text:
Book recommendations for evolutionary models
I was recently working on getting a statistical model of a DNA sequence. To do this I found that understanding evolution quantitatively seems to be quite important. I would really appreciate any book recommendations on the basics of evolution.
I come from an Electrical Engineering background and have a limited knowledge of evolution and biology.

You're looking for a introductory textbook that explain the principles of evolution, explain what is speciation and how it occurs, what is a gene, an allele, a locus, etc… explain stuff about phylogeny and so on. Or you want a book of population genetics (mathematical formulations of how an allele change in frequency in response to selection, to genetic drift. How does the population structure influence the probability of fixation of one allele etc..). Or something else more specific to bioinformatics.It's probably wiser to start with a book that gives an general introduction of evolution.

I was looking for something more quantitative. I did read Dawkins'  'The Selfish Gene', which was quite brilliant in my opinion.

Ok, so I think you might want to try one of the book given in the second paragraph of the answer of this other post

I actually wouldn't have recommended Dawkins as a first book on evolution. He has some interesting ideas, but he is also has very radical views away from what the mainstream science agrees on. You cannot undo it now, of course, but for future reference for other people who see this question, it's probably better to start with a more basic and conservative text. And if you later read Dawkins or a similar author, you then have the basis to recognize what part of his arguments is consistent with the widely recognized knowledge, and what part makes large philosophical leaps.

I agree that Dawkins has an idiosyncratic perspective, and I think he's very wrong about a lot of things, but for an entertaining book oriented to the general public, The Selfish Gene does a pretty good job of introducing a lot of real biological thought, some of it based on serious and still-influential work by George Williams, William Hamilton, John Maynard-Smith etc.  So I personally would not necessarily steer people away from TSG, but would recommend reading something else later and not taking Dawkins' view to be the last word.

You either want a introductory book in evolutionary biology or a book that offers mathematical models of evolutionary processes.
In my first class of evolutionary biology I had this textbook: Futuyama, Evolution I think it gives a good start to the field and offers a good overview of the difference subfields.
If you think you already know enough about the concepts selection, genetic drift, molecular evolution, etc… and you want a book that provides mathematical formulations of evolution, then you might want to have a look into the field of population genetics. On this post you'll find some book-recommendations
If you are particularly interested into molecular evolution, I'd suggest: Yang, Computational molecular evolution
Maybe you are particularly interested into the statistical methodology used in DNA annotation or in phylogeny. Then…. I don't know! It's not quite my field!

Thanks a lot. By evolutionary models, I meant mathematical formulations.

I really good intro to evolution book is The Evolution of Vertebrate Design by Leonard Radinski.
Also, for a more math based approach you could look into Narrow Roads of Gene Land. These are collected papers of W.D Hamilton.

I'd like to add a few books to to the above suggestions. The book by Sean Rice "Evolutionary Theory: Mathematical and Conceptual Foundations" covers a lot of ground, including allele-based models, quantitative genetics, Price's formalism, and MLS. If you're interested in social evolutionary models, I found R. McElreath and R. Boyd "Mathematical Models for Social Evolution" to be extremely accessible for those that don't have a solid math background. Another great book on social evolution is S. Frank's "Foundations of Social Evolution" but it is not as easy to follow as McElreath and Boyd's book.


text:
The dominance variance on a single locus
I was reading the book "Genetics and Analysis of Quantitative Traits", by Lynch and Walsh. I how the covariance between two individuals with IBD $\Theta$ gets divided into just the additive variance and dominance variance component, even in the simple $1$ locus case.
Here my understanding of the modelling (for the simple one allele case):
Given a genotypic value $G_{i,j}$ of mean $0$, $i,j \in \{0,1\}$ we find numbers $\alpha_0$ and $\alpha_1$ minimising the least squares of the following form $\mathbb{E}(G_{i,j}-\alpha_i-\alpha_j)^2$, where the expectation is over the population.
We next define the error terms in each case as $\delta_{i,j}=G_{i,j}-\alpha_i-\alpha_j$. From the properties, viewed as functions of the population $\alpha_i$ is independent of $\delta_{i,j}$, and both have
mean $0$.
The claim made in the book is that given two individuals, with IBD $\Theta$ and probability that the genotype is equal $\Delta$, the covariance of the genotypes $G_{i,j}$ and $G_{k,l}$ is given by,
$$\text{cov}(G_{i,j},G_{k,l}) = 2\Theta \sigma_A^2 +\Delta \sigma_D^2,$$
where $\sigma_A^2= \text{Var}(\alpha_i)$, and $\sigma_D^2 = \text{Var}(\delta_{i,j})$.
Expanding the LHS of the expression, showing that $\mathbb{E}[(\alpha_i +\alpha_j)(\alpha_k+\alpha_l)] =\Theta \sigma_A^2$ is quite easy. It also seems to follow from the  that the the terms $\mathbb{E}[(\alpha_i +\alpha_j)\delta_{k,l}]=0$ from independence of errors from the $\alpha$.
On analysing $\mathbb{E}[\delta_{i,j}\delta_{k,l}]$, we see that if both genotypes are equal, which occurs with probability $\Delta$, then this reduces to $\sigma_D^2$. This gives us a term $\Theta \sigma_D^2$. Further, if both $i,j$ and $k,l$ are not IBD then the covariance is $0$. However when one of the two alleles are IBD, then it is not clear to me that this the covariance will still be $0$.
The book seems to claim that unless both alleles are IBD,  $\delta_{i,j}$ and $\delta_{k,l}$ are independent. I do not see why this is the case. Am I missing anything here? I'd appreciate any help wrt this.

