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Why do mitochondria waste energy?
In a mitochondria, it makes ATP by using energy from NADH and FADH2 electron to pump H+ into the inter-membrane space then use the ATP synthase to bring the H+ back into the matrix while using the proton motive force to create ATP.
My question here is, why does mitochondria do this, I mean, in terms of energy I think it is a waste of energy. For example using energy to put water on the top, then generating energy by making to water come down should make some unneeded energy loss.

Welcome to Biology SE! The answer to this question lies in the fact that, it would only be a waste if the mitochondria did not break even. Which it does, it uses energy to produce energy. Therefore, it isn't a waste

Thank you for your answer! What I meant to say was that, for example, let's say that you use a water power plant to make electricity. Then use that electricity(energy) to pump water high so that you can use the water power plant to make electricity(energy). Each time you do that, you lose bits of energy, until you have no energy left. In terms of physics, it's known that when you transfer energy from A to B, you cannot transfer 100% of A's energy to B. You must lose some through heat, friction or whatever.

You are picturing the system as closed one. The cell by no means is a closed system. You convert, nutrients(glucose) into energy. In your analogy, the power plant should have an external source of water providing the basic minimum to drive this pumping of water so that it can produce more energy. Then it is an almost proper analogy.

So what your saying is that, by pumping H+ in and out of the intermembrane, your creating additional energy? I don't think this true... Then, where is the extra energy coming from??

I did not say that. Take a look at this image: https://en.wikipedia.org/wiki/Cellular_respiration#/media/File:CellRespiration.svg and article https://en.wikipedia.org/wiki/Cellular_respiration#Citric_acid_cycle

@KoustavPal — Please do as it says and do not use the comment facility to answer questions.

Could you please explain in chemical / thermodynamic terms where you think energy is being wasted? When you talk about "the energy from NADH" what you mean is the Gibbs free energy change when NADH is oxidized to NAD+ in the electron transport chain. When we talk about energy being wasted in biochemical reactions we usually mean that the free energy lost in the reaction is in a form (usually as heat)  that does not benefit the cell (e.g. by the production of ATP from ADP). So, where do you think this occurs? Are you sure you don't mean why is the method of generating ATP the way it is?

I guess the OP is asking - "why pump H+ into the intermembrane space and then harvest it when H+ is on its way back. Why not directly?" This is what I could make out from the question!

This question is actually very reasonable, and your premise is not wrong.
Certainly it's true that some potential energy is wasted in the process of creating the proton gradient (when electrons are transferred from NADH to O2) and then using the proton gradient to create ATP (by ATP synthase). And you're right, it would be much more efficient to somehow link NADH oxidation to ATP synthesis more directly. Physically, this is trivially true (and it's also true for every other series of reactions).
The problem is that biochemically, it's completely unclear how to actually do this! In fact, there was an enormous mystery about this in the field for a very long time. It was known that somehow electrons were transferred to oxygen, and that this was linked to ATP synthesis, but no one knew how the energy was transferred. People postulated that there was another high energy intermediate such as ATP, but no one was able to find such a molecule. The current theory, known as the chemiosmotic theory, was proposed in 1961 and eventually won Peter Mitchell the nobel prize (https://en.wikipedia.org/wiki/Chemiosmosis#The_chemiosmotic_theory).
If you want to take the water analogy, it's as if biology just doesn't have access to a water wheel to generate energy directly from the flowing water. But it has something that can generate electricity from water falling to the ground. So it pumps up the water, uses the tools it has to generate electricity, and accepts whatever small thermodynamic loss is associated. This is a common motif -- there simply aren't biological molecules that can catalyze every single possible chemical reaction.

This answer is incorrect in accepting the poster’s premise that the two-step process wastes energy compared with a one-step process. The Gibbs free energy change for the reaction Xred +  Yox + ADP + Pi → Xox + Yred + ATP is exactly the same as if one adds in the energy change of establishing a proton gradient on the left and an extra reaction exacty reversing this on the right. There is, of course, energy lost as heat in the overall process — complete efficiency is impossible, and one needs this to drive the oxidation of NADH (as with any other reaction or reaction series).

I disagree. For instance, consider proton leak across the membrane.

I suggest that leakage per se through the lipid bilayer is insignificant, and that which does occur is regulated and used to maintain the basal metabolic rate of the organism. In any case the key question is waste, and thus whether a direct coupling mechanism would be able to convert more of the free energy to ATP. (No space to cover this in my last comment.) The problem with direct coupling is you can only release energy in ATP-size chunks — so in the real world there is a loss (the poster would call it a waste) in any case. Use of the electrochemical gradient may even be more flexible.

I don't dispute that there are other reasons why the proton gradient is incredibly useful. That would be a good alternative answer.

I may add one later in the week when I have time. But that really requires changing the question from why? to does? Some people may not like that.

Its because NADH is a powerful reducing agent. If you leave high concentrations of NADH in the cell, it would actually wreak havoc on the cell.
This is actually the reason why peroxisomes just remove FADH2s because they find no use for the extra energy and simply remove it.
So heres the simple answer. Energy is not always a good thing, because stability also matters. ATP is simply a good way to store and convert such energy.

Thank you. Now I understand. Also after reading your answer I realized that lots of enzymes and stuff needs ATP as an energy source, which means that converting all the energy to ATP(although that might lose some energy) will be easier

This is nonsense. Mitochondria do NOT waste energy in the sense the questioner implied, but was unable to explain in response to my comment. Certainly not all of the free energy change is captured as ATP, but that's no different from anaerobic glycolysis. If there is sufficient ATP in the cell this decreases the reduction of NAD by regulating the relevant  metabolic pathways.

@David what I took from the question was that why would mitochondrias not use NADH directly, as it does indeed has more free energy. Is it nonsense that NADH is a reducing agent, that it would reduce oxygens when not coupled to ATP synthesis and produce hydrogen peroxide?

First, the premise of the question is incorrect, so any answer that accepts it is nonsense. Second there is an equilibrium between NAD and NADH in cells, and the reductive power of NADH can only be used in enzyme reactions that take the reaction over the activation energy barrier that prevents spontaneous reaction. Third the conversation of chemical energy into the electro chemical potential is one of the most sublime and beautiful things in biological chemistry. An answer that regards it as a device for preventing hydrogen peroxide formation is nonsense.

So you're telling me that by pointing out what would happen in case of the questioners premise was the case, that makes it nonsense? Equilibrium shouldn't be the case since I've made it clear if it was in high concentration, which would be the case of questioner's incorrect premise. So an answer that's not practical but points out what the questioner is not seeing is nonsense? There are a lot of nonsense out there but, I don't think someone else's beauty should matter in making someone else get out of their loophole?


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Heteroduplex and Products of cleavage of Holliday Junction (Resolution)
In homologous recombination (Holliday model), the last process i.e resolution can occur in two ways (horizontl and vertical cuts) leading to formation of either "splice" or crossover products or "patch" or non-crossovers product (as shown in the image).
The two possible products confuse me with what are crossovers. I could not understand why the "patch" product (Fig. (g) in the image) is called a non-crossover. Is it because one strand of both the homologous helices are same?
Also please do explain what is the hetero-duplex in this model?

Hello @SanjuktaGhosh.
My question did come out to be a duplicate. My apologies.
The question you linked is exactly what I wanted to know. I read your answer to the same. But I still couldn't understand the concept. Can you please elaborate on the complimentary part?
Thank you.

Yeah. I'll. Give me some time. I'll elaborate as soon as I have some time.

I'm done explaining my answer you may go through it now.

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What is the use of an antibody that is non-neutralizing?
When we generally speak of the immune response to viral infections, we talk of neutralising antibodies. These are antibodies that can neutralise the effect of the virus and reduce its load.
My question is, what do the rest of the antibodies produced, which are not neutralising, even do?
Is it a failure of the immune response of the body to produce antibodies that are not neutralising? But isn't binding enough for opsonisation?
How is 'neutralising' even defined? Are such antibodies neutralising just based on binding (since I assume neutralisation assays are in-vitro) or do even these antibodies require downstream antibody effector mechanisms like complement, opsonisation, ADCC etc. for neutralisation?

Which antibodies do you mean with "not neutralizing"? The ones which are generated in the process of making highly specific antibodies in the process which do not fit or the majority of antibodies which are always present in the circulation?

@Chris I dont know. I just assumed that if some antibodies are called neutralising antibodies, the others must be non-neutralising. I know, not a safe assumption, but still...

Ok , what is your knowledge about antibody maturation?

@Chris I know that the activated B-cell undergoes somatic hypermutation in the germinal centre, followed by selection of better ones by FDCs

The term "neutralizing" depends on context. In virology, it generally (not always) means it prevents the virus from binding to its receptor(s) and getting its genetic material inside the now-infected cell. Other antibodies can bind other epitopes besides the sites of binding between capsid and receptor (or enveloping membrane and receptor), yet still contribute to the immune response. Such antibodies are often opsonizing. Still more antibodies are just ineffective, a byproduct of the antibody maturation process.

Are there neutralising antibodies elsewhere? I mean, in a context other than virology?

@Polisetty sure. One example is in enzyme replacement therapy, where patients genetically lacking an enzyme in a metabolic pathway can have it replaced by injecting recombinant protein into the bloodstream. These proteins have a certain glycosylation pattern, such as high levels of terminal mannose-6-phosphate residues, and they bind the M6P receptor on target cells and are internalized. Since the injected protein is foreign to the patient's immune system, they can raise a variety of antibody responses against it. A neutralizing antibody could bind to the protein's active site, for example,

and prevent the enzyme from catalyzing its reaction. Another response, which is sometimes called neutralizing, has antibodies binding the M6P residues and preventing the protein from binding the M6P receptor. You can read about other neutralizing responses here. Typically they are discussed in the context of virology, but the diphtheria antitoxin antibody response is another good example of a non-viral response.

"Neutralizing" is not a general concept; it's context-dependent.  Most often (in virology anyway) it means that the antibodies, by themselves in a tissue culture plate, can prevent infection of the cells by the virus. Many antibodies that are "non-neutralizing" in tissue culture are probably protective in the animal, in the context of complement and phagocytic cells and so on.
That said, there's no reason why antibodies should be protective, let alone neutralizing.  Antibodies don't arise in a guided manner with foreknowledge; antibody development is driven by physical interactions between the antibody and its binding partner. If they happen to arise to something irrelevant -- an internal protein of a virus, or a pollen grain, perhaps -- then they can still be driven through priming and development and maturation and still be functionally useless, or even harmful.
On top of that, of course it would be beneficial for pathogens to be resistant to antibodies, and at least a few have evolved this ability, so for those pathogens many antibodies would be non-neutralizing and non-protective.

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Animals walking backward?
Have you ever noticed that we humans can walk forward and backward but animals don't walk backwards?I guess this is true with most of the animals.What is the reason behind this?

Most animals can walk backwards if they really want to, or if you make them. The reason they, and we, tend not to walk backwards most of the time is that most animals and people don't have eyes in the back of their heads, and would risk running into things or falling off cliffs. You might try walking backwards all day and see what is the result, but please do not hold me liable if you end up in hospital.

I'm voting to close this question as off-topic because it's based on a false premise.

Sorry but I never noticed them do so.Anyways thank you

Your premise is incorrect other animals can and do walk backwards. Like humans, other animals do most of their walking forward both for biomechanical reasons and for the obvious reason that it is easier to see where you are going when walking forward.


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Wolf or Coyote?
I took the following pictures in the Yellowstone National Park of a Coyote-like animal. However, when comparing with pictures from the Internet, I see also quite some similarities with a grey wolf. So my question: Is this really a coyote?

Note that these two species have recently formed a hybrid as well: https://en.wikipedia.org/wiki/Coywolf

PBS did a documentary about coywolves: 53 minute video

Related: https://biology.stackexchange.com/questions/93010/did-my-wildlife-camera-take-pictures-of-coyotes

It's a coyote - I think it's too slender for a wolf and has pointed ears...


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Sources of Mutations
I'm looking for a reference that gives some information quantifying sources of mutations that occur within cells. These can be general, but I'm interested in some percentage of mutations caused by external vs internal sources (like mutagens vs replication errors).

This is going to strongly depend on the cell type, where it's located in the body, the type of organism, etc. Are you interested in looking at cancer, which occurs in pretty much all cell types, or heredity, in which the mutations must occur in the germ cells, or what?

There is an issue of epistemology when talking about the "sources of mutations". The question makes little sense and you should rather be asking about the "factors causing variation in mutation rates".

See this: http://dx.doi.org/10.1038/nature12477

An extensive collection of the various mutation rates (from which you could reverse-engineer their fraction on the total share of mutations):
http://www.bionumbers.hms.harvard.edu/search.aspx?log=y&task=searchbytrmorg&trm=mutations&org=&rpp=100

cool site I'll take a look.

I actually found this in the following paper:
http://science.sciencemag.org/content/348/6237/880.full
This group shows estimated governing forces in mutation incidence by tissue types.


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Evidence of condition-dependent sex-allocation in regards to humans
Coming from zero background in biology, I am looking for expert opinion on evidence regarding Trivers-Willard hypothesis (1973) and humans.
In short the hypothesis states that
if

"Condition" of offspring during their whole life are correlated
to that of their mother during pregnancy
Males have better on average better reproductive success (more genes in next generation) than female when in "good condition", and vice versa if you compare male/females in "bad condition".
Females objective is "eventual reproductive success" down the
generations.

Then it makes sense for females to vary sex ratio, more males when in "good condition" and more females when in "bad condition".
I think it is safe to say that plenty of evidence exists on assumption one. The second assumption seems more nuance in todays environment, but one would imagine that during most human history it does hold true. On the third one I think is safe to assume it is true based on the theory of evolution by natural selection.
Any (rigorous) reference (articles, researchers, journals) or comments would be superb!
Reported association that I am already aware of are:

Reduced gender ratio at times of war and famine (Ansari-Lari & Saadat, 2002; Song, 2012; Valente, 2015) and after natural disasters (Fukuda et al. 1998).
Darwin (Descent of man); Norberg, 2004; Almond & Edlund, (2007); Hamoudi & Nobles, (2014) divorce or "unmarriedness" correlated with lowered gende ratio.
Negative association between parents age and gender-ratio,  Jacobsen, Møller, & Mouritsen, (1999).

Have you looked at http://www.ncbi.nlm.nih.gov/pubmed/?term=trivers-willard+human+%22sex+ratio%22 ? -  although  see @Remi.b's comments about statistical issues ...

Yes, I've looked around but have not found anything that seems to settle the debate. But most things I find point towards the same direction as Trivers-Willard. For example: http://humrep.oxfordjournals.org/content/13/8/2321.short

Interestingly Darwin had spotted a pattern: excess of male over female births is less when they are illegitimate than when legitimate - The Descent of Man

@snoram Be sure there has been a lot of work on the evolution of sex-ratio since Darwin made this claim. You could start with West and Sheldon 2002 for a review but you will very likely have to start with a very introductory course to evolutionary biology (such as Understanding Evolution for example) as you were unfamiliar with the term 'fitness'.

The paper you link to does not mentions humans specifically, but they state "the extent to which data on mammals fit this prediction is disputed". I wonder how much that has changes since 2002.

I am not aware of any such evidence in humans but I know little about this literature. If you happen to have data showing that, then it would probably be a relatively big thing! Below is a series of comments that might be of interest.
Evidence from Hyena
The evolution of the sex-ratio variation in hyena have been quite extensively studied. This very short article (not peer-reviewed) cite a number of key papers on the subject.
Logic behind the second assumption
In case clarification is needed. The variance in fitness is indeed often higher in males than in females. The reason is that females (by definition) produce the larger gametes, the one that don't leave the body and therefore often pay a much higher cost when reproducing than males do. As such, females are the limiting factors. As a consequence, males compete a lot to access females and "good males" receive a lot of mating opportunities while "bad males" receive little mating opportunity causing the higher variance in fitness among males than among females.
Statistics
IMHO, there is a tradition of horrible statistics when dealing with human sex-ratio data. It is particularly the case as these papers are often published in journals where reviewer have little knowledge in statistics (e.g. medicine). Typically, "windowing" data is generally a very bad idea and previous papers in the field have reported very bad interpretation from data due to cherry picking specific ways to classify observations. Please be cautious in your statistical analysis!
About the post
The formulation of the hypothesis is clear enough but some sentences are misleading

it makes "natural selection" sense for females to vary sex ratio`

This sentence sounds very wrong. You should rather say "females that are able to vary the sex-ratio among their offspring will be have a higher fitness".
Note that I said "among their offspring" because while this would cause variation in sex-ratio in the population, genotypes are selected based on their ability to vary the sex-ratio among their offspring and not in the population. In fact, any given individual, would appreciate if all the other would produce the exact opposite sex-ratio than the one they actually produce among their offspring.

better chance of reproductive success

This sentence a little clumsy as well and should be replaced with higher fitness

Great. Thanks! But not sure I understand your last comment "replaced with higher fitness". The second assumption (as I understand) is that at some point on the "fitness scale" males start to have a reproductive advantage over females.

You are misusing the terms "fitness" and "reproductive success". reproductive success is the realized number of offspring of an individual for a chosen duration (often the whole life). Fitness is a function of survival and reproductive fitness and is generally defined as (but might differ slightly from one model to another) the expected lifetime reproductive fitness of an individual. Therefore "Better chance of reproductive success" translate into "higher fitness" and we usually use this expression.

Fitness just means good health. Agreed? (I checked the dictionary). By saying "better chance of reproductive success" I mean exactly higher expected number of offspring.  Good health causes "Better chance of reproductive success" not the other way around.

You are getting confused with the use of the term fitness in the sense physical fitness and in the sense "biological fitness" (which is just termed "fitness").  In evolution, "fitness" does not mean "good health". In evolutionary biology we sometimes talk about "overall health" of an organism (which would mean something like "physical fitness") as an extremely multivariate trait that is eventually (but not necessarily) a good proxy for fitness.

I will do some small edits to my original posts based on your comments. But to clear I never used the word "fitness" (nor do Trivers and Williard) and use instead "condition" for something like "physical fitness".


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Modeling population growth - Variance
I've been studing population growth models, but there's something I can not find that's fustrating. That's a formula for the variance in population growth. I know that other models can be aplied, but I want to start with the simplest case.
Let's assume a population is growing exponentially as defined by:
$N(t) = N(0)W^{t}$
The parameters $W$(absolute fitness in my definition) tell us that the time for division (if the species reproduces binarally) is given by an exponential distribution with $\lambda = \dfrac{\ln W}{\ln 2}$
So I see a model for $N(t)$ and a random variable associated with this model. What is the pdf, expected value and variance of $N(t)$? The expected value I expect it to be given by the first equation (or the value to be the same) but what about the variance?

The exponential growth without noise is the deterministic approximation. Now knowing that this means that the time for division is given by an exponential distribution, what is the variance in the population size?

My bad, I didn't read the question right. Removing my embarrassing comment.

Basically, you have a Poisson process where the rate doubles whenever there's a (birth) event. The mean grows exponentially, and the variance should be overdispersed since it's a mixture of Poisson...

Not exactly...   Because whenever there's a birth the time for the birth from the individuals that did not divide is the same as before minus the time of birth... But there is also the two new individuals...

By the way, as my final interest is the frequency of this in a larger population, I think diffusion theory, and Kolgomorov forward and backward equations might help... I just don't know enough to use it

Sorry, I meant increased by one, not double. Poisson process where rate grows by one after each event.

Check out Kendall (1949), section 2. He shows that the pdf is a geometric distribution. In your notation, it's $P_n(t) = N(0)W^{-t}\left(1-W^{-t}\right)^{n-1}$, which implies that the mean is indeed $E[N(t)] = N(0)W^t$ and the variance is $\text{Var}[N(t)] = N(0) W^t(W^t-1)$. (Be careful -- his definition of $\lambda$ differs from yours by a factor of $\ln 2$.)

so, my answer isn't incorrect (I'll go ahead and leave it up), but this is the full solution.

yes... I accepted this one but yours already point to the right direction

If $W$ is a parameter, I'd expect (in the simplest case) that $W$ itself is a constant (i.e. it doesn't have a distribution). (By the way, I would normally use $T_{1/2}$ to denote the doubling time, $\ln 2/\ln W$, and would use $\lambda = \ln W$ for the exponential rate, i.e. $W^t= \exp(\ln W)^t = \exp(t \ln W) = \exp(\lambda t)$. I don't normally see people express rates scaled by $\ln 2$.)
In the case of a continuous-time birth-death process (the technical jargon for your model), I believe the analytical answer will be that the standard deviation of the population size at time $t$ will grow at the same exponential rate as the mean population size, and that the variance will grow twice as fast (because it has units of $\textrm{population size}^2$), i.e. $\propto \exp(2 \lambda t)$)
I don't have a derivation/reference handy, will dig around for one. This is fairly basic stochastic-process math, but stochastic-process math also gets pretty hairy-looking (to a biologist) quickly. Bartlett 1960 (Stochastic population models in ecology and epidemiology) is one place to look for basic results, although I'm sure there are many others. This recent PhD thesis gives a thorough introduction to the math of birth-death processes ... although, not to my disappointment, a canned derivation of the variance result I'm too lazy to derive for you.


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Identify this roadside plant in Montserrat, Spain
Photographed in April; growing abundantly on the side of a rocky path in Montserrat, Spain.  Up to maybe 1 foot (30 cm) in height.

The blackish "eye-like" objects seem to be cyathium inflorescence, a sort of "false flower" found in the genus Euphorbia.

The genus Euphorbia is bizarre in the sense its species are very different-looking, and often impossible to correlate from superficial shape

This plant is in the genus Euphorbia, which is a large and diverse group.  The members take wildly different forms, but the general form of this plant is shared by many Euphorbia members.  I'm not sure of the species, but think it is most likely Mediterranean Spurge, Euphorbia characias:
 Photo: Macro63
 Photo: cc-by-sa-2.0 Bernard Dupont.

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Will the climate change help the trees to grow?
I've heard several contradictory views and I'm not sure which factor do climatologists count with. Counting with all the effects of the current climate change (including changes of biotopes on places such as Siberia, as well as the higher percent of CO2 in the atmosphere), will the conditions help make better conditions for growing trees (I know the effect on biosphere is usually claimed to be synergic, e.i. for example coral reefs will have less CaCO3 to work with so they will make the global warming appear faster. So please consider just the average effect on trees)

I think it's safe to say that a changing climate will be a selective force, making many species extinct. The cream will rise and the the diversity will decline. Diversity takes many years... diversity is a sign of a (previously) stable climate. The ability to adapt is/was the selective advantage for humans. The earth is experiencing a dramatic extinction event, and we are a major part of it.

@BenWelborn — Please do like it says when you click in the box and do not use comments for answering questions.

@david It's hardly an answer.... at least not one about various factors or biotypes of siberia, and certainly not containing references. So for these reasons, such an answer is liable to be voted down, despite being a relavant truth. What the comment does do (appropriately), is help clarify that a comment such as the one above would not be an answer to the question despite the relevance. So it really is a clarification and/or embellishment of the existing question.

I don't think anyone knows for sure. It will certainly depend on which spatial location, and which tree species, you're thinking of: while "global average effect on growth (e.g. measured by change in net ecosystem exchange of forested ecosystems) of all tree species" is at least well-defined, it will be an average across an enormously variable set of communities, and species within communities. Some of the relevant factors:

if you count the direct effects of increased CO$_2$, this will generally increase growth rates, although it will be highly variable across ontogeny (life stage, i.e. seedling vs sapling vs adult) and species. In general changes in growth rate will be higher for seedlings and for early-successional/fast-growing species, which may in turn change community structure: see Bolker et al. 1995 for one synthetic study of this.
increased temperature would be expected on average to increase growth rates
decreased moisture availability (potential evapotranspiration) would be expected on average to decrease growth rates
increased microbial activity (e.g., due to increased temperature and/or moisture availability) would be expected to lead on average to increased nutrient availability, increasing growth rates
if you're just measuring "net biomass accrual to trees", then changes in large-scale disturbance (wildfire, windstorms, pest and pathogen outbreaks ...) will tend to decrease standing biomass (although it may also lead to temporary pulses of increased carbon accrual as forests re-grow after disturbance)
note that almost all of these driving factors (temperature, precipitation, water availability, frequency of disturbance) will themselves vary a lot in space.

For a summary, you could start by looking at Purves and Pacala 2008 for some of the ways in which people are trying to put these pieces together.


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What is nastic movement due to growth?
I have read in my biology book that

"nastic movement is the movement that occur due to difference in the rate of growth on two opposite sides of a plant organ" ,

but I can't visualize how this movement take place and how the rate of growth cause this movement?

All sort of plant movement (including tropic, nastic, everything) and even bending of human hand and fish, take place in quite similar way. Have you ever read about "bi-metallic strip"? it is just like that.

Hmm want to visualize. Draw a rainbow. take a measuring tape, and measure the length of the curves. You'll find that the curves from convex, "outer" regions, are longer, and the curves towards concave, "inner" regions are shorter and shorter. Like this.
.
In reverse, if you take 2 rods or sheets of different length, and try to fuse them side-by-side, the whole thing will get bent. The longer object will try to face "outwards", and the shorter object will try to face "inwards". The whole thing would look like a bow.

To test this, you could take 2 paper-strips, of slightly different lengths. Now, stepple their end-portions (so-that no-one lag-behind the other, and whole length of long strip (here 10 cm) interact with whole length of short strip (here 8 cm)). Now if you gently try to stretch the whole thing, you will obtain a bent structure. Longer strip outwards and shorter strip inwards.
We see a similar situation when one side of a masonite-board or a cardboard is wiped with wet cloth, the wet surface soon bent-out, this is plausibly because the wet surface expands.
Now , for continuously growing structure, such as a plant's axis, the all sides grow in almost same speed, if one side grow/expand slightly faster than its opposite side, then faster side will accumulate some more length. Now since all the layers of plant-tissues are tightly attached, no-side will be lagged from the other's but the whole thing will become bent. The "faster" side will try to stay "outer" of the curve, and the "slower" side will try to stay "inner" face of the curve.
A more-similar situation is bi-metallic strip which is made up of 2 layers of separate metals. The 2 metals have difference in their linear thermal expansion coefficients, so, when the strip heated/ cooled, the 2 sides of the strip expands/contracts in separate rate with temperature change; as a result, the strip bents (or if it was already bent, then change its curvature).
 Image source wikipedia.

Btw "Growth-movement" is not exactly same as "nastic movement". Plants show many-kind of movements. Some of them  are "growth-movement" (due to variation of growth rate in different tissues), and some-other movements are due to variation in turgor-pressure.
Nastic movement is one type of movement out of many. It is non-directional response to stimuli (non-directional induced-movement) (in contrast, directional induced movement is called tropic movement such as phototropic movement by-which the photosynthetic axis bend towards light).
A nastic movement could be of growth-type or turgidity-type. Growth-difference is not the defining criterion for the term nastic movement. so the statement  "nastic movement is the movement that occur due to difference in the rate of growth on two opposite sides of a plant organ" is technically incorrect.
Let look an example of a nastic movement
photonasty in Oxalis triangularis

 on light
 on dark

Photos from Wikipedia. Photonasty in Oxalis triangularis.
https://commons.wikimedia.org/wiki/File:Oxalis_Triangularis_Photonasty_Timelapse.ogg
Note that, in this induced-movement (depending on light), there is no relation between direction of light and direction of leaflet movement. From whatever direction you give the light, the leaflets will arouse ~90 degrees from the axis.
In contrast, if there were any effect of direction of the stimulus, it will be called a tropic movement, such as this positive phototropism image from wikipedia.
Positive phototropism in Arabidopsis thaliana shoot, photo from wikipedia. (Phototropic movements are most common movement in all green plants and we watch it in germinated seedlings from our kid-hood)
There are autonomous (non-induced) movements, too. Such as in Desmodium gyrans or telegraph-plant, a kind of autonomous turgor movement is seen.
. Photo from http://www.biologydiscussion.com/plants/movement/movement-in-plants-with-diagram/23622
youtube links here and here . (However yet I've not the fortune to see this plant directly) .

This classification scheme of plant movements would give a quite better idea.
brief classification scheme of plant movements, slightly modified from ** , a college-textbook.
And the most examples of Nastic and Pulvinar movements are of turgidity-type.
Nastic movement in Oxalis sp. is also due to turgor-variation; not due to growth-movement.**

** Reference : Studies in Botany; Vol. 2; D.Mitra, J.Guha, S.K.Chowdhury; Moulik Library kolkata.

any feedback welcome.

I think you are considering only the movement of leaves and flowers which are indeed non directional. Flower will always close or open no matter from what direction the light is coming from but what about in stems, roots and tendrils which can only show movement in one direction due to difference in the ratio of growth on two opposite sides? Isn't this type of directional movement ?

Stems can show versatile movements. If you are telling about tropic movement (phototropic, geotropic, etc), it's quite easy to imagine if you've understood what I've told. Such as you've grown some seedlings in a pot, and put the pot near window in your room. What movement you can see they're performing (turning to light), is phototropism, a sort of tropic movement. Not Nastic movement. However that bending is a growth movement

for climbers there is a complicated mixture of movements. 2 kind of spontaneous movements, nutation and circumnutation, and a tropic movement, Thigmotropism (tropic movement where the stimulus is touch). All them are growth-movements and they ultimately give the ultimate shape of  climbers and tendrils.

@AksaK Which class or standard are you in?

But in my textbook both nutation and circumnutation are classified under nastic movements (directional) and on the other side are nastic movements(non directional) which are induced . I am preparing for entrance test of medical college.

I'm not aware about any such classification. Btw which class/grade/standard are you in?

You could check the  page on nastic movement on wikipedia.

Ok then its not any kid's book after all. I am not aware of any such classification. Thats all I could tell.

OK I will check.

Think about say the left side of a shoot growing more than the right side. That way the left side will be longer and will be pulled back by the right side. This causes the shoot to turn to the right. By controlling the differences in the rates of growth in the two sides (using plant hormones) the plant can control exactly how much the shoot will turn.
Most nastic movements however, are not directional. For example, in Thigmonasty, or the movement due to touch, of the Mimosa pudica (or the touch-me-not), cells at the base of the leaves pump out K+ ions and Cl- ions, while taking in Ca+2 ions, thus create a osmotic gradient and lose water. This loss in water results in a drop in turgor pressure of the leaves and they droop.
https://en.wikipedia.org/wiki/Thigmonasty#Thigmonasty_in_the_Fabaceae

You've wrote " Most nastic movement not directional". is there any nastic movement which is "directional"? (All nastic movement take place in definite directions, but  they've no relation with direction of stimulus, by definition). If it had a relationship with direction of the stimulus, it would not be called nastic movement by-definition. It would then called tropic movement.

I assume you were trying to write "Most nastic movements are not growth-movements ". Is that?

Thanks for mentioning the molecular process behind turgor change.


text:
How can there be a one-to-one correspondence between RNA and genes?
From what I know, multiple strands of DNA make up a gene, so how can for each gene there can only be one RNA corresponding to it and vice versa? Is my knowledge incorrect?

how are you defining "gene"?

By multiple strands do you mean two strands of DNA ? By what I have understood from your question you seem to ask how can a single RNA be formed when a gene is a fragment of a DNA (ds DNA) . Isn't it?

No, I mean doesn't a combination of DNA molecules form a gene?

No. Each gene is on a single molecule of DNA.

Very few things are that clear cut in biology. There are three main things to consider here.
1. Gene to RNA
Most eukaryotic genes are spliced. This is basically a process by which a single gene can be transcribed to multiple, different, mRNAs each of which will then be translated to a different protein.
Therefore, there is usually (some genes aren't spliced) not a one-to-one correspondance between a gene and the mRNAs it can produce.
2. RNA to Gene
The next issue is that some genes exist in multiple, similar copies in the genome. For such genes, it is not always possible to know which of the duplicates was actually read to produce a given mRNA.
There is, therefore, not always a direct one-to-one correspondance between an mRNA and the gene it was transcribed from. This, however, is far less common than the splicing issue mentioned above and can, in most cases, be ignored.
3. Each gene is only on a single strand
Each gene is only on a single strand of DNA. Yes, DNA is double stranded, but each gene resides on only one of the two strands (the other strand will be the reverse complement of the gene).

Despite the points made above, it is actually usually possible to map an mRNA molecule to the gene that produced it. In the case of duplicate genes you'll just get multiple hits. The programs that exist to do this sort of analysis can mostly deal with splicing. So, for example, if you have the sequence of the human chromosome 21 and the mRNA sequence of the ERG gene, you can do (on a *nix system with exonerate installed):
exonerate -m coding2genome -t chr21.fasta -q dscam.fasta > out

Which will produce:
Command line: [exonerate -m est2genome -n 1 -t chr21.fasta -q erg.fasta]
Hostname: [oregano]

C4 Alignment:
------------
         Query: gi|609878487|ref|NM_001291391.1| Homo sapiens ERG, ETS transcription factor (ERG), transcript variant 8, mRNA
        Target: gi|528476536|ref|NC_018932.2| Homo sapiens chromosome 21, alternate assembly CHM1_1.1, whole genome shotgun sequence:[revcomp]
         Model: est2genome
     Raw score: 7669
   Query range: 0 -> 1546
  Target range: 39594417 -> 39332536

        1 : GTTTTCACTTGGTCGGAATGGGGAGAGTGTGCAAGAGATCGCTGCGGGACAGGT :       54
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39594417 : GTTTTCACTTGGTCGGAATGGGGAGAGTGTGCAAGAGATCGCTGCGGGACAGGT : 39594364

       55 : TCCTAGAGATCGCTCCGGGACGGTCGTGACGGCCCCCGAGGGACATGAGAGAAG :      108
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39594363 : TCCTAGAGATCGCTCCGGGACGGTCGTGACGGCCCCCGAGGGACATGAGAGAAG : 39594310

      109 : AGGAGCGGCGCTCAG  >>>> Target Intron 1 >>>>  GTTATTCCAG :      133
            |||||||||||||||++         76685 bp        ++||||||||||
 39594309 : AGGAGCGGCGCTCAGgt.........................agGTTATTCCAG : 39517600

      134 : GATCTTTGGAGACCCGAGGAAAGCCGTGTTGACCAAAAGCAAGACAAATGACTC :      187
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39517599 : GATCTTTGGAGACCCGAGGAAAGCCGTGTTGACCAAAAGCAAGACAAATGACTC : 39517546

      188 : ACAGAGAAAAAAGATGGCAGAACCAAGGGCAACTAAAG  >>>> Target In :      226
            ||||||||||||||||||||||||||||||||||||||++         9093
 39517545 : ACAGAGAAAAAAGATGGCAGAACCAAGGGCAACTAAAGgt.............. : 39517505

      227 : tron 2 >>>>  CCGTCAGGTTCTGAACAGCTGGTAGATGGGCTGGCTTACTG :      266
            bp         ++|||||||||||||||||||||||||||||||||||||||||
 39517504 : ...........agCCGTCAGGTTCTGAACAGCTGGTAGATGGGCTGGCTTACTG : 39508374

      267 : AAGGACATGATTCAGACTGTCCCGGACCCAGCAGCTCATATCAAG  >>>> Ta :      312
            |||||||||||||||||||||||||||||||||||||||||||||++
 39508373 : AAGGACATGATTCAGACTGTCCCGGACCCAGCAGCTCATATCAAGgt....... : 39508326

      313 : rget Intron 3 >>>>  GAAGCCTTATCAGTTGTGAGTGAGGACCAGTCGT :      345
             130340 bp        ++||||||||||||||||||||||||||||||||||
 39508325 : ..................agGAAGCCTTATCAGTTGTGAGTGAGGACCAGTCGT : 39377955

      346 : TGTTTGAGTGTGCCTACGGAACGCCACACCTGGCTAAGACAGAGATGACCGCGT :      399
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377954 : TGTTTGAGTGTGCCTACGGAACGCCACACCTGGCTAAGACAGAGATGACCGCGT : 39377901

      400 : CCTCCTCCAGCGACTATGGACAGACTTCCAAGATGAGCCCACGCGTCCCTCAGC :      453
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377900 : CCTCCTCCAGCGACTATGGACAGACTTCCAAGATGAGCCCACGCGTCCCTCAGC : 39377847

      454 : AGGATTGGCTGTCTCAACCCCCAGCCAGGGTCACCATCAAAATGGAATGTAACC :      507
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377846 : AGGATTGGCTGTCTCAACCCCCAGCCAGGGTCACCATCAAAATGGAATGTAACC : 39377793

      508 : CTAGCCAGGTGAATGGCTCAAG  >>>> Target Intron 4 >>>>  GAA :      532
            ||||||||||||||||||||||++         21741 bp        ++|||
 39377792 : CTAGCCAGGTGAATGGCTCAAGgt.........................agGAA : 39356027

      533 : CTCTCCTGATGAATGCAGTGTGGCCAAAGGCGGGAAGATGGTGGGCAGCCCAGA :      586
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39356026 : CTCTCCTGATGAATGCAGTGTGGCCAAAGGCGGGAAGATGGTGGGCAGCCCAGA : 39355973

      587 : CACCGTTGGGATGAACTACGGCAGCTACATGGAGGAGAAGCACATGCCACCCCC :      640
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39355972 : CACCGTTGGGATGAACTACGGCAGCTACATGGAGGAGAAGCACATGCCACCCCC : 39355919

      641 : AAACATGACCACGAACGAGCGCAGAGTTATCGTGCCAGCAG  >>>> Target :      682
            |||||||||||||||||||||||||||||||||||||||||++         19
 39355918 : AAACATGACCACGAACGAGCGCAGAGTTATCGTGCCAGCAGgt........... : 39355875

      683 :  Intron 5 >>>>  ATCCTACGCTATGGAGTACAGACCATGTGCGGCAGTGG :      719
            698 bp        ++||||||||||||||||||||||||||||||||||||||
 39355874 : ..............agATCCTACGCTATGGAGTACAGACCATGTGCGGCAGTGG : 39336142

      720 : CTGGAGTGGGCGGTGAAAGAATATGGCCTTCCAGACGTCAACATCTTGTTATTC :      773
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336141 : CTGGAGTGGGCGGTGAAAGAATATGGCCTTCCAGACGTCAACATCTTGTTATTC : 39336088

      774 : CAGAACATCGATGGGAAGGAACTGTGCAAGATGACCAAGGACGACTTCCAGAGG :      827
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336087 : CAGAACATCGATGGGAAGGAACTGTGCAAGATGACCAAGGACGACTTCCAGAGG : 39336034

      828 : CTCACCCCCAGCTACAACGCCGACATCCTTCTCTCACATCTCCACTACCTCAGA :      881
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336033 : CTCACCCCCAGCTACAACGCCGACATCCTTCTCTCACATCTCCACTACCTCAGA : 39335980

      882 : GAGA  >>>> Target Intron 6 >>>>  CTCCTCTTCCACATTTGACTT :      906
            ||||++          867 bp         ++|||||||||||||||||||||
 39335979 : GAGAgt.........................agCTCCTCTTCCACATTTGACTT : 39335088

      907 : CAGATGATGTTGATAAAGCCTTACAAAACTCTCCACGGTTAATGCATGCTAGAA :      960
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39335087 : CAGATGATGTTGATAAAGCCTTACAAAACTCTCCACGGTTAATGCATGCTAGAA : 39335034

      961 : ACACAG  >>>> Target Intron 7 >>>>  GGGGTGCAGCTTTTATTTT :      985
            ||||||++         1911 bp         ++|||||||||||||||||||
 39335033 : ACACAGgt.........................agGGGGTGCAGCTTTTATTTT : 39333098

      986 : CCCAAATACTTCAGTATATCCTGAAGCTACGCAAAGAATTACAACTAGGCCAGG :     1039
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39333097 : CCCAAATACTTCAGTATATCCTGAAGCTACGCAAAGAATTACAACTAGGCCAGG : 39333044

     1040 : TACGAAAACACCCCTGTGTGATCTCTTCATTGAGAGACATCCCAGATGTCCTGC :     1093
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39333043 : TACGAAAACACCCCTGTGTGATCTCTTCATTGAGAGACATCCCAGATGTCCTGC : 39332990

     1094 : TGAGATCCGTGCCCTAAGTCACGTGATACAAAGAGAGCTGATCCCGGAGCTGAA :     1147
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332989 : TGAGATCCGTGCCCTAAGTCACGTGATACAAAGAGAGCTGATCCCGGAGCTGAA : 39332936

     1148 : GCCAGTCCCAGACAGTCTTATTCTGCCTCTGTTGATTTGGAGACTAAATCCACT :     1201
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332935 : GCCAGTCCCAGACAGTCTTATTCTGCCTCTGTTGATTTGGAGACTAAATCCACT : 39332882

     1202 : CAAACCATTTCATTCAAAGACCACACTAAAGGAATTAAGAGCAGATTAGCCCTT :     1255
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332881 : CAAACCATTTCATTCAAAGACCACACTAAAGGAATTAAGAGCAGATTAGCCCTT : 39332828

     1256 : TAACTAGCTTTTCAGAAAGACAGATGGGCAAAGAAGGCATCCTGGATGCCTGGC :     1309
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332827 : TAACTAGCTTTTCAGAAAGACAGATGGGCAAAGAAGGCATCCTGGATGCCTGGC : 39332774

     1310 : AGTTAGGAATAGGCCGACTTTTGAACTAACAGAAGGATCTGTCCCTCCTCGGGG :     1363
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332773 : AGTTAGGAATAGGCCGACTTTTGAACTAACAGAAGGATCTGTCCCTCCTCGGGG : 39332720

     1364 : GAAGAGCACAAAACAAGGACACTCCCCAGATTCACAGTGACCGATTATCAGTAT :     1417
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332719 : GAAGAGCACAAAACAAGGACACTCCCCAGATTCACAGTGACCGATTATCAGTAT : 39332666

     1418 : GTCACAAGAAGCCAGTCTTGCAGAGCAGAAGCATGCAACCAGTAGTATTTACAT :     1471
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332665 : GTCACAAGAAGCCAGTCTTGCAGAGCAGAAGCATGCAACCAGTAGTATTTACAT : 39332612

     1472 : CTGAATCTTACTGCCTGTCCTCCAAATGATTTAATTAGGTAATAAATTTACATG :     1525
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332611 : CTGAATCTTACTGCCTGTCCTCCAAATGATTTAATTAGGTAATAAATTTACATG : 39332558

     1526 : CCATTCATGCAAAAAAAAAAA :     1546
            ||||||||||||||| ||| |
 39332557 : CCATTCATGCAAAAATAAACA : 39332537

vulgar: gi|609878487|ref|NM_001291391.1| 0 1546 + gi|528476536|ref|NC_018932.2| 39594417 39332536 - 7669 M 123 123 5 0 2 I 0 76681 3 0 2 M 102 102 5 0 2 I 0 9089 3 0 2 M 86 86 5 0 2 I 0 130336 3 0 2 M 218 218 5 0 2 I 0 21737 3 0 2 M 152 152 5 0 2 I 0 19694 3 0 2 M 204 204 5 0 2 I 0 863 3 0 2 M 81 81 5 0 2 I 0 1907 3 0 2 M 580 580
-- completed exonerate analysis

Alternatively, you can use an online resource like the UCSC's BLAT page to align the mRNA against the genome. You can see the results here and in the image below:

As you can see, our query mRNA sequence (NM_001291391.1) overlaps perfectly with the ERC gene.

There is no one-to-one correspondance between RNA and genes but not so much for the reason you seem to have in mind (although I am not sure what you have in mind).
You should read the wikipedia article on RNA splicing, it will teach you a lot of what you will need to get to the answer you might be looking for.
You might also want to follow an introductory course such as the series DNA to RNA to protein from Khan Academy.

So if I am given an RNA like MIR382, I would not be able to figure out which gene it corresponds to? Because that is what I am trying to do.

@Bob Just a thought: perhaps try posting your specific question as a separate question, and see if you can get a more specific answer for it. As it is, this current question might be a little too broad or different to get the answer you're looking for.

I'll guess that I'll do that, but I don't know if I can get a specific gene corresponding to a specific RNA molecule?

Yes, you can match an RNA to a gene. However, a given gene can yield to different RNAs and different alleles can yield to different or the same RNA. You should have a look at the sources of information I posted above. It is not very long and you'll understand a lot of what you are looking for.


text:
What is the gene corresponding to MIR382 RNA molecule?
Where can I find information such as this?

Did you try a Google search first before asking here? We ask that you thoroughly research your question and try to answer it yourself before asking here. Otherwise, the post may be downvoted and/or closed.

I did. Look at the comments in the answer, which I couldn't find from google search.

You find such information on ncbi gene (or ensembl gene)
http://www.ncbi.nlm.nih.gov/gene/494331
Note that Mir 382 still only is provisional.

So where's the gene?

The section on genomic context lists the physical location of the entrez gene 494331 which is the gene encoding Mir 382 in humans

Does it not give a specific name as to what gene it is?

The second line at the top has the entry for "Official Full Name". In this case the name of the gene is "microRNA 382" . For the human gene, this name comes from HGNC, which is the official naming committee of human genes. (see the entry on "provided by"). For additional non-standardized names you might also want to see the "also known as" and "Summary" fields at ncbi gene (which is basically one of the two major official resources for genes)


text:
How did mitochondria make energy long ago?
I've learned that mitochondria is thought to have been eaten by a larger cell, resulting the mitochondria to be part of a bigger cell. Well, here's my Q. If you look at how mitochondria works, you find that in order to initiate the TCA cycle, you need to have pyruvate acid.
Then does this mean that when mitochondria was all by itself, there were pyruvate acid around it? I mean, isn't pyruvate acid a complex molecule, therefore, cannot be abundant??? How could this be?
Furthermore, if cell A swallowed a mitochondria, then that cell A should provide mitochondria with NADH and pyruvate acid. How could this be? Did ancient cells produce NADH and pyruvate??

Actually it is acetyl CoA that is required for the TCA cycle, not pyruvate. The acetyl CoA can come from other sources, e.g. fatty acids. I agree this doesn't alter the substance of your question. You might do better to wait until you have assimilated more of your course material before posting questions about evolution of metabolism. If you haven't covered photosynthesis yet you can't even start thinking about it.

Umm sorry... What I mean was, you need acetyl CoA for TCA, but that acetyl CoA is made from pyruvate acid, which

Must be entered from outside the mitochondria. In other words, you need pyruvate acid to make mitochondria work.

No. As I said, acetyl CoA can come from the breakdown of fatty acids without any involvement of pyruvate. It can come from other intermediates as well. I assume you haven't met these areas of metabolism yet.

@David Though the OP mentioned pyruvate in specific, there is no real contradiction on it being a substrate. Just that it is not the only substrate. I would rather call Ac-CoA as a reactive intermediate and not a substrate. Organic acids like fatty acids and pyruvic acid (alpha keto acids) are substrates. I see your point but that is not really the central idea of the question. IMO, the idea is where did the ancient mitochondrion obtain its substrates from. An edit would resolve this confusion.

@DannyHan Perhaps you would want to edit your question.

You are asking a very interesting question.
As you correctly mention, the substrates of mitochondrial metabolism (TCA or Krebs Cycle) are pyruvate and NADH, and, through oxidative reactions, ATP is produced. Indeed, it seems unrealistic that when the "mitochondria" were by themselves there was pyruvate and NADH in the environment. Let's take a step back.
In the 1970s, Dr. Lynn Margulis proposed the extracellular origin of mitochondria. What does this mean? Margulis suggested that, due to the bacteria-like characteristics of mitochondria (e.g. circular DNA), it is plausible that the first mitochondrion was in fact a bacterial cell that had been introduced into another cell by endocytosis. Therefore, we cannot really describe mitochondria as having been "by themselves", since originally they were (most likely) bacteria. (I am emphasizing this because in your statement it seems like perhaps there is some misunderstanding with this point.)
Where were we? Ah, yes, so we have a bacterium (pre-mitochondrion) inside another (host) bacterium. Consider that the combination of one bacterium inside another works and, voilà!, we have symbiosis and, more precisely, endosymbiosis. This means that the two bacteria collaborate to survive, they benefit from interacting with each other (symbiosis) and one of them is inside another (endo-).
But, of course, the combination is not optimal: the two bacteria have common steps in their metabolism and this is a waste of energy. And evolution does not like that. Evolution encourages organisms to minimize their energy expenditure through natural selection: those organisms that manage to make the most out of their energy supplies will survive and thrive. This means that the pairs of endosymbiont bacteria that manage to use less energy to carry out the same actions will be positively selected for.
Indeed, what this possibly lead to was the host bacterium keeping its basic glucose metabolism (glycolysis), and the "inside"-bacterium exclusively keeping its TCA metabolism, effectively becoming a mitochondrion. Hence, the current arrangement of glycolysis in the cytosol and respiration in the mitochondria.
In short, it is important to look at the bigger picture: were there ever really "free" mitochondria? No, according to Margulis' Endosymbiosis Theory there mitochondria-precursors, which were bacteria. Once these bacteria were introduced into the cytoplasm of another cell, their metabolism degenerated and was reduced to the minimum necessary. This is a success story: the mitochondria are evolved bacteria that have managed to survive and thrive, and have made themselves fundamental for survival of many lifeforms, including humans.
I hope this is a useful answer to your question. Feel free to ask for clarifications in case I did not describe something well enough :)

As a fun fact, mitochondrial DNA has an extremely low mutation rate, estimated to be one base pair per 7884 years... crazy!
Source: http://www.genetics.org/content/156/1/297.full

I have a further question... Bacteria originally had 1 cell membrane, 1 cell wall, and 1 capsule. So then the cell wall and capsule was degenerated while the membrane didn't??

It is thought that a primitive nucleated eukaryote acquired the proteobacterium that gave rise to the mitochondrion — not another bacterium. The later makes little sense and would still have to evolve a nucleus and other features of eukaryotes, lose its cell wall etc. Your answer would be better if you cut 95% out and left the key fact (or hypothesis) that mitochondria were bacteria acquired by primitive eukaryotes that lacked aerobic metabolism.

@rlluc Since the nature of the ancient eukaryotic ancestor (the host cell) is not really known, you should refrain from calling it a bacteria. Just simply call it a host. This propagates a wrong notion. Unfortunately, there are even some articles that are propagating this unreferenced claim as a statement (not even as a speculation). Perhaps you may also add a reference (a book or wikpedia would do) for the endosymbiotic theory. Everything else is fine :)

@DannyHan If you have additional questions then you may post them separately. Look at other Q&As on this subject, in this site or some basic resources elsewhere (like wikipedia) before asking a question; we appreciate some research effort from your side.

@David It is fine to ask someone to remove the 95% of the answer if that was really irrelevant. I don't think that is the case here.

@WYSIWYG Thanks for your comment! I appreciate the knowledge, I was not aware of the uncertainty about the "host".

@David I also appreciate you letting me know about the possibility of a proteobacterium being acquired and not another bacterium. However, you can spread knowledge without being condescendent.

@rlluc proteobacteria is a class of bacteria and extant α-proteobacteria and mitochondria fall under the same phylogenetic group (clade). Therefore it is believed that the ancient mitochondrial ancestor would have been a bacteria of the α-proteobacteria group. The details of how this happened are still unknown.

@WYSIWYG — What will you take then? 90%, 85%? I'm afraid that  "Where were we? Ah, yes…" in an answer is a flag that it is verbose (and can I say self-indulgent). This turns out to he the case. The answer spends so long in unnecessarily describing the history of the idea that it ends up with the nonsensical suggestion that one bacterium engulfed another. When this attracts four up-votes, somebody has to point out that the emperor is naked. One would hope that the feedback will help the answerer improve and thus help improve the site as a whole.


text:
What are hiccups?
What are hiccups?How are they generated and are they involuntary?Does it happen when we eat something tart?Or is there any other cause?I tried to find the solution but I always got different answers

This can be answered by a simple Google search. https://en.wikipedia.org/wiki/Hiccup

It is essentially the phrenic nerve being irritated and as such the diaphragm (innervated by the phrenic nerve) contracts when involuntary signals are generated as a result of the irritation.
This irritation can occur for a variety of reasons.

Overall great answer; however, it is highly recommended that you add some references, otherwise the answer may be downvoted and/or removed.


text:
How to introduce predators to a simulated ecosystem?
I made an evolution simulator and observed that when a marginally competent predator appears, it quickly multiplies and hunts down all of the prey animals, which leads to their own extinction soon after. This seem unlike the real world.
About the simulator
The animals are controlled by neural networks, herbivores must consume spontaneously generated food particles to obtain energy, predators can sap energy out of a prey without killing it, but this significantly hinders the prey's well-being. Animals reproduce asexually with mutations.
There are about 50 animals when the predator appears. All herbivores tend to resemble one another.
The ideal result
This simulator was initially meant to explore the development of individual organism through evolution, but the phenomenon I observed made me aware of the importance of whole ecosystems. I want a modified simulator to produce a ecosystems with multiple niches and stable final state, in short, I want biodiversity.
Some proposed modification

Add different habitats: different habitats vary in naturally spawned food particle, and their difference can be detected by the animals
larger population
arbitrarily increase the reproductive period of predators (?)

Please inform me if more information about the simulator is needed, I will also accept general guide lines to such a simulator.

have you set up so that individuals (both predator and prey) need to gather energy above a set rate to reproduce and survive? In the real world many predators would die of starvation as the prey population shrinks so dramatically, this allows the prey population to recover, and the predator population will recover with some lag

Just a point of ecology: a predator that "can sap energy out of a prey without killing it, but this significantly hinders the prey's well-being" sounds like a micropredator to me. Generally an organism will have one or the other feeding mode, it can't choose between them (although you could have a fixed probability of a mutation evolving that switches feeding mode)

I may write a full answer at some point but you definitely need larger populations. It depends on the range they can move over, but if I put fifty rabbits into a sealed empty warehouse with randomly-placed bowls of food and then added a fox, I wouldn't expect the rabbits to last long.

Don't forget parasites and disease. I took an ecology course and the that we used simulator was underwhelming... but the net result was that predator/prey population lags. Predators kill prey, until there are not enough to sustain the poulation. The fewer the prey, the more difficult they are to capture. After the predators population declines (starvation), the prey population blooms... and then the predator population increases again, like two sinusoidal waves with the predator population a couple years behind.

@rg255: Yes, all animals slowly lose energy overtime, and predators especially.

You may be able to take some insight from the Madingley Model, which is very similar to what your doing but on a global scale. http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001841

What you're trying to do sounds really cool. I feel that you can do the following:
1) Increase reproductive period of predators
2) Increase prey to predator ratio (see Lotka-Volterra equation)
3) Make the reproductive speed/ ability of an individual to be in relation with the number of energy 'points'
What kind of set-up are you working with, a unicellular model or a larger scale?
Maybe you could start with a solely herbivorous setup, but give all individuals the ability to harm/sap a small amount of energy out of another individual.
Is there some way you could send me your project? I want to have a look at it

I think the first thing to consider is adding immigration of prey animals from outside populations. In the real world if a predator hunts it's prey to extinction (or close to it), the predator will slowly die off. In that time period of low/no prey species and low predator density is a perfect opportunity for outsiders of the prey species to come in a fill that empty niche in that area.
Another thing is that predators eating prey is easy at first because prey numbers are large. As prey becomes rare they become harder to find and potentially smarter, so harder to catch once you do find them.
Also the fact that predators can "sap energy" out of prey makes them more of a parasite, not a predator. Just something to consider when you read about predator/prey dynamics.

You have a parasite or parasitoid, since they dont kill and eat preys. Assuming real predators,I think that these need too:

add some kind of defense behavior or defense structure to preys. in real world this occurs as potential prey is capable to run, or have a thick skin.
add variation in both prey and predator, things like individuals faster then others, etc
Good evolutionary novelties for predators (biger claws) drives selection of good evolutionary novelties for preys (thicker skin), that drives  again selection of good evolutionary novelties for predators (group hunting), that selects good evolutionary novelties for preys (big horns and agressive behaviour) and so on...
add diseases, death and life spam to preys and predators

Add the option of cannibalism and maybe increase predator mutation rate such that new species that feed of each other quickly evolve. Also insure that herbivores have the capacity to evolve defense mechanisms such as speed herd protection or the ability to harm predators back.


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Which of the response is faster? voice or hand action?
After taking certain stimuli and making the the decision to do certain action, which one response (output) (out of 2 possible output-ways, voice and hand-movement) would act faster?
For example lets say I'm playing a car video game that can be controlled by voice.
If i say "left" it will turn left and so on.
If I'm controlling that car by hand then I could just steer to the left.
So, if i'm not considering energy required for hand to move and all.
Which will get the signal to my brain faster, my mouth or my hand?

The title and concluding sentence don't seem to match: is your question which output is faster (title) or which stimulus is registered quicker by the brain (last sentence)?

Which output is faster, using voice or hand?

Maybe it is hand action for me.

This question is not a bad question. why it received so little attention

You could also ask a related question in Psychology & Neuroscience

Assuming that we are talking about a situation at the physical limit of the brain:
Speaking a word will always be slower than pushing a button.
A whole word requires a contraction of the diaphragm to push out air so this air can be modulated by another sequence of contractions and relaxations of the vocal chords.
So contracting finger muscles is very similar to speech initiation however for a computer to respond (in the example you were playing a video game) the computer needs to recognize the full word and then map it to an output before actually implementing the left turn.
So adding the extra processing time of the computer and the actual extra production time of the vocalization you're better off pushing buttons.
As a matter of curiosity if the physical limit situation is relaxed; whenever there is a mismatch in both sensory receptors as well as outputs, the brain does its best to compensate. Think of something dropping on your foot, the visual information is actually delayed so that the sensory stream (that has to go up all of your leg and spine) catches up.


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What is the typical amount of full length clones in a cDNA library?
For a Yeast Two Hybrid project we need to make a cDNA library from a single celled organism. We used the Cloneminer II kit from Thermo. We followed the manual and performed all the quality control steps and everything checked out. However out of curiosity we sent 10 individual colonies for sequencing and while all of those give hits in our organism only 40% seem to be even approaching full length in the coding sequence (80-90% coverage).
Is this normal or did we have poor input material/made a mistake? What is the average number of full length clones for a typical cDNA library?


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What's the probability of a non-pathogenic strain becoming pathogenic from plasmids transmitted through the air?
So the thing is, I was getting a bacterial CRISPR kit for biology class, which is overall pretty simple and I'm just doing this for practice, and my dad was saying he was concerned it would accidentally make the non-pathogenic bacteria I was using pathogenic.  I told him that it was basically impossible for me to accidentally genetically engineer bacteria to be pathogenic because infectious bacteria need a bunch of adhesins to infect the human body.  However, that did make me think, what chances would there be of non-pathogenic bacteria (e coli hme63) becoming pathogenic because of some bacteria in the air getting in the culture and transferring plasmids to become infectious?   Again, I don't think this is likely at all, but I would like to ask those with more knowledge than me.
Edit: it would appear to me that if it was that easy for bacteria to get what they need to be infectious people would be getting sick a lot more than they are.

You have found the reason why genetical work is usually done in confined spaces with defined security measures to avoid even unlikely risks. The CrispR system is safe in this respect, since you need to have some fitting DNA present. The exchange of plasmids however, is a risk which happens in the wild.

But even so, what would have to happen is infectious bacteria would have to be in the air and get into the container with the non-infectious bacteria while it was getting resistance plasmids and give the non-infectious bacteria all the DNA needed to be able to get into and infect the body.  Also, aren't bacteria that grow outside the body not as good growing inside?  Like if some bacteria had extra plasmids they would need more nutrients to grow and they would be outcompeted while growing?  I'm just saying that under normal circumstances, is it almost impossible?


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Why do we feel sleepy when we wake up
Why do we feel sleepy, tired, and feel like we need to sleep more when we wake up? (Like, is there a special chemical in the brain that causes that?).
Are there any ways to wake up without feeling such things?

Possible duplicate of http://biology.stackexchange.com/questions/6829/why-do-we-feel-tired-if-we-sleep-excessively?rq=1

It is not tired by sleeping excessively, the question was why do we feel sleepy when we just wake up from being asleep.

Let say you are hungry and I stop you in the middle of your lunch. With high probability... you will be still hungry %))

I don't know if anyone else experiences this, but for me I always wake up six hours after falling asleep (and that's usually as soon as my head touches the pillow). At that precise moment when I wake up, I'm wide awake. Any sooner I feel sleepy and any later I feel groggy.

It is true I feel more sleepy in a vacation morning when I'd slept early, (with no factor of anxiety or stress) and normally rise on morning; than the end of an extremely busy, anxious, unslept night.

Probably it is not solely due to lack of sleep

maybe the brain stays in a state of "inertia" that take time to become fully alert.


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How long is one generation for a mosquito?
For instance, humans are said to have an average generation time of 20 years. I've heard that mosquitos go through 10 generations in a year. Is that information correct?

This  http://www.mosquito.org/life-cycle  is the first hit if you google "mosquito generation time".  14 days, apparently.

it's variable depending on the species, temperature, and feeding.

@Roland I think you can make an answer out of your comment. There will probably be no need to further the answer much more than what the comments currently say.

I feel the need to add that there are thousands of different mosquito species, but I'm guessing you're mostly interested in the ones that cause humans problems? (These should be the ones that the American Mosquito Control Association talk about, too.)

According to this information page from the American Mosquito Control Association, the generation time for a mosquito at 70${}^\circ$ F is about 14 days. The precise generation time depends on temperature and access to nutrients, but yes, it seems reasonable that mosquitos can go through 10 generations or more in a year.


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After getting fully vaccinated for HBV why does the antiHBs titer last for so long?
When a newborn child is fully vaccinated with HBV and let's assume he's responsive, his antiHBs titers will be high. But since the antigenic stimulus is withdrawn, shouldn't the titre fall to nill in some time? Rather, the titers stay significant for around 40 more years. (>10 IU/L is significant)
So, how are there circulating antibodies for so long if there is no more antigenic stimulus?
I understand that memory cells have large half lives but what is producing the antibodies is the plasma cells which have very short half lives.
So how do the antibodies persist for so long?

There is such a thing as memory plasma cells, discovered only relatively recently. Here is a review from 2010 discussing them, here is another review from 2012, and here is a pre-publication manuscript of an upcoming review in Leukemia (I apologize if any are behind paywalls, let me know if you can't access any of them).

Thanks!! Great! I also read up that the anamnestic response stays longer than the long lived/memory plasma cells. So are there other vaccines too where a continuous titre is maintained?

@Polisetty check out page 2 of this PDF from the Immunisation Advisory Centre of New Zealand out of the University of Auckland. It's a table of the average duration of response to a number of common vaccines.


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Sequencing two strands of dna
My background is not genetics. 2.I am not interested in knowing how dna sequencing or genotyping is done. 3. I am interested just in the nature of the results as described here.
Now coming to the question: Humans have two sets of chromosome in each cell. So if I say sequencing chromosome1, what does that actually mean? Which of the two chromosome's gets sequenced? Of genotyping-do comparison take place between two+two=four chromosome1's? Or is my entire undertanding flawed?

What is your own research about this question? To avoid closure as "homework question" (which is also used as a synonym for low effort questions), please add this information using the edit function.

From your question I gather that you do not have a basic understanding of sequencing....The answer can get pretty long....It would be advantageous to know your background and as Chris mentioned to know your research on the matter.

No I don't.My background is electronics engineering. But I am keenly interested in this topic and is eagerly waiting for the answer. Please do explain in simple words how it is done and more importantly about the two strands getting sequenced.

http://www.genomenewsnetwork.org/resources/whats_a_genome/Chp2_2.shtml. I have a rough idea that dna is cut into pieces ,stained etc. What I am concerned about is not the process,but the nature of the output. In what order will the output be presented? Or is it completely random?

I am interested just in the nature of the results as described here.

By aligning this sequence to all nucleotides of all organisms, we would realize that the given (short) sequence occurs in various organisms besides humans. Therefore it might come from a species with only one chromosome see NCBI Blast !
For the sake of the example, let's assume that the species had multiple instances of each chromosome (e.g. one by human mother, and one by human father), and look at "the results as described here". As no detail is given on the protocol, let's further assume the most common scenario - namely that there was no experimental distinction or separation of the individual instances of chromosomes.
Looking at the results, we would realize that is not "next generation sequencing", but Sanger-sequencing.
Now we look at the provided scheme again (note: this is not real experimental data): clearly the bands on the left side only occur for one letter/base, and at a given position of the sequence, there only is one very clear peak on the right hand side (as opposed to the possibility, to have multiple peaks corresponding to different bases).
We would have to conclude that every instance of the chromosome has an absolutely identical sequence. Thus we would conclude that it would not be important to distinguish individual instances.
But wait - aren't maternal and paternal chromosomes different? Absolutely, the given example however only looks at 25 bases rather than the full chromosome - and it would quite possible that they are absolutely identical. (note: there are various experimental techniques to select only specific regions of DNA or RNA for analysis).

I would say your understanding here isn't necessarily flawed - rather, there's a little trick being played on you.
The figure depicts typical results of Sanger sequencing. This type of sequencing always requires a so-called primer, a short sequence of around 20 bases which are known. The code following those 20 bases will be sequenced. Using this technique alone, you can't practically sequence a whole chromosome - it's usually only good for about 700-1200 bases after the primer.
The bands in the graphic on the left and the peaks on the right side correspond to the base at position "primer + n" (n being the number of bands/peaks starting to count at the bottom of the graphic).
Now consider that in practice, this technique is performed on a liquid sample containing of course a huge number of DNA molecules. In an ideal scenario, every single molecule is identical. In that case, the sequence behind the 20 primer bases is identical and you will get clear bands or peaks as shown in the graphic.
When you take a sample from an organism like a human, there will be a variety of DNA molecules in the mix.
What gets sequenced? Simple, everything that sits behind the primer you're using to sequence. If different molecules have different sequences there, the result will be bands in different columns at the same position on the gel (left side of the graphic) or two different-coloured peaks at the same location in the chromatography (right side of the graphic).
Example: Genotyping
We consider the XYZ gene. There are two variants of this gene in humans, and the only difference is at position 167 of the gene, where one variant has an A and the other a G. Thanks to the human genome project, I know the full sequence of the XYZ gene, so I design my primer to span positions 50-70 of XYZ. Therefore, my sequencing result should yield the XYZ gene, starting somewhere around position 100 (even the highest quality sequencing reactions miss out a few bases after the primer). If I take a sample from a human who has the same XYZ variant on both sister chromosomes, I will only get a single sequencing result - either with A or G at position ~67 of my sequencing. If my sample came from a human who has one variant on one chromosome and the other variant on the other, my sequencing will be ambiguous at position ~67, and upon closer inspection I sequenced two variants from this sample: one with an A and one with a G at this ambiguous position. This way I can determine a human's genotype for this gene: homozygous XYZA/A, XYZB/B or heterozygous XYZA/B.
PS: Don't let the double-stranded nature of DNA confuse your thinking here, Sanger sequencing always only sequences one strand (the one that you designed the primer for)! So two sister chromosomes = two double strands = four single strands, of which two will be sequenced because the other two contain the complementary sequences.
PPS: The way this works can cause huge problems if the primer isn't designed properly. With 20 bases, it's possible that the same 20 bases appear elsewhere in the genome, and suddenly the sequences following the primer aren't only different in one or two positions, but everywhere.

That's a picture of Sanger sequencing.  If that sequencing had been done in a region where a diploid organism was heterozygous for a simple SNP, the trace file would instead of having single clean peaks, would at the point of the SNP have two half sized peaks of two colors for the two letters present at that site.  If the difference between the two alleles was more involve than a single nucleotide polymorphism, the trace file might look quite different.

So if I say sequencing chromosome1, what does that actually mean?

People don't often just sequence a whole chromosome like that, and pretty much no one would do it with Sanger technology anymore.  But if you were sequencing a diploid non-inbred organism, you would expect at points of heterozygosity to get a mix of signals.

Of genotyping-do comparison take place between two+two=four
  chromosome1's?

Diploid organisms have 2 copies of a given chromosome, not 4.  Each chromosome has two strands, but the information on complementary strands is identical.

UPDATE

Before coming to sequencing you have to consider that you are not sequencing a single chromosome from a single cell. You are sequencing a DNA sample corresponding to a population of cells, containing all the chromosomes. I do not know of a procedure to target a single chromosome, targeted procedures for specific regions on the genome sorrounding genes are in existence.

Or is my entire undertanding flawed?

Yes, I would say lacking not flawed.
That said,

So if I say sequencing chromosome1, what does that actually mean?

Hypothetically that would mean you are sequencing DNA from chromosome 1 corresponding to a population of cells. Meaning you are retrieving the sequence of chromosome 1 for usage in downstream analysis by polymerizing its complementary DNA sequence by taking advantage of the procedure of DNA replication.

Which of the two chromosome's gets sequenced?

There is no way to differentiate between two chromosomes in mainstream sequencing experiments. The cell does not have an idea about which chromosome is which and neither do you, so both chromosomes get sequenced at the same time. Please note, I said no way to differentiate between two chromosomes in mainstream sequencing experiments

do comparison take place between two+two=four chromosome1's?

This has two parts. What do you mean by four?
If you are implying that chromosome 1 has two strands and that equates to 4 then no, the two strands together make one chromosome. Your cell has 2n or two chromosome 1's. If you are sequencing a population of cells (let's say 1000), you have two thousand chromosome 1's which are being sequenced all of which are present in pairs across 1000 cells.
Do comparisons take place?
In mainstream experiments we do not compare. That said, methods for differentiating between the two chromosome 1's exist. The oldest I could find is an article by M Nagano on allele specific sequencing. In this case, since your parents equally contribute towards your DNA, each of them carry some mutations specific for their DNA. Using this feature we can differentiate between the paternal and maternal chromosome 1.
There's also single cell sequencing, in this case you would be sequencing the two chromosome 1's from a single cell, theoretically you can then also do allele specific sequencing on a single cell allowing you to differentiate between the two chromosome 1's present in the cell.
Finally, there is no way to differentiate the two strands, after sequencing when you align your data back to the reference genome, you will get to know the strandedness of the data.
Answer to old question

Nowadays the word sequencing is synonymous with High-throughput sequencing, and the article you linked to in the comment relates also to high-throughput sequencing techniques (I got this from a cursory glance).

While sequencing dna which of the two strands get sequenced?

Both get sequenced.

In what order is the results provided

Random

while sequencing how are these two strands sequenced?

If it is single end sequencing, we do not know which strand was sequenced first. (There are ways, but for simplicity's sake let's not go there)
If it is paired end sequencing, one read originates from the sense strand and the other read originates from the opposite strand.
You can watch a youtube video here to find out what is the difference

Is it that result of one strand is provide first followed by the other or is it that only one of the two strands get sequenced?

Both are reported.
The question you have asked is very broad, I can go on for a handful of A4 pages and still not finish. Coming to your first question, I said both get sequenced, because we have no way of knowing while sequencing which strand is getting sequenced (there are stranded sequencing techniques, but you should digest what is mentioned/linked here first and later on with some more research come back with a question on stranded sequencing).
After sequencing you get your result in random order, because what you get is not really result but more raw data files which are called FASTQ files. Read up on FASTQ a bit. After sequencing you don't really get a FASTQ but you get a BCL or base call file, which must be converted to FASTQ. These FASTQ must then be either filtered or not based on quality then aligned to a reference genome. This is where you get to know which read came from which strand.
You should read up more on single end sequencing and paired end sequencing to better understand how DNA is sequenced. Also check out this video. This is the most simplified version which I could find. It should make you curious without bombarding you with too much information.
Last of all, in a single end sequencing you have no way of knowing without alignment which strand got sequenced, but in paired end (where a DNA fragment is sequenced from both ends, generating two paired reads) generally, one mate aligns to the sense strand while the other aligns to the antisense strand.

I do not know of a procedure to target a single chromosome Check out single cell sequencing. I'm more familiar with it in terms of RNA-Seq, but one can perform single-cell genomic sequencing as well.

I meant that I do not know of any procedure till date, which isolates an entire chromosome for sequencing...there are targeted protocols for sure...but targeting an entire chromosome? I'm yet to encounter a procedure which employs isolation of a chromosome before sequencing.

OK, I understand. I doubt such a thing is possible in somatic cells, as there is no way to differentiate between maternal and paternal chromosomes. However, I don't think there is a scientific need to do that. If you want to know where a particular SNP or other mutation comes from, just sequence the subject's parents (if possible).

This poster is asking about Sanger sequencing, not next gen.  There are no bcl files in Sanger sequencing, and it's not clear to me that returning Sanger data in FASTQ format is standard.  It wasn't in the years that I worked in Sanger sequencing.


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Problem in understanding Operon
Is there a good book that explains operons: lac operon and trp operon in details.
I was reading  the functioning of the trp repressor protein from 'Principles of genetics-by Snustard and Simmons',they have mentioned that the binding of the repressor-corepressor complex to O$_t$$_r$$_p$ prevents the transcription of the structural genes. But they don't explain how.
Khan academy says that the repressor-corepressor complex physically comes in the way of the RNA polymerase. They have used this diagram below which shows that the large RNA polymerase cannot bind to the promoter site due to steric hindrance.

I'm looking for a more authentic source to study exactly how this RNA polymerase is being prevented from transcribing the DNA in both the operons.

Chapter 31 in the Voet and Voet biochemistry book (I have the 4th edition) link has a rather extensive explanation on this subject. It is rather pricey but you can find a copy of this one in nearly every university library. It generally is a good resource if you want to know more about the DNA or Protein structure of a basic process


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Can someone identify this tree?
It appears to be a kind of fig tree (perhaps similar to the fiddle leaf fig tree but without the fiddle?), although the leaf shape doesn't match. It didn't seem very appealing to eat (!), it was oozing white sap from the stem and from the fruit itself when i broke it apart.
The fruit felt like a hard sponge.
I found the tree in Israel, although, in this location there are a number of non-indigenous trees.
Here are some pictures:

(NOTE: photo of full tree was taken in March, not at the same time as the first two photos)

Something similar to Ficus macrophylla that grows in Israel? https://en.wikipedia.org/wiki/Ficus_macrophylla

Fruit and sap are certainly reminiscent of a fig, but the leaves make me think Ericaceae. @skymningen's find of F. macrophylla, however, suggests to me that some figs do in fact have eliptic coriaceous leaves....I'll dive in to see what I find

Can you provide an image of the tree itself (demonstrating its overall growth form)? Additional images of the leaves would be helpful as would sizes of the leaves and plant overall. Thanks.

@theforestecologist I walked past the tree today, and took a photo. It should be noted that the first two photos were taken in August 2016, and the third photo was taken March 2019!

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


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DNA Sequencing and genotyping
Before going to the details of the question let me post a few other details-
(I posted something similar and got no useful answers-probably because I didn't explain things properly or something else)-
1. My background is not genetics.
2.I am not interested in knowing how dna sequencing or genotyping is done.
3. I am interested just in the nature of the results as in-https://en.wikipedia.org/wiki/DNA_sequencing#/media/File:Radioactive_Fluorescent_Seq.jpg
Now coming to the question- Humans have two sets of chromosome in each cell. So if I say sequencing chromosome1,what does that actually mean? Which of the two chromosome's gets sequenced?
Of genotyping-do comparison take place between two+two=four chromosome1's?
Or is my entire undertanding flawed?

You should first read up on the linked pages on the other question. If you have more questions (to incite curiosity was the point of the answer), you should ask in the comments section. If you think that your question was wrongly worded you can reword the question mentioning UPDATE. And lastly, you are touching too many topics. Until further clarification I am marking this as a duplicate to the first one which you asked.

Double question. Will be merged with http://biology.stackexchange.com/questions/50755/sequencing-two-strands-of-dna


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Variance of frequency in expanding populations
I'm trying to understand the variance in frequency of some strain after some time as passed in a growing population. The idea is to then plug this in kolmorov foward equations and get the classic results (probability of fixation, time to fixations, mean fitness).
However, I got a weird result.
I started with the model definde here
$N(t) = N(0)W^{t}$
and from the answers I got that the variance of $N(t)$ would be
$\text{Var}[N(t)] = N(0) W^t(W^t-1)$
Now, the frequency of strain $N_{m}$ is
$f_{m}(t) = \dfrac{N_{m}(t)}{N_{m}(t) + N_{b}(t)}$
assuming only two sub populations. From there I need only the variance of $f_{m}(t)$ and this and this helped me build a formula. However, the variance of the frequency is not $0$ when $f_{m}(0) = 1 $ and it has units much larger than 1...
My question is, have I done something wrong?

You suddenly talk about two strains while it was no present in the beginning of your model. Can you please link the existence of these two strains to the beginning of your model. Where is your calculation of the variance of this frequency which you state is wrong?

Indeed I had made a mistaken when calculating the variance. As the formula is very large, I will just point to the fact that using the references I gave it is possible to get the variance of the frequency.


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How much energy is in a human brain's electromagnetic activity?
Lately there has been an increased interest on worldbuilding.se about a realistic depiction of fictional creatures who would feed off thoughts and dreams, with some answers proposing feeding off the electromagnetic emissions of the brain.
As a first guess I would think the energy in those emissions is very small. However, has there been any study to give an approximate amount? Most information a quick search provides stems from sensationalist articles which don't look too trustworthy.
The brain does use up almost 20% of the whole body's energy balance, but I would guess most of it is turned into heat.
If one could extract useful work out of the electromagnetic field generated by an average human brain with 100% efficiency, without any physical intrusion (so, the energy potentially available outside of our head), how much would it approximately be? An order of magnitude approximation would be enough.

EEGs pick up about 0.5 to 100 µV on the scalp and about and about 1-2 mV when measured on the surface of the brain, it's about 100 times lower than ECG (heart) signals.
Brain waves have been categorized into four basic groups

beta (>13 Hz),
alpha (8-13 Hz),
theta (4-8 Hz),
delta (0.5-4 Hz).

Votage times current = power. In this case, the amount of current would be/is hypothetical as it would be based on a "salt water" bridge; neurons contain Na+, K+, Ca++, and Cl- ions which are the basis of the current.
EEG measurements must be amplified simply to be seen. An amplifier has to provide a gain of 100 - 100,000 in order to move a delicate needle (and draw the EEG). So, using the amplifier gain as a indication of the amount of current, let's suppose you need as much force to move a pen back and forth as would be required to accelerate a feather one inch in one second.
A feather weighs 0.0082 grams and an inch is 2.54cm. That's about 2 newtons or 2 watts. So, since the current from the brain is amplified 100 - 10,000 times then the wattage picted up by an EEG would be between 0.2 to 20 milliwatts. Supposing that an EEG was only 1% efficient at absorbing the power, then the wattage could be on the order of 20 milliwatts and 2 watts. Altogether brain power might possibly enough to accelerate a feather one inch per second... at around 100% harvesting efficiency.


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The most reliable way of identifying deer antler measurements?
I am creating a (theoretical) study on how males use antlers to assess fellow males' abilities. I thus would need to have accurate measurements of antlers, including length, width, number of tines etc.
The papers I am reading are either really vague, using data already available, or they are relying on antlers which are cast each year to obtain the measurements. In a real life study, the last would be least intrusive and the most ethical, but would it be the most reliable?
I am equally unsure of the efficacy of waiting for deer to cast their antlers to then obtain measurements, as well as having the issue of changes / potential misidentification. I could take the DNA from the antler and use that to identify the deer that they came from.
Does anyone have any experience of this / any input as to what would be the most ethical, reliable method of doing this?
I understand there are confounding factors in this study, with other traits likely affecting deer fights. They seem to be largely un-dealt with in the literature, and I am giving them thought also.
With thanks.

Since antler size is important for hunting regulations, I imagine hunters and related organizations (such as rangers or game wardens) might compile such data. Hunted animals could also provide a source of data that does not require antlers to be shed.


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What is the attachment after this gene name, following the comma: SULF1,hCG18956?
What is this part mean: hCG18956? Is it an alternate naming convention for genes? I am trying to read in a list of gene names using R, but I don't have an extensive biology background.
There are some rows where gene names is not listed. Only something like this: hCG1809003. Does that mean there is no appropriate gene name?

Here, hCG stands for "human Celera Genome". hCG-prefixed protein and gene descriptors are used as a last resort for genes which are found only in Celera's database.
See for example http://www.ncbi.nlm.nih.gov/protein/119619226 , the gene you referred to as "hCG1809003". As the entry says, this was submitted by Celera in 2005 as a putative gene, after being found by "conceptual translation", that is, scanning the Genome Project data for start and stop codons. It is likely this gene has yet to be found as RNA or protein - because the only references for that gene are Celera's submission and the Genome Project paper. Nevertheless, Celera's sequencing (and microarray!) software and chips still look for it.
Your two example genes eventually made it to GenBank. The first example even has a proper name and function assigned - sulfatase 1. Many genes remain in hCG limbo.