasn't until a chiropractor recommended I see a sports medicine specialist, who recommended an MRI, that I learned I had herniated a disc in my back that was the cause of the pain in my arm, which didn't go away until over a year later.

@moonpoint It is not uncommon that disc herniation is not immediatly diagnosed. The pain may go away, or it may not, not even after surgery :-(

Just as an FYI, the answer is emphatically yes.  I have two separate areas of my body which exhibit those symptoms.  But my answer does not "track" those of others here.  They talk about (I would guess) some relatively standard off-site pain actions.  In my case, it appears to be more simply the action of (for want of a better term) CrossedNerves.  As one example, there is an area of about two square inches, just right of center, on my chest which, when poked with a sharp object, will cause a stabbing  pain to appear on the back of my right shoulder just below the shoulder blade. This is repeatable and has been that way since as long as I can remember.
Glad to see I'm not the only one with these strange biological oddities.

interesting answer - is there any cited literature on this phenomena that you describe? could you cite that in your answer - it would improve your answer significantly

@VanceLAlbaugh to me this sounds like a specific form of synesthesia.


text:
How two genomes adopt when cell goes to recipient's body from donor's body?
We often give blood to another following the blood giving compatibility chart. Heart transplant and similar transplants also brings one's cell to another's body.
My curiosity is, when a cell goes to the recipient's body from the donor's body, what actually happens with respect to the genome?
If the genomes do not merge to one, then how to identify one identically? How does DNA fingerprints, parent detection etc. work correctly? More generally, how does it maintain consistency?
Remarks:
My assumption was : "All the cells of one particular person's body carry the same genome or DNA information. And every individual has a distinct genome or DNA information". But after some study and some comments, I found that the statement is actually wrong.
However,  this article led me to break my wrong notion.

The genomes don't merge. Red blood cells (the vast majority of cells in blood) do not contain a nucleus, and therefore no DNA. White blood cells do contain DNA, but they remain as independent cells and don't "merge" with anything. The same situation applies with the microbes in your gut - they are separate organisms, and don't "merge" with the epithelial cells in our intestines to form some sort of bacteria-human hybrid.

@MattDMo Interesting. That means when one gets blood from another's body, then his blood cells contain two types of information. And if I get blood from several persons, then I would have several types of information in my blood cells. Does not it create any problem when it sees genome in body cells are not identical with genome in blood cells?

I've tried to determine what you are concerned about, place it in a more appropriate context, and answer a reformulated question. Could you please see if this does, in fact, address your concerns. If so, the whole question (and my answer) could be rephrased.

@David Thanks for your cooperation. I have tried my best to rephrase it. Have a look on it. Thanks once again.

@manetsus Fine. Have modified my answer accordingly.

Have you considered the term "alloantigen" which is not a very common one, to be found in the context of MHC. I nteresting to me that there are two alleles  of each gene in one body, and the antigens they both express seem to be identical. I haven't heard of "iso-antigens" - except for MHC.

My previous answer was to the original question which focused on red blood cells which do not contain DNA. Now the question has been revised to focus on tissue transplantation, where the cells do contain foreign DNA, my amended answer deals with a couple of the points raised, but only briefly with the question of identification.
Incorporation of foreign DNA into the human genome
It is extremely unlikely that any of the DNA from the tissue of the donor would be incorporated into the DNA of the cells of the recipient. The donor cells would have to be broken (i.e. die) to release the DNA, which is most likely to be degraded in the process. Even if it survived it would then have to be taken up by the host cells, which is unlikely as there is no specific mechanism to allow this. However if foreign DNA somehow got to the nucleus it would need specific machinery to be incorporated into the host DNA. This involves enzymes making staggered cuts in the foreign and host DNA to allow annealing and enzymes to ligate the two together. We know about this sort of thing because retroviruses and viruses that can exist in the genome in a latent state have specific mechanisms for doing this. It is unlikely to happen just by chance.
Even if foreign DNA did get incorporated, it still has to be in an environment that allows it to be expressed (appropriate promoters). A more likely possibility is insertion in a position that affects a host gene. This can result in uncontrolled division of cells, i.e. they become cancerous, and is a problem that has been encountered using viruses of the type mentioned to insert genes into genomes in gene therapy.
Do the differences in the DNA of transplanted tissue matter?
Obviously differences in the DNA of different individuals has an effect on the individual. It is genetic differences that cause people to differ in size, shape, features, hair colour etc. Oh, and some are girls and some are boys. But when the tissues and organs have finished developing it probably doesn't matter if a piece of transplanted liver is from a male or female donor. The genetic programme that causes sexual differentiation and function isn't the one being expressed in the adult liver. The genes that are being expressed are those for the enzymes the liver needs to play its metabolic role (too numerous to list), and if they work, they work, even if the proteins differ in amino acid sequence by the odd amino acid that doesn’t impair its function.
The problem of identification by DNA
I would have thought that this would not really be a problem. After all, if you want to take a DNA sample from a person you can do it with hair roots, white blood cells or scrapings from mouth skin. You wouldn't need to resort to liver biopsies and the like.
Doctor of Philosophy
Finally, I can see there is a general philosophical concern over who one is if one has tissue or organs from another donor, but until we have brain transplantation I’m not going to worry about that. (And when that comes, I won’t be answering questions on the subject.)


text:
How genetically similar are worker ants from the same colony?
I've been reading https://en.wikipedia.org/wiki/Ant and it says

If the egg is fertilised, the progeny will be female diploid; if not, it will be male haploid.

Since the males have only one set of chromosomes to pass on to the queen, all of their direct offspring (which can only be female) will contain all of their DNA. How similar is the DNA that the queen provides? Is there a high likelihood that there will be genetically identical individuals within a single colony, even if they were hatched at different times?

Relatedness of ants within a colony vary from species to species (as different species may use different mating systems) and from colony to colony. I will consider a basic (simplified) model of a honeybee colony and describe it a little bit to try to address your question.
Simplified Model of an ant colony
There is quite a lot of diversity in mating systems among ant lineages. See for example the amazing case described in Fournier et al. 2005 (which is quickly summarized at the end of this answer). I will assume a general and simplified model below.
In general, a queen can have several mates. The queen is storing the sperm of these males in her spermatheca. As you noted, the queen is diploid while the males are haploids. The queen will use the stored sperm for all of her life. Each egg that is fertilized will give rise to a worker. Although, a worker does not reproduce (in our simplified model), a worker is still considered a female for morphological reasons. At some point in the life of the colony, some larvea that could have become workers are fed with royal jelly and they will then develop into queen. These queens will fly away to mate with multiple males and make up a new colony. The queen also produce males. The males are haploids. The queen only uses her own gametes to make up a male.
Relatedness
In our simplified colony, a male has no father and has the same mother than any other male and any other worker. Two workers may or may not have the same father. Let's imagine to simplify the story that the queen mated with a single male so that all the workers have the same parents (they are sisters).

queen-worker: 1/2
worker-worker: 1/2

This relatedness decreases with the number of father. At the extreme when there are an infinite number of fathers, the relatedness between two workers drops down to 1/4.

queen-male: 1/2
male-male: 1
male-worker: 1/4

The calculation of relatedness is a little bit problematic when comparing individuals that differ in ploidy (queen - male comparison for example).
Consequences of these relatedness
The fact that the workers are more closely related to their sisters than to their brothers have been suggested to cause a queen-worker conflict for the sex-ratio. Indeed if workers are more closely related to their sisters than to their brothers we might think that they would tend to bias the sex-ratio of the colony toward more sisters to a degree that would not be optimal for the queen. The degree of relatedness between workers depends on the number of fathers. There more fathers there are, the lower is the relatedness among workers and the lower is the incentive to bias the sex-ratio. As a consequence, while the queen would wish a sex-ratio of 0.5, the workers will deviate this sex-ratio toward more workers with a strength that is decreasing with the number of father.
Personally, I have some trouble with these predictions (that I won't express here) but empirical evidences (Chapuisat et al. 1997; Passera et al. 2001) support that the sex-ratio differ depending on the number of fathers (and therefore on the worker - worker relatedness).

"At some point in the life of the colony, some larvea that could have become workers are fed with royal jelly and they will then develop into queen." Are you confusing this with bees, or do some or all ants use a specific foodstuff to make queens? All the sources I've found refer to differences in nutrition but make it sound like it can just be a matter of how much food the larvae get, not what kind.

Also, with one father shouldn't worker-worker relatedness be 3/4, because the males are haploid so workers share 100% of the genes they get from their father instead of 50%? And similarly male-male should be 1/2 because their mother is diploid; they all have half of her genetic material but don't all have the same half.


text:
Breeding Southern Right Whales Genetics
I don't know much about biology. I just like watching David Attenborough videos and this made me curious.
I just watched this video about breeding Southern Right Whales, and these two quotes puzzled me:
Quote 1 occurs at 1:54

"The males barge and jostle one another to reach her"

Quote 2 occurs at 3:51

"One coupling can flush out whatever preceded it, so it may not be the
  first male who succeeded in copulating who becomes a father it
  (will/would?) be the last."

Quote 1 suggests my first assumption.
Males compete to be the first to mate with a female
Quote 2 suggests that a male's chance of being a father is decreased each time a subsequent male copulates with the female. This leads me to my next assumption.
The last male to mate with the female has the best chance of being the father
Beyond what was said in the video, I just have a general assumption that the healthiest male (best genes) will mate first because he's faster, stronger, etc. So here is my third assumption.
The last male to mate is the male carrying the worst genes.
All together, this seems pretty bad for the species. I mean, if the worst genes are the ones most likely to get passed down, wouldn't that make the species evolve in a bad direction? So here is my conclusion.
The breeding habits of southern right whales are bad for the species.
Is this true? If so, does this occur in other species, and does it have a name? If not, where did I go wrong with my logic?
Thanks.

The keyword here is may in "it may not be the first". Most likely the first male will have the highest change. It is unlikely that all his semen is removed by the next and even if so, it might already be to late.


text:
Does the use of RNA as a primer affect the accuracy of DNA replication in E.coli?
DNA polymerases have proof-reading ability, but RNA polymerase does not. Does the use of RNA as a primer affect the accuracy of DNA replication in E.coli? Explain

E.coli use DNA polymerase for DNA replication too. Primase creates a short oligonucleotid (primer) in the start of string and DNA polymerase continues in work. RNA polymerase is using in synthesis of RNA molecules.


text:
Which of these versions of allopatric speciation is correct?
I'm confused with the illustrations of allopatric speciation. Here are two diagrams-

Which one of them is correct and why?
According to wikipedia the second figure is correct but I'd like to know why is it so, or why can't be the first one be right?
All I know about allopatric speciation is that it is a process of formation of new species from existing species in the following way-

A large ancestral population is firstly spatially divided into two subpopulation
Evolutionary forces act on the subpopulations
Eventually with large span of time reproductive isolation develops between them and finally lead to new species

According to my concept fig 1 is correct but I find the other diagram all over the internet.

For the millionth time, when asking homework questions, you must show your attempt at an answer. "Because I read it on Wikipedia" is not an attempt at answering. With all of the low-quality questions you ask, you are at risk of being question-banned on this site. PLEASE improve your questions.

@MattDMo I've added some information. I didn't write this before because it was not related to my question directly.

Both are correct. From Wikipedia, the causes of genetic change within each now-separate population are: (a) they become subjected to different selective pressures, (b) they independently undergo genetic drift, and (c) different mutations arise in the gene pools of the populations.
It is possible that factors a, b, and c cause the emergence of 2 new species -- or just 1 (which is possible considering that the original species probably is well-suited to its current habitat).


text:
Role of Intermediate Filaments in cell - cell signalling
A passage in my textbook mentions briefly that the role of intermediate filaments in the cytoskeleton is to enable cell to cell signalling by extending between special junctions and alowing cells to adhere to basement membrane
What does this mean?

There are desmosomes and gap junctions (cell-cell-contact), and hemidesmosomes (cell-basal membrane-contact) which enable a stable united cell structure. I'm not so aware with this topic, but I found some papers which may help you :)
Intermediate filament in cell architecture
Desmosomes and hemidesmosomes
Review on gap junctions
Blood-testis barrier and different cell-cell-contact structures


text:
Is it possible and how could it possible for plant to survive in naked space
I heard that there are fungi could survive on space station in the naked space. I want to know if any plant could be able to do the same
How many limitation of plant differ from fungi
And could it possible for them really grow with photosynthesis from the sun. At least growing out of space station which we may fed them with our carbon and water but not limited to only inside of our shell

Do you have a link to show that fungi can live in naked space?
From what I know, the space fungi are all living inside the space stations.

@GrahamChiu Sorry but I remember it wrong, it is lichen https://www.sciencedaily.com/releases/2012/06/120623145623.htm


text:
Cellulose Branching
I understand that humans cannot digest cellulose because there are no branches to break down the polysaccharide chain.
But why can cellulose not form branches?

Cellulose is, by definition, unbranched. If it is branched, it becomes another compound. This is like asking why blue-eyed people can't have brown eyes. If they did, they'd no longer be blue-eyed.

You misunderstand. It has nothing to do with branching. (And, as @MattDMo writes, you are attacking the problem from the wrong end.) Humans cannot digest cellulose because they do not have the enzymes needed to do so. These are called cellulases, which you can read about here. The problem seems to be one, not only of breaking the β(1→4) glucose linkage, but disrupting the higher-order structure formed by the interaction of individual cellulose chains.
Ruminants, that need to digest the cellulose in grass, also cannot produce cellulases, but they host bacteria to do the job for them in their rumen. Presumably if we humans needed to live on grass our stomach evolution would have followed a similar path.


text:
How is excess semen removed if ejaculation does not occur?
There are some attempts to answer the question that I found via cursory Google search, but none of them were appropriately sourced.
This site claims that they are "recycled like blood cells", but the blood cells are recycled using the spleen, and I don't think spermatozoa normally enter the blood stream at any point in time.
This other site contradicts the first site, and claims that they are removed from the body by "dripping" them, therefore expelling them in the normal urine stream.
What is the actual process through which semen is removed if ejaculation does not occur?

Well as far as my knowledge goes in this aspect..
If sperms are not ejaculated then they are simply reabsorbed by the epididymis and recycled.
I would say the first website you have linked up there is what is a more appropriate explanation.


text:
What is A in IgA?
What is the significance of letter A in immunoglobulinA?
What are the significance of other letters D, M , G, E in diffeternt types of antibodies?

The letter suffix in the name or abbreviation of an immunoglobulin specifies which type of "heavy chain" the immunoglobin contains. The heavy chain is the large polypeptide (amino acid chain) found in the antibody.  In mammals there are five different classes or types of heavy chains, and these types are given Greek letters to differentiate them.
As Wikipedia says,

The different suffixes of the antibody isotypes denote the different
  types of heavy chains the antibody contains, with each heavy chain
  class named alphabetically: α, γ, δ, ε, and μ. This gives rise to IgA,
  IgG, IgD, IgE, and IgM, respectively.

Thus the Ig suffix letter is the Roman letter corresponding to the equivalent Greek letter of the heavy chain that Ig contains.

Does the heavy chain has name A or it's an abbreviation?

For igA, the heavy chain is of type α (Greek letter alpha, not Roman A).

@mgkrebbs whoever named these proteins named the chains with similar greek letters for compatibility. I don't think they were named based on the chains they have. See the linked post. I think the answer there explains the possible origin of these names.


text:
Has Staphylococcus aureus ever been used against cancer?
Treating inoperable tumors with bacteria appears to be very effective, albeit being toxic to the patient as well. Has (live attenuated) Staphylococcus aureus ever been used against cancer? If the answer is yes, can you give me a link to some papers on this topic as well?

Amy sources to your claim?  I've never heard of using bacteria against cancer?!

@Christiaan I actually interviewed recently at a company that's doing just that. It's really interesting.

Is OP talking about Coley's toxins? http://www.cancerresearchuk.org/about-cancer/cancers-in-general/cancer-questions/coleys-toxins-cancer-treatment and Streptococcus pyogenes and Serratia marcescens are currently used, not Staph.


text:
Deducing amino acid sequence from a DNA sequence
The suggested answer to the question is the following: "M L S C D K S D Stop". I do not understand how they get that result.
The question is as follows:
An RNA polymerase transcribes the following DNA sequence, in the direction of the arrow. Which amino acid sequence will be generated?

Thanks in advance!

I get that, and the first ATG is at 5' CCA CC ATG TTA. I thought it always reads the code in triplets? Thats why that option doesn't make any sense to me.

@OLi4 The polymerase certainly does NOT search for a start codon to start transcription. The polymerase produces a mRNA with a 5' untranslated region before the start codon. However this question is not about RNA polymerase, its a theoretical question about the genetic code.

This is a deceptively and badly worded trick question. Your confusion is because it starts with a mention of RNA polymerase, which transcribes DNA into mRNA, but asks about the protein, which is produced by the translation of the mRNA on ribosomes.
The first step in solving the problem is asking what is the sequence of the mRNA produced by the transcription. The question doesn't actually say which strand is copied, but the 5'-end of the mRNA is synthesized first, so you can assume the mRNA is the complement of the bottom strand, which is copied. (The convention of direction presumably tells you the same thing). Thus, the mRNA has the sequence:

CCACCAUGUUA...

Now you need to go along the sequence (as a ribosome) looking for where to start translating. However the question doesn’t tell you whether this is a prokaryote or a eukaryote (unless you omitted to tell us). In order to solve the problem we have to assume it is a eukaryote where the ribosome normally scans along from the cap to the first AUG to initiate translation (the region italicized above):

AUG (ATG) = M
UUA (TTA) = L
etc

(If it were a prokaryote you’d need to look for a Shine and Dalgarno ribosome-binding site.)
You might wish to raise my criticisms with your instructor (although I doubt that he will thank you for doing so).


text:
Why I cannot find dendritic cells in blood smear?
According to many sources including Wikipedia, there are haematopoietic stem cell derived dendritic cells in the blood.

figure 1 - haematopoietic cell lines - ref

Despite of this, when I examine a blood smear, I cannot find dendritic cells and I did not find any blood smear example on the internet, which depicts dendritic cells.

figure 2 - blood smear cell lines - ref

Why is that?

I've identified both plasmacytoid and myeloid DCs (albeit at very low numbers) in PBMCs derived from whole blood of (presumably healthy) volunteers by flow, so they are there. I don't recall off the top of my head the exact numbers, but it was far less than 1% of PBMCs (dozens to hundreds of counts in a 1-2 million cell sample, IIRC), meaning an incredibly small proportion of overall cells in the blood. Therefore, the chances of seeing and correctly identifying them in a smear are rather low.

@MattDMo Does it look like this? https://www.google.hu/search?docid=pK94a0h-wQhUsM&bih=730&biw=1536&tbm=isch&tbs=simg:CAQSJgmQDCJQTlxphRoSCxCwjKcIGgAMCxCOrv4IGgAMIaSveGtIfsEI&sa=X&ved=0ahUKEwj-4LO8zqfMAhUIJpoKHZz0BUYQ2A4IGSgB#tbs=simg%3Am00&tbnid=kAwiUE5caYWUhM%3A&docid=pK94a0h-wQhUsM&tbm=isch&imgrc=kAwiUE5caYWUhM%3A It is extremely hard to find an image about them. In theory this is an activated mature DC moving from the skin to the lymph nodes. It appears to present antigens in the blood too. Actually I don't have deep knowledge about them right now, I just want to show an image to somebody.

@MattDMo According to this http://www.sciencedirect.com/science/article/pii/S0022175916300217?np=y normally about 0.5% of the WBC-s are some kind of DCs. Interesting. :D I probably confuse them with monocytes, and the image I linked is probably fake. Not sure yet.

This was by regular flow cytometry, so I wasn't taking images of them. All the images I've seen of DC in vivo are along the lines of these - the staining is somewhat diffuse because of all the ruffles and extensions. If you do a search for "mature dendritic cell SEM" you'll find a bunch of scanning electron microscopy images of the cells in 3D.

The dendritic cells are antigen presenting cells that process and present pathogens to the T Cells.
As such they are present in interfaces where foreign organisms are frequently present. Eg: Skin.
When these cells get activated i.e. come in contact with pathogens, they process them and move to lymph nodes to present the processed antigen.
Thus these immune cells do not circulate in blood once they reach the target tissue but reside in the tissues and found in lymph nodes on activation.
Further, from Kuby's Immunology:

Dendritic cells can be difficult to isolate because the conventional procedures for cell isolation tend to damage their long extensions. The development of isolation techniques that employ enzymes and gentler dispersion has facilitated isolation of these cells for study in vitro. - Kuby Immunology 5Ed. P.42
Since blood is the most accessible tissue for clinical studies, we set out to extend the findings that were reported in mouse blood to humans. However, when we tried to induce DC growth by adding GM-CSF to human blood, we identified actively proliferating DC aggregates only infrequently -
Proliferating Dendritic Cell Progenitors in Human Blood
By Nikolaus Romani, Stefan Gruner, et.al.

I need some references about the "do not circulate in blood" part. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809702/figure/fig02/

"conventional procedures for cell isolation tend to damage their long extensions" - I think this is about flow cytometry. I don't think that blood smear creation would damage their long extensions. E.g. sickle cells and reactive lymphocytes are not damaged by this procedure. According to my previous link DC-s in blood do not have such long extensions, they are not mature enough... I believe they can easily confused with other cells, and some of them are derived from monocytes.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Why do many people seem to prefer unhealthy compared to healthy foods?
I don't have any concrete statistics on this but many of us seem to love the taste of food that is unhealthy for us.
Over the centuries, wouldn't it have been a non negligible advantage to those who preferred (and hence ate) healthier food?
So, why don't most of us inherently find healthier food to also be tastier?
Apologies if this is a silly question or something that is frequently asked. I know very little about biology in general.

I blame cavemen and biochemists....

It's a very simple answer. "Unhealthy" foods, for example potato chips, sugary drinks, and other fatty, cheesy or sugary edible items, have only been around a few hundred (at most) years. In prehistoric times (before agriculture, when the primary source of food was hunting and gathering), when food was scarce, fatty and sugary foods would be of great importance. They would supply the body with large quantities of energy (a gramme of fat gives about 9 calories, a gramme of carbs gives around 4 calories). Since we survived mostly on fruits, vegetables, meat, and whatever roots we could find, something as energy rich as, say, a serving of deep fried cheese covered bacon would have sustained us for days. So eating anything with high calorific value, like a fat rich tuber would release 'feel-good' chemicals, like dopamine and serotonin, among others, which make us feel happy (dopamine is also released in response to hugs and accomplishing goals, serotonin is released, in very large quantities, during nicotine consumption).
Our body these days just isn't used to our relatively sedentary lifestyle with  guaranteed food. Our body still hoards fat like it did during our time as hunter-gatherers, and our body still secretes dopamine everytime we dig into a sumptuous serving of cake.
A couple of good sources:
http://www.ncbi.nlm.nih.gov/pubmed/8697046

Serotonin-releasing brain neurons are unique in that the amount of neurotransmitter they release is normally controlled by food intake: Carbohydrate consumption--acting via insulin secretion and the "plasma tryptophan ratio"--increases serotonin release; protein intake lacks this effect. This ability of neurons to couple neuronal signaling properties to food consumption is a link in the feedback mechanism that normally keeps carbohydrate and protein intakes more or less constant. However, serotonin release is also involved in such functions as sleep onset, pain sensitivity, blood pressure regulation, and control of the mood. Hence many patients learn to overeat carbohydrates (particularly snack foods, like potato chips or pastries, which are rich in carbohydrates and fats) to make themselves feel better. This tendency to use certain foods as though they were drugs is a frequent cause of weight gain, and can also be seen in patients who become fat when exposed to stress, or in women with premenstrual syndrome, or in patients with "winter depression," or in people who are attempting to give up smoking. (Nicotine, like dietary carbohydrates, increases brain serotonin secretion; nicotine withdrawal has the opposite effect.)

http://www.scientificamerican.com/article/addicted-to-fat-eating/

Like many pleasurable behaviors—including sex and drug use—eating can trigger the release of dopamine, a feel-good neurotransmitter in the brain. This internal chemical reward, in turn, increases the likelihood that the associated action will eventually become habitual through positive reinforcement conditioning.

http://www.ncbi.nlm.nih.gov/pubmed/8697045

There is an intimate relationship between nutritional intake (eating) and serotonin activity. ...
Traditionally, serotonin has been linked to the macronutrient carbohydrate via the intermediary step of plasma amino acid ratios.

TL;DR:
You would have starved if you didn't eat fatty foods back before we had food so readily available, so your body automatically stocks up in case you ever run out.
Watch this video for more information:
Why our brains love junk food

You had me at "deep fried cheese covered bacon"

@MattDMo deep fried cheese covered bacon is a health food, though - right?

http://theawkwardyeti.com/comic/salad/

The primary source of animal fat was probably the marrow inside animal long bones, which was inaccessible without tools.  So, it's an evolutionary advantage to like animal fat.

@MalharKhushu It would be great if you can add a citation. Youtube videos are fine as a learning/teaching tool but are not, by themselves, strong references. The video does cite a PNAS paper and some other references. Can you please add those references (and others, like cross references from the paper, if necessary) along with the video link?

Great reply, Malhar Khushu!
One additional point... In reference to the cal/g energy densities of fats and carbohydrates, Alcoholism may be positively influenced by the 7cal/g density of ethanol!!! Yay science

sorry for a not scientific answer, this is general knowledge.
you can try to search for proofs you need.
there are several different types of unhealthy food and the resulting addiction/desire to eat them. the unhealthy food tricks the brain.
cholesterol/carbohydrates:
the brain is built from cholesterol partially.
the brain can make cholesterol from carbohydrates.
so so-called "unhealthy" food it is good for you kind of. unless you are sick.
so some times a moderate amount of cholesterol is good for you in general, the brain can make its own cholesterol. cholesterol supports memory.
cholesterol is bad if you have an internal wound like an inflammation, maybe of blood vessels or heart arteries. cholesterol made by the liver usually patches the would holes. later to be fixed using protein(if there is also vitamin c). however, if there is an inflammation going and there is a wound filled with cholesterol, new cholesterol will stick to already existing cholesterol. and clog arteries worse.
depriving the brain of cholesterol deprives memory. because neurons make vesicles - like small soap bubbles filled with dopamine that marginally pre-excite neurons. those vesicles are made of cholesterol. if you ingest something that dissolves cholesterol for a long time like a statin or antioxidant you will lose memory and lose the ability to form memory.
also, the brain is energy hungry, so it brain gets activated on high energy foods. however, if fructose or sugar is ingested with food. a large percent of it is stored into fat. using insulin that is made from sugar.
chemical foods:
like things that make the brain make neurotransmitters like acids, ions, and sweet poisons are bad for you.
they trick the brain and stress the brain. things like coffee and sugar and sodium glutamate. coffee makes adrenaline and ticks you to release saved energy.
sugar acts on dopamine center and tricks you think you do something good even if it is bad. sugar also gives you some glucose. however, all dopamine from sugar is consumed immediately.
some other things dopamine-making:
the brain seeks dopamine, and while on dopamine the brain does not think rather acts as before in an automatic manner. like, do the same thing again. also if the situation not as before the brain will mistake. sometimes brain confuses one thing to another. because they both make the same level of result. one real one fake. the fake quicker and you need to do it again and again. so people fall for a quicker and easier way. the solution is to delay time, to prevent instant action and try to solve basic body needs like rest and food


text:
Voltage sensitive dyes technique: What is the underlying measure?
I just discovered voltage sensitive dyes technique: first of all what imaging techniques do we use? And I have seen that figures are labeled with ΔF/F0, what does it stands for?

As for imaging method, many kinds of fluorescence microscopes can been used (two-photon, confocal, widefield, etc.). Depends what spatial scale you're interested in (e.g. subcellular compartments vs. large patches of cortex) and the context of the measurements (e.g. cell culture vs. behaving animals).

Since these are fluorescent dyes, the most likely method of use is with some sort of fluorescent (likely confocal) microscope. The various types of dyes have different hydrophobic tails, so they target different types of membranes (plasma membrane, mitochondrial membranes, etc.). An excitatory light source (typically a laser, with a single wavelength) is applied to the sample, and the $F_0$ or baseline fluorescence intensity at time zero is measured. When an event happens, such as the contraction of a muscle, the $\Delta F$ or change in fluorescence intensity is measured. This difference is then divided by the baseline, and called the fractional fluorescence (${\Delta F}/{F_0}$). It is plotted like so:

Bu G et al. Biophys J. 2009 Mar 18;96(6):2532-46.


text:
How big advantage had a trait have to bring to evolve in the human evolution?
Yes, I've heard that we have evolved from the common ancestor with primates as intesively, as the chimpanzees. Sometimes I read about some enormously complex traits, evolutionary psychologists think have evolved in humans, such like religion, night owls or art (which don't seem to require a specific complex mutation). On the other hand we still grow many unnecessary organs, so I really wonder: What is the percentage advantage a trait had to provide to humans (so that no other species share it) to actually evolve continuously?
OR (I'm not sure if it can be calculated generally) I can get by with this question: What is the correct formula how to calculate the average probability of survival a trait had to increase to preserve over some time (with the gene expression calculated in it)?

"we still grow many unnecessary organs" - huh? Which organs are unnecessary? The liver? Kidneys? Stomach?

I think a clear way to rephrase this question would be "How beneficial a mutation needs to be to behave really differently from neutral mutations?". I am answering to this question.
Neutral mutations and nearly neutral mutations
The probability of fixation of a new neutral mutation is $P_{neutral}=\frac{1}{2N}$, where $N$ is the population size. An intuitive way to understand why this is true is that, after an infinite amount of time (constant population size and in absence of speciation), the whole population will necessarily descend from a single individual. In absence of selection pressure every single individual has the same probability to be the ancestor. As a fraction of $\frac{1}{2N}$ of the population is carrying the mutant allele when it first occur, then the probability that his allele reaches fixation is $\frac{1}{2N}$. In fact, this result can be generalize to say that the probability of fixation of a neutral mutation present at frequency $p$ at a given time in the population has a probability $P_{neutral}=p$ to get fixed.
Given the selection coefficient $s$, a good approximation is that whenever $2Ns<<1$, then the probability of fixation is essentially not different from $P_{neutral}$.
This qualitative boundary ($2Ns<<1$ or $2Ns>>1$) is the boundary you were interested in. In your post you talk about "percentage advantage". This percentage advantage is just $s\cdot 100$.
Beneficial mutations
For "significantly" beneficial mutations, a good approximation to the probability of fixation of a newly arisen mutation given $s$ and $N$ is
$$\frac{1-e^{-s}}{1-e^{-2Ns}}$$
Source of information
Your question shows a few misunderstanding and is nested within the field of population genetics. Plus, in absence of good understanding equations and just vague symbols. I recommend that you have a look at an introductory source of information in population genetics. You will find recommendation of books in population genetics here. For a complete and relatively accessible (might still be a bit complicated) introduction to population genetics, I would recommend  Gillespie's Population Genetics: A Concise Guide for you. This book will so offer proofs for the equations I gave you above.

Sorry, I don't understand what does the N mean. But thanks for rewriting the question. And about the neutral mutation: Shouldn't the probability be just random? There is nothing else we can say about an individual with a neutral mutation, except from he has something that doesn't affect his fitnes.

Sorry, I forgot to indicate what $N$ means. $N$ is the population size. To make it more general $N$ should be replaced with the effective population size $Ne$.

You said Shouldn't the probability be just random?. This sentence makes no sense. You either don't understand the definition of "probability" or of "random" (or both). If a probability is different from 0 or 1, then there is randomness (=stochasticity). Yes, the probability of fixation of a mutation (neutral or not) is subject to certain level of stochasticity in finite populations (it is the very nature of genetic drift at play).

Yeah, sorry, I meant probability 0,5. It's the same probability that the bearer of my gene is a good one, as that he is a looser (comparing to the rest of the population). So the equation should somehow work only for population of 1 individual.

I added an intuitive explanation for why the probability of fixation of a newly arisen neutral mutation is $/frac{1}{2N}$. This equation holds true for a population of any size (however should be more correct to talk about "effective population size" but I did not want to add another concept you might not know of).


text:
What happens to the brain during sleep versus unconsciousness?
How does being unconsciousness differ from being asleep and whether it causes breaks in consciousness?

I'd recommend you to formulate the question on the basis of the mechanisms stopping the brain to control the body during dreams.

sounds like a great question for an anesthesiologist


text:
What information do bipolar cells encode?
Short version: I don't see what information on-centre bipolar cells are actually capturing.
Longer:
Actually, the question could be extended to on-centre retinal cells as well, but I'll focus on bipolar cells for now.
On-centre cells will fire when a spot of light hits the centre of their receptive fields and doesn't touch their surround, off-centres are the reverse (light in the centre is inhibitory, surround is excitatory).
Here's an over-simplified illustration that I made, red is hyperpolarized (excited), blue is hypopolarized (inhibited). Let's pretend that horizontal cell effects have already happened, and ignoring overlapping receptive fields for simplicity.

So my question is, if off-centre cells would be useful to highlight contrasts like edges (as I understand it, though eventually edges get detected further down in the complex cells), what are on-centre bipolar cells used for?
From my perspective it looks like they'd be good for single points in light which are small enough to hit the small number of rods that encompass the centre of a receptive field but not hit the surround. But when would this ever be the case? The centre of a receptive field would be incredibly tiny given the large number of rods in say the fovea (though, granted, maybe on-centre cells become more important in the periphery?).
One source:
http://thebrain.mcgill.ca/flash/a/a_02/a_02_cl/a_02_cl_vis/a_02_cl_vis.html

Recent nature neuroscience review on bipolar cells says that bipolar cells are classified into 13 (12 cone bipolar + 1 rod bipolar) different types.
Depending on the polarity of their light response, bipolar cells can be grouped into ON and OFF cells.
Answering your question, what are on bipolar cells used for ? ON bipolar cells predominantly depolarize at light-onset and stratify in the Inner Plexiform layer (ON).
Considering rod - rod bipolar path way: Eyes are sensitive to very low light level. Imagine you are seeing a star during night. As the number of photon reaching retinal layer will be very small. It reaches order of few rod photo receptors (receptive field) & then converge to rod bipolar cell for efficient signal processing. It makes vision at dim light really interesting and promising.

In case with central surround organization, It is one of the classical stimulus study which has been explored further in detail with various complex stimuli.
I recommend you to go through The Neuronal Organization of the Retina for more details.
I am absolute beginner in visual neuroscience field. Please correct me if am wrong.
-Sathish


text:
True or False: Dideoxynucleotide sequence analysis Question
True or false: Dideoxynucleotide sequence analysis is a template-directed method that makes use of chain terminators that stop DNA synthesis because they lack a 2'OH group.
The answer is false.
However I thought it would be true because dideoxynucleotide sequences stop DNA synthesis due to a lack of an OH group on a 2' and 3' group. What have I misunderstood?

you probably want to edit your question given that it's for homework...check out this link to understand how we handle homework questions on this site... http://biology.stackexchange.com/help/homework

Instead of posting here you should look up the structures of deoxy- and dideoxy-ribose, and that of the phospho-diester bond in DNA. (Learning them would be good.). Then the answer to the question will become obvious to you and you will have learnt something.

It is false, because DNA synthesis occurs via DNA polymerase,5' to 3'
By hydrolyzing activated nucleotides together. This occurs by nucleophilic attack of 3'-OH, of the last nucleotide in sequence, on alpha phosphate of a corresponding nucleotide triphosphates.

You should explicitly state that the 2' OH does not matter in this case, because all DNA nucleotides are missing the 2' OH, it's not needed for DNA synthesis and wouldn't affect chain termination.


text:
What is the most stable globular protein?
What is the most thermodynamically stable globular protein?
I am looking for a small (ideally less than 50kDa) soluble globular protein motif which folds easily/reliably and is known to be extremely stable and resistant to unfolding once folded.  Also very resistant to proteolysis and degradation.
Any ideas?

ubitquitin is very stable, you could double check, but my supervisor was saying that people initially thought it wasn't a protein because it was so heat resistant

RNAse A was used to prove that a protein's structural information was stored in its sequence by unfolding it and refolding it, so it must be pretty stable. I've also worked with Bee Venom PLA2, which has 5 disulfide bonds. It's so stable, I've left solutions out on the bench over the weekend and the activity wasn't harmed at all. I've conjugated the protein with peptides and/or oligosaccharides with minimal activity loss. I've iodinated the protein under harsh conditions and retained 25% activity.

After I left the lab, another student has been able to pass Bee Venom PLA2 through an HPLC column with an acetonitrile and dilute TFA gradient ( the same kind you'd use for small molecules ) and recover the enzyme with full activity. It's really stable. As for MOST stable, that's probably a thermodynamics problem. These are just my anecdotal experiences with a very stable enzyme.


text:
Spatial dimensions for an animal
I'm reading a review paper. They say:

The position of an object in head-centered coordinates (that is, relative to an animal's head) can be defined along three axes: the medio-lateral (radial) axis, the rostro-caudal (horizontal) axis and the dorso-central (vertical) axis.

I'm having a little bit of difficulty understanding this coordinate system as the paper doesn't provide a picture. Usually I would think of the three axis as an x-y-z coordinate system where the rat's head is the "origin" (from a mathematical standpoint), but the terminology here seems to be a bit different, so I'd like to understand from a biologist's point-of-view how these three axes are drawn relative from a rat's head.
Paper can be found here: http://www.nature.com/nrn/journal/v9/n8/full/nrn2411.html (bottom of page 602)

@Remi.b Thank you for the edits and I have included a link to the paper.

Rereading the quote, I realize that in parenthesis, the common meaning of the three axes are indicated. Are the terms "radial", "horizontal" and "vertical" unclear to you in this context?

@Remi Yes they are unclear, specifically they're unclear to me what they referring to relative to a rat's head (e.g. is horizontal axis from the rat's head through it's body, or is it perpendicular to the body through the head? If it's the latter, then what is the axis through the rat's body called?, etc.)

Wikipedia has a quite didactic article on this: https://en.wikipedia.org/wiki/Anatomical_terms_of_location#Axes
These terms are complementary with a mathematical coordinate system: if you are describing a system of axis for a cylinder, you will need to specify that (e.g.) $z$ is along its symmetry axis, here you will say that $z$ is along the rostro-caudal (or antero-posterior) axis. Also, in biology, axes do not have to be straight lines, see the neuraxis:

The so called horizontal axis (rosto-caudal) is parallel to the body of the rat.  Vertical is just vertical when the rat is in its normal standing position and medio-lateral is horizonral and perpendicular to the rat's body. The head is the origin.