@rg255 : It is chapter 7 on page 143-144. They handle the multiple allele case, but I was simplifying it to the single allele case here.

It looks like I could solve the question. My understanding is as follows.
Let $(X_1,Y_1)$, $(X_2,Y_2)$ (corresponds to $i,j$ and $k,l$ in the question) be the genotypes of two individuals
 at some location. We assume that neither individual
 is in-bred. In this case define,
 \begin{align*}
  \Delta_7&= \text{Pr}(\text{Both alleles $\{X_1,Y_1\}$ and $\{X_2, Y_2\}$ are IBD}),\\
  \Delta_8&= \text{Pr}(\text{Exactly one allele pair of the four pairs is  IBD}),\\
  \Delta_9&= \text{Pr}(\text{ No IBD between the two individuals}).
 \end{align*}
 $\Delta_7$, $\Delta_8$ and $\Delta_9$ are calculated from the pedigrees.
 For example, for non-twin siblings, $\Delta_7 = \frac{1}{4}$, $\Delta_8=\frac{1}{2}$,
 $\Delta_9 =\frac{1}{4}$.
We note that the IBD coefficient (also called kinship coefficient) $\Theta$ is
 \begin{align*}
  \Theta = \frac{1}{2} \Delta_7 + \frac{1}{4} \Delta_8.
 \end{align*}
 Also the fraternity coefficient, $\Delta =\Delta_7$.
Thus we have that the covariance between the genotypic
 value of two individuals is given by
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)] =& \Delta_7 \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{both IBD}] + \\
  &\Delta_8 \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{one IBD}] + \Delta_9  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{no IBD}].
 \end{align*}
Further note that,
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{both IBD}] &= \mathbb{E}[G^2(X_1,Y_1)],\\
  &= \sigma_A^2 +\sigma_D^2.
 \end{align*}
\begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{no IBD}] &= \mathbb{E}[G(X_1,Y_1)] \mathbb{E}[G(X_2,Y_2)],\\
  &=0.
 \end{align*}
\begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{one IBD}] &= \mathbb{E}[(\alpha(X)+\alpha(Y_1)+\delta(X,Y_1))(\alpha(X)+\alpha(Y_2)+\delta(X,Y_2))],\\
  &=\mathbb{E}[\alpha^2(X)] + 2 \mathbb{E}(\alpha(X) \delta(X,Y_1)) + \mathbb{E} [\delta(X,Y_1)\delta(X,Y_2)],\\
  &= \frac{1}{2} \sigma_A^2 + 2 \mathbb{E} [ \alpha(X) \mathbb{E}[\delta(X,Y_1) | X] ] +  \mathbb{E} [\mathbb{E}[\delta(X,Y_1)|X]\mathbb{E}[\delta(X,Y_2)|X]],\\
  &= \frac{1}{2} \sigma_A^2.
 \end{align*}
Thus we have that,
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)] =& \left(\frac{1}{2}\Delta_7 + \frac{1}{4}\Delta_8\right) 2 \sigma_A^2 + \Delta_7 \sigma_D^2,\\
  &= 2\Theta \sigma_A^2 + \Delta \sigma_D^2,
 \end{align*}
 which is as claimed.

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Identity by descent among unrelated individuals
I was reading a couple of papers which talk about IBD (Identity by descent) among unrelated individuals (for eg. http://www.pnas.org/content/109/4/1193.long). However they do not seem to clearly define what they mean there. I was wondering how IBD is defined in such a context. I'd appreciate any help (especially suggested references to look this up).

They are not close relatives of each other I suppose. You are right I think, there should be an exact definition.

I formulated an answer on this post that is very relevant. I was however quite confused and I am not sure whether or not several definitions of IBD exist in the literature.

In the context of GWA studies the IBD is usually different than what defined in population genetics. It represents the relatedness across individuals defined simply as the genotypic correlation between them. In other words, you run a linear regression using two individual genotypes to get an r-sq that can be interpreted as the proportion of similarity in their genetic material. r-squares of 0.5, 0.25 and 0.125 represent respectively parent–offspring, full-sibs, first cousins relationship. This is used as a  control as GWAS statistical tools assume a population of unrelated individuals.

The definition of IBD is always the same - an allele or segment of alleles which is shared between two individuals because of descent from a common ancstor.
In the context of this paper, the authors are referring to segments of the genome between individuals which are IBD. In this case, they are looking at recently isolated populations who are likely to share longer stretches of IBD with one another. This is the case because each individual within a relatively isolated population is likely to be, on avergae, more related to another individual than in an outbred population. In general, it it much easier to detect longer segments of IBD than shorter segments, and this is why they choose to study isolated populations. Also, you can be much more sure that longer IBD segments will share a common ancestor with one another.
More specifically, they define a 'large' IBD segment is one which is longer than L centimorgans of length. Additionally, they define 'IBD-sharing' level between two individuals, as the probability that a randomly chosen genomic position on homologous chromosomes from each of the individuals lies in a large IBD segment shared by the two individuals. Thus IBD sharing takes values between 0 and 1.
There are several different methods, such as PLINK, fastIBD and GERMLINE which can identify IBD segments and their corresponding lengths from genotype data.
If you are interested in a relatively accessible guide to understand the principles of both single locus and segmented IBD, then I would recommended checking out Graham Coops's population genetics notes, section 2.2.

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text:
How do penicillin resistant bacteria grow slower in the presence of penicillin?
We put 2 flasks inoculated with Bacillus cereus in 37⁰C: one with 100μg/ml penicillin +  50μg/ml chloramphenicol and the other without penicillin. We found that the OD is higher in the one without the penicillin. These strains are supposedly penicillin resistant as verified by growing them in a test-tube containing penicillin (5mg/ml) at 30⁰C. It contradicts my hypothesis that they should have the same growth rate because of the $\beta$-lactamase secretion that would destroy the penicillin. I can't find any explanation in the web.
help me

You need to add a lot more detail for any answer to be possible. Which kind of bacteria were in there? Were they resistant to Penicillin. Did you work sterile?

the bacteria was bacillus cereus. as far as i know weve worked sterile (they gave us the bacteria). i didnt mention two other things: 1. we onother erenmyer that contain penicillin (0.2 ml) and chloranphenicol (0.1 ml). 2. the real changes in the OD began after 90 min.

Can you please edit your question and add information about the bacteria, resistances and, media and all the other things that may be important. Additionally: This sounds a lot like a homework question, so please add some interpretation of yourself.

You could also show a diagram with OD measurements over time for both cultures.

Resistance to penicillin in B cereus is due to chromosomal genes, but not all B cereus strains are penicillin resistant. Do you know for certain  that you used a resistant strain?

@ebeginner To make it short: You used a penicillin resistant strain of B. cereus and the culture that was grown without the presence of penicillin was growing faster? How was the difference in OD? Was it 0.05 or 0.5 or what?

the differnce was between 0.05-0.1.

i dont know for certain. but later on we put the bacteria in a test tube that contain penicillin (in a higher concentration) and it pruduce penicillinase.

forgot to mention: we put that in 30 degrees

@ebeginner So please use the edit function of your question (directly below it) and edit your post so it contains all relevant acts of the experiment. I don't want to collect them from the comments. If you could add a figure with the growth curves, that would be great.

ey chris, ill add the curves later (they are not available now). do you think that the low concentration of penicillin (100 ml/u) wasnt inough to induce penicillinase ? later we put it in 5000 ml/u and it induce it/

@ebeginner One last time: Please add all info to the question. Then I will answer them.

@ebeginner: I edited your question.. see if it is consistent with your experiments. Add more details such as 1) When did you finally take OD measurements 2) Did second flask contain chloramphenicol 3) Did you perform any other tests for penicillin resistance

Your hypothesis is incorrect.
You must be assuming that lactamase destroys the antibiotic with perfect efficiency. This is incorrect.
You must be assuming that the population will remain genetically stable. This is doubly incorrect. Firstly the penicillin will select highly resistant bacteria which suffer a greater fitness burden from expressing the lactamase. Second, in absence of penicillin, spontaneously arising mutants which suppress the lactamase are free to proliferate.
You must be assuming that carrying capacity is identical for Pen+ and Pen- media. Trivially, you claim your experiment disproves this, but the assumption is also baseless since this need not be the case.
Furthermore, your results are inconclusive. You lack crucial controls, such as putting the bacteria from the Pen+ into Pen- and vice versa to see if the growth difference is intrinsic. You have not only failed to provide the error of your measurements, but have failed to provide the quantitative measurements themselves, so we do not even know if the difference is statistically significant.
Lastly, there are several basic things which you could rightfully expect us to assume, but have nevertheless failed to provide. For instance, you do not say if the populations are clonal.

Can you provide a ref. for "suffer a greater fitness burden from expressing the lactamase," and explain why it would slow growth, if that's what you are getting at? Thanks.

@daniel Assuming not every cell in the population expresses the exact same amount of lactamase, it stands to reason that some of them make more of it than others. It is well known that expressing arbitrary proteins, or antibiotic resistance, by itself constitutes an energy burden. I cannot provide references unless OP clarifies the experiment.

Not questioning your assertion, just wanted to read further if you had a ref. The question is a bit vague and I think your second paragraph is correct. If the results are qualitatively accurate it's an interesting question. How is the difference in growth rates allocated between the 'fitness burden' of resistance and the ability of non-resistant mutations to proliferate in the pen.-free nutrient? That's why I was interested in a ref if you have one. +1


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Why are cancer rates low in large animals?
Large animals generally have more cells and live longer than smaller animals. For example, bowhead whales live up to 200 years and weigh up to 100 tonnes, as opposed to humans (living ~71 years and weigh ~75 kg) and mice (10–25 g, <1 year in the wild). Hence, whales have an immense number of cells and those cells are subjected to environmental carcinogenic influences (chemicals, UV) for a longer period of time.
Cancer is caused by random mutations and those random mutations are basically stochastic processes. Given their long life span and larger number of cells, shouldn't larger animals have a substantially higher chance to develop cancer? In fact, story goes that bowhead whales in fact only very rarely contract cancer, and less so compared to humans?

Can you please provide a peer reviewed source backing up your claim that they do not, in fact develop cancer.

@AMR - just checked - at least for sharks it's a myth

Short answer
Large animals do get cancer. They may contract cancer with an incidence less than that estimated by absolute cell numbers, but there seems to be a lack of data on cancer rates in large animals to support this hypothesis conclusively.
Background
Whales contract cancer (Martineau et al, 2002). There does, however, seem to be a lack of correlation between body mass and cancer risk, which is counterintuitive since larger animals have more cells. This is known as Peto’s paradox (Caulin & Maley, 2011), after epidemiologist Richard Peto of Oxford University in the UK, who noted it in the 1970s. He reasoned that larger organisms have more potentially carcinogenic cells, tend to live longer and require more ontogenic cell divisions. Therefore, statistically, cancer incidence should scale with body size (Nagi et al., 2007).
It is thought that larger animals use protective mechanisms that many smaller animals do not. For example, blue whales have 1000 times more cells than us, if they would contract cancer at rates 1,000 times higher than humans, they would die before they were able to reproduce and the species would quickly go extinct. However, the paradox itself has been scrutinized, because there may simply be a lack of data on cancer rates in large animals (Source: Nature News, 2013). In addition, it is thought that malignant tumors are disadvantaged in larger hosts. In larger organisms, tumors may need more time to reach lethal size, so tumors have more time to evolve without becoming lethal. Hence, in large organisms, cancer may in fact be more common, but less lethal (Nagi et al., 2007).
The persistent myth that sharks don't get cancer seems to stem from clinical evidence that cartilage has antiangiogenic properties, i.e., it inhibits the development of blood vessels, which are crucial to the growth of many cancerous tumors. Since shark skeletons are made of cartilage, it was thought that they can't get cancer. Recent studies have found that while the incidence of cancer in sharks and related fishes such as rays does seem to be low, cancerous tumors, including chondromas (cancers of the cartilage), have in fact been found in sharks. The reasons for the apparently low incidence are not necessarily related to their high cartilage content, but may simply be a matter of lack of directed research on cancer in sharks and related fishes (Source: American Museum of Natural History). Indeed, tumors have been found in 23 species of sharks, measuring up to 30 cm in a Great White (Source: Scientific American, 2013).
References
- Caulin & Maley, Trends Ecol Evol (2011); 26(4): 175–82
- Martineau et al., Environ Health Perspect (2002); 110(3): 285–92
- Nagi et al., Integr Comp Biol (2007); 47(2): 317-28
P.S. All animals, including whales, age and die, otherwise the oceans would've been pretty crowded, at least before whaling started.

@AlekseyBelikov, no worries. This one question was particularly interesting, because I was also under the assumption that sharks could not contract cancer. I never really delved into the topic up until now :)

@AlekseyBelikov If the answer answers your question, you can check it so that future users know you received the answer you expected (I am not sure you can still accept an answer now that the post is being closed). Accepting an answer also reward the one who answers with extra reputation points and may eventually bring more effort answering your future questions.


text:
Mechanisms and Assumptions of the Species-Area Realtionship
I would like to choose a model to use to describe a species area relationship based on plant species richness data that I have collected.  Rather than choosing the power model a priori, I am considering all options (eg. exponential, untransformed, etc).
Does anyone know of any good recent synthesis work on how to choose the best model?  Of particular interest are the assumptions behind each model, and the ecological mechanisms that each model might imply.

Disclaimer: I am NOT an ecologist! What do you mean species-area relationship? Do you mean number of species, or presence/absence of a particular species. I don't understand what the "species" variable is.

@Remi.b It's referring to the relationship between the species richness of a particular region/site and the area of that site. Such plots often follow a power function (i.e. linear on the log-log scale)

Dengler 2009 would be a good start.

I'm sure this paper, his citations and papers citing Dengler's paper will get you well on your way.


text:
Can growth rate be used as an indicator of fitness in fish populations?
I would like to calculate selection gradients in order to gain insight into the strength and type of selection influencing my study population.
(see here for review. http://jgking.web.unc.edu/files/2012/06/Kingsolveretal.AmNat_.Mar2001.pdf )
(see here for what I would like too do in the end. http://onlinelibrary.wiley.com/doi/10.1111/evo.12077/epdf).
For this I need an indication of fitness.
My question is this:

Does it make sense to use growth rates (in mm. per year or other) as a "proxy" for fitness?

Thanks in advance for your time

Welcome to Biology.SE!
Possible confusion
When talking about growth rate as a proxy for fitness, most authors think of population growth rate (whether in terms of the Malthusian parameter or the net reproductive rate). Such methods are typically used for unicellular that have very short generation time. You seem to be referring to the individual growth rate.
Possible proxies for fitness
There are a number of different proxies for fitness one can use.

growth rate
Some phenotypic trait correlated with fitness such as:

seed production
body size
etc..

Competitive abilities
Experimental evolution

How to chose a proxy
The proxy you want to use depends:

The accuracy you need
The organism you are working with
The a priori knowledge on the biology of the organism of interest.

For example, if you have little knowledge of what phenotypic trait could be correlated with fitness and if the organism of interest have a very short generation time, then growth rate might be good (and accurate) proxy to use indeed.
Ressource
You should probably read some papers that have used a method of potential interest before doing it yourself.
At page 1232 of Kawecki and Ebert 2002, there are a few paragraphs reviewing the different proxies and their usage. They cite key papers you might want to have a look at.
Proxy for fitness in fishes
I know little about fish biology in general but I doubt there is such thing as a generalization of whether "individual growth rate" is a good proxy or not. As you don't specify what species of fish you are working on, I don't think it is possible to answer this question accurately.
You should look at previous work done on the species (or related species) you are working on in order to figure out what would be a good proxy.
Issue in your post

I think it is clear from above that you should indicate what species you are working on.
The paper you link should come with more explanation. You say a paper is a review but a review about what?
You cannot say "I would like to do something like them" and link a paper. You should describe with you own word what you are trying to achieve.

Excellent and thanks for your time :) .... I did not want go into to much detail of the study and so I omitted some info. The species I am studying is small benthic (dwarf) Arctic charr and I am aware that individual growth rate in fish populations in particular can vary greatly among individuals and that in some instances these differences in growth rate do not translate directly into differences in individual fitnes. That is to say, fish with variable growth rates can have very similar fitness.


text:
Meaning of "non-homologous virus"
From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

More recently, concerns have been raised that HGT from genetically modified organisms (GMOs) could have adverse effects (Pontiroli et al., 2007). HGT of an introduced gene in a GMO may confer a novel trait in another organism, which could be a source of potential harm to the health of people or the environment. For example, the transfer of antibiotic resistance genes to a pathogen has the potential to compromise human or animal therapy (Bennett et al., 2004), transfer of a viral gene to a non-homologous virus may result in an emerging disease (Falk and Bruening, 1994) or gene transfer to humans has been controversially proposed as a potential trigger for oncogenesis (Ho et al., 2000).

What is a "non-homologous virus"? A virus whose species is the same but the strain is different from the virus taken as the donor for the GMO? Or just any virus (including viruses from different species) whose DNA or RNA sequence is different from the GMO donor virus?
Excuse me if the question seems too simple.

It is not a standard term. What it means is unrelated viruses.

It simply means a two dissimilar viruses. If you read the paper Falk and Bruening, they are worried that if you place a viral gene in a plant (here we call that the transgenic gene), then natural viruses may "mix" it's genes with the transgenic genes and create a superior virus. The thought is, you are speeding up the evolution of the virus by taking a beneficial gene from a non related (non homologous virus), something that would probably take a long time.

Thank you! And this wild\natural non-homologous virus could be of the same species with the donor virus, the difference being only that it lacks this 'beneficial' gene sequence that was introduced into the GM plant?


text:
What is the name of the bond between phosphate and the sugar in a nucleotide?
I am slightly confused about what the name of the bond is between the phosphate and sugar within a nucleotide. All my research comes up with is a phosphodiester bond being the backbone of DNA. But within a single nucleotide, would we perhaps call it a phosphoester bond (all of my searches of phosphoester bond correct it to phosphodiester, so I don't think the term 'phosphoester' is in use...); or maybe it would be an O-glycosidic bond as it is a sugar molecule covalently bonded to another molecule via an O atom?

Please do not ask multiple questions.

@another 'Homo sapien' Glycosidic bonds certainly do not always involve an O atom (heard of N,C and S glycosidic bonds? Now THAT is something you can find out on Wikipedia). And I do not get your point- even if a glycosidic bond required an O atom, there is one between the sugar and the phosphate group.

@another'Homosapien' see above comment.

Phosophoester is a valid term. There are at least a 1000 peer-reviewed articles that use this term. IUPAC Goldbook defines nucleotides as:

Compounds formally obtained by esterification of the 3 or 5 hydroxy group of nucleosides with phosphoric acid. They are the monomers of nucleic acids and are formed from them by hydrolytic cleavage."

Phosphoester or phosphoric ester means an ester of phosphoric acid.

Expanding on WIYSIWG's correct answer:
Each nucleotide contains one phosphoester bond (between a phosphate O and sugar 5'-C). Additionally, two nucleotides are connected by one phosphoester bond (between a phosphate O and sugar 3'-C). So in a polymer of multiple nucleotides (DNA, RNA), the repeating monomer unit contains two phosphoester bonds, on "top" (5') and "below" (3') the sugar. Since the repeating unit contains two phosphoester bonds, and the phosphates alternate with the sugars in the sequence, we call this a sugar-phosphate backbone held together by phosphodiester bonds/linkages.
Schematic of single nucelotide  featuring vertical line as phosphoester bond (to 5' C):
$P \\
| \\
[sugar]-[base]\\
\\$
Two nucleotides, each with an internal phosphoester bond and with a new phosphoester bond connecting them (spanning 5' of one sugar to 3' of the next):
$P \\
| \\
[sugar]-[base]\\
|\\
P\\
| \\
[sugar]-[base]\\
\\$
Repeating unit in nucleotide polymer, with alternating sugar-phosphate backbone and one phosphodiester bond/linkage per unit/nucleotide residue (the ... ellipses indicate pattern continues for the entire nucleic acid polymer, with hydroxyls capping the very ends):
$...\\
P\\
| \\
[sugar]-[base]\\
|\\
...\\$

phosphomonoester is also a common term for the first case


text:
Independence of Light independent reaction in photosynthesis?
Inspired by a question asked to me by a classmate, I have the following question about Light-independent (dark phase) reactions in photosynthesis:-

Let us suppose an algae sample was exposed to light for a considerable
  time so that maximum( if there is a limit) NADPH concentration was
  achieved. Now if the sample is placed in dark and radioactive
  ¹⁴CO₂ bubbled, will the cell be radiolabelled after some time of
  bubbling continuously?

I guess the answer depends on the active life of ATP and NADPH , the products of light reaction. If they are considerably stable, such that they are in sufficient concentration for executing Calvin cycle although their production (apart from respiratory ATP production) has ceased due to absence of light. If they are, then the ATP and NADPH produced during the initial exposure period will carry out carbon fixation with radioactive carbon and hence radio labelled sugars will be recoverable from the sample. If not, they will quickly degenerate (by hydrolysis, utilization or likewise) and they will be unable to carry out fixation after some fixed time after stopping the light.
What, under normal conditions, should be the time after which the light-reaction products are no longer capable of fixing CO₂ by Calvin cycle? And, ultimately, will the presence of radioactivity in sugars for the scenario above depend on the species of plant?
[I am ignoring all radioactivity due to dissolution of ¹⁴CO₂ in cytoplasm]

It turns out that the so-called light independent reactions are not light-independent at all: there are several regulatory mechanisms in place to prevent the turning of the Calvin Cycle when there is no light energy available to produce ATP/NADPH. The hypothetical situation you described in your question demonstrates the necessity of such regulation. The cell cannot allow levels of ATP and NADPH to drop too low because those two factors are required for everything. So if you let the Calvin Cycle run when there is no means of fueling it (ultimately) from light energy, then the Calvin Cycle will run until ATP/NADPH is too low to sustain it further, at which point the cell dies. So several key enzymes in the Calvin cycle are activated indirectly by light.
One of the most well-studied regulatory mechanisms is the ferrodoxin/thioredoxin regulatory system. The enzyme Ferredoxin-Thioredoxin reductase takes electrons from ferredoxin (which is reduced by light energy via the photosystems) and transfers it to thioredoxin, a disulfide-based redox protein. Then thioredoxin reduces several key enzymes in the Calvin Cycle, which activates them (through conformational changes induced by disulfide bonds). The upshot is that when light is around to facilitate reduction, the metabolic enzymes of the Calvin cycle can work, but in the dark the cell oxidizes and these enzymes are turned off, switching off the Calvin cycle and arresting CO$_2$ fixation.
An orthogonal direction of light regulation of the "light-independent" reactions is RuBisCO Activase, which is required to modify the RuBisCO active site to be active. This requires ATP hydrolysis, which amplifies the sensitivity of the Calvin Cycle to ATP availability.
The takeaway is the light-independent reactions may not directly require light as an input, but they are regulated by light availability. I tried to look up how much time in the dark would be required to shift the redox balance such that the Calvin Cycle enzymes would be inactivated, but I couldn't find that data. People in the literature, however, seem to believe it would be quick (1).
There is some description of this at Wikipedia. If you want to look further, Bob Buchanan at Berkeley made a lot of seminal advances in this area; a review of his you might want to check out is (2).
(1): Ruelland E, Miginiac-Maslow M. (1999). Trends in Plant Science. 4(4): 136-141
(2): Buchanan BB. (1980). Annual Review of Plant Physiology. 31:341-374.

+1 for the comprehensive answer:) On an imaginative side note, had these regulatory mechanisms been absent, what then would have been the time delay before the light reaction products at saturation would go below the minimum concentration required to execute Calvin cycle (just an order of magnitude, i.e. seconds? minutes? hours?)? Would ATP & NADPH utilisation be the only way of their depletion or would their natural decomposition (hydrolysis) also play a part?

@Satwik I am not sure but I think before they would naturally dgrade, ATP and NADPH utilisation would limit them


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Difference between inbreeding and interbreeding
Is inbreeding the same as interbreeding?
On this site interbreeding is defined as (http://www.thefreedictionary.com/interbreeding):

To breed with another kind or species; hybridize.
To breed within a narrow range or with closely related types or individuals; inbreed.

But I am sure that interbreeding is not the same as inbreeding. Inbreeding would be between genetically related members of a species and interbreeding would be between genetically un-related members of the same or different species.
after looking at wikepedia pages for both terms as well as searching the english oxford dictionar I am certain they are different

You are basically correct. Most common usage in my experience:
Inbreeding refers to sexual reproduction between genetically closely related individuals, within a species. Inbreeding will increase the relatedness between individuals in a population.
Interbreeding refers to reproduction with another species (or race), and is often used as a synonym to crossbreeding or hybridization (when referring to hybrid offspring from two different species/races/breeds, not DNA hybridization). This is also how 'Interbreeding' is defined in the Oxford English Dictionary. However, 'Interbreeding' is sometimes used just to signify that two individuals can breed and have viable offspring ("...these two individuals can interbreed..."), and under this usage this can also include/overlap with inbreeding.
The latter usage can be seen in the Species article in Encyclopædia Britannica, online:

Species, in biology, classification comprising related organisms that share common characteristics and are capable of interbreeding.
  ...
  Interbreeding only within the species is of great importance for evolution in that individuals of one species share a common gene pool that members of other species do not.

interbreeding is a process in which same kind of species are breed together such as(male and female)but outer breeding is a process in which different kind of species are breed together such as(means horse is a specie it will breed with bitch those are different species


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Author statements (Readers) in biological nomenclature
I know that a binomial name may be followed by the name of the reader who has been the first to identify the species and to give it that binomial name.
It is not completely clear to me what the same of a botanist, zoologist etc. means if it is placed between parentheses, as in Blysmus compressus (L.) Panzer. Does it mean that Panzer gave that species the binomial name Blysmus compressus but it was Linnaeus that identified it as a species? I cannot find precise information on line, nor in my books...
Moreover, the pattern may get more complicated if we introduce the subspecies, for example another Cyperacea: Carex ferruginea Scop. subsp. macrostachys (Bertol.) Arcang.. It seems quite trivial to me that Scopoli (Scop.) identified and gave the species the name Carex ferruginea; as to the subspecies,  did Arcangeli (Arcang.) named it macrostachys after that Bertoloni (Bertol.) had identified it as a subspecies?
I thank any answerer very much.

If I remember correctly, a name in parenthesis means that that person (eg. L.) discovered and named the species, but the species was later on re-categorized into a new genus/family/etc. and then given a new name. The person who re-categorized and renamed it has their name appear after the parenthesis (eg. Panzer)

@CactusWoman Thank you very much for your comment! Am I right if I understand it to mean that L. gave Blysmus compressus the name X compressus (where X is name other than Blysmus) and then Panzer identified it as a member of the Blysmus genus? Analogously, I would think that Bertol. gave Carex ferruginea macrostachys the name X Y macrostachys but it was Arcang. that attributed it to the Carex ferruginea species... Or have I misunderstood? Thank you again!

Yes, that seems to be correct. Blysmus compressus, according to the Flora of China, was originally named Schoenus compressus by Linnaeus, then underwent a number of reclassifications before ending up with the current classification.

It is important to note that classifications of species can be very complicated, with the same organism being reclassified many times by many different people. Also, an organism needn't keep its species epithet (the second part of the binomial) after being reclassified. If species Foo barus is later reclassified into the Baz genus, but a species with the name Baz barus already exists, the species will be given a new species epithet, ending up with a name like Baz spamus. Nomenclature can actually get rather complicated!

As @C_Z_ mentions, the double author citation is due to a naming revision. In your case, 'Panzer' has revised the name given by 'L' (Linneus). It can for instance be due to an assignment to a new genus or a change in rank status (e.g. going from subspecies to species).
Note that author citations differ between botany and zoology, where changes in authorship are usually not recognized in zoology (as long as there is a proper and complete species description in the first place), while the botanical code allows for multiple author citations. From Wikipedia: Author citation (botany):

... in contrast to the situation in zoology, where no authorship change is recognized within family-group, genus-group, and species-group names, thus a change from subspecies to species, or subgenus to genus, is not associated with any change in cited authorship

So under the Zoological code, the old author name is kept when a species is reassinged to a new genus, e.g. when Seriola gracilis (Lowe, 1843) --> Cubiceps gracilis (Lowe, 1843). On the other hand, the Botanical code allows for multiple and sequential revisions, so you can have situations as "Dummy species (L.) Thom. emend. Müll.".


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Big Bug from Peru
I'd like to have a name for this guy.  There were 5 or 6 of them zipping around the flower bed on the coast of Peru about 120 kms south of Lima.

Nice photo! :) :)

That is a hawkmoth, probably Hyles annei (Guerin-Meneville, 1839). It is one of a number of moth species commonly called "hummingbird," "sphinx," or "hawk" moths in the family Sphingidae.
Beautiful, isn't it? :)
edit - sorry, I originally misidentified this as Hyles lineata - the pattern is slightly different.

Image search on "hawkmoth" turns up some stellar photos. Here is a close-up of an eye.

@DavidS That is amazing.


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Molecules responsible for reading amino acid language

The molecules responsible for reading the language of amino acids and nucleotides is:

RNA polymerase enzyme
mRNA
tRNA
DNA

I don't actually understand what "reading amino acid language" means!
Does saying nucleotides refer to those on the DNA molecule? If so then RNA-polymerase is then responsible for synthesizing mRNA molecules which carries the same genetic code of the amino acids; or is it something else?

Is this a homework question?  I guess that "amino acid language" refers to the genetic code,  https://en.wikipedia.org/wiki/Genetic_code

This is a homework question I assume? You should show what effort you've made so far to be well received on the site. I agree it's not very well worded, however. My interpretation is that you can think of the question as asking you: "What molecule is responsible for converting between the 'code' of DNA and the 'code' of Amino Acids"

It means which molecule participates in the process of turning a sequence of nucleotides into amino acids, i.e. "reads" the sequence of nucleotides and "knows" to which amino acids it corresponds.

It is not a homework question unless studying for un upcoming exam is considered a homework question.... sorry for any inconvenience and thank you

Do you mean which molecules turn RNA into amino acids? Because that would be those in the ribosome complex.

@KoenvdH Unfortunately, I don't fully understand the question. Also it's u multiple choices questions....

Yeah, that’s one badly worded question! I’m assuming that the required answer is one/all of: ribosome/tRNAs/aminoacyl tRNA synthetase. However, this would actually be inaccurate or even wrong: these molecules read the codon language, not the amino acid language. I’m not aware of any molecule which actually reads amino acids, except maybe immunoglobulins. However, I’ve never heard of “language” in this context. Another candidate would be post-translational modification (e.g. glycosylation). But, once again, I don’t know of anything that would qualify that as a language.

Please use commas to separate the choices or bullets, it makes your question more clear.

Clarifying the premise
As mentioned in my comment, the term “amino acid language” doesn’t really make sense as far as I’m concerned. Worse: nothing, to my knowledge, is ever reading an amino acid sequence in living systems.
Yet here we are. The term “amino acid language” itself is definitely used (though, once again, I’ve never heard of anything “reading” this language).
So, to answer the question, let’s define a meaning for the term “amino acid language”:

The amino acid language is a language written by amino acids. In other words, a set of sequences consisting of amino acids.

The candidates
Now, your question is multiple choice so it’s sufficient to go through all possible choices and see if they fit:

RNA polymerase enzyme

RNA polymerase reads either DNA (DNA-dependent RNA polymerase) or RNA (RNA-dependent RNA polymerase) and produces RNA. There are no amino acids involved. This is clearly not the right answer.

mRNA

mRNA is an information-carrying molecule. But it does not “read” anything (at least not in its canonical function). Note that other RNAs are involved in recognising/reading things, but not mRNA. So, not the answer.

tRNA

tRNAs (transfer RNAs) are RNAs that carry individual amino acids. Each individual tRNA recognises a codon on an mRNA via complementary base pairing and thus “translates” the codon into a specific amino acid by the rules of the genetic code. In the context of this question, it’s fair to say that tRNAs (in combination with other molecules) are writing the amino acid language.

DNA

DNA, like mRNA, is an information-carrying molecule that does not read anything. Moving on.
The answer
tRNAs do not read amino acids in the conventional meaning of the phrase. But it’s the closest candidate here: not only does it indeed read a language, it translates symbols into amino acids. This is therefore almost certainly the expected answer, unless an acceptable answer is “none of the above”.

Thank you for your effort..... This was really confusing as I got like 3 different answers from 3 different people and I never actually came across the word reading an amino acid language which made the question far more confusing... thanks again.

I think what the question was trying to get at, though I agree it was poorly written, is that the "codes" in DNA, RNA polymerase, and mRNA have no direct connection to the amino acids; when we say a given sequence "codes for" a particular amino acid, the only thing mediating that code, connecting it to a particular amino acid, is the tRNA (though the aminoacylation process is at least if not more important).


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Can anyone identify this caterpillar?
Can anyone identify this caterpillar we found on a cauliflower? This was the only photo we could get of it.
Location : Ceres, Fife, Scotland

Can you tell us where you found this caterpillar?

Hi Chris it was found in Ceres, Fife, Scotland. I thought it could perhaps be a Green-veined White caterpillar?

It might be an imported cabbageworm:

or a green-veined white:

Both exist where you are, and the former is more common than the latter. I can't tell them apart, but consulting the pages might help.


text:
If the haploid prothallium of a fern fertilizes itself into a diploid sporophyte, does this make all ferns clones?
From what I understand in the alternation of generations in ferns, mature spores germinate into a haploid prothallium. But how does this gametophyte produce recombinant gametes if it itself develops mitotically from a haploid spore? And if the gametophyte produces its own (haploid?) eggs and sperm, how does it ultimately produce a diploid sporophyte with the same number of chromosomes as its parent? If the haploid prothallium fertilizes itself, that means it possesses two identical copies of its parent's chromosomes, which themselves are identical - there is no outcrossing between plants. So are all ferns genetic clones? Why even bother with meiosis if you don't have a recombinant mixing of alleles? Or do I have this totally confused?

No, it would not be accurate to label them clones, and the organism still goes through sexual reproduction even if they are selfed. Selfed offspring would get two copies of the "same" chromosome (when selfed within the same prothallus), when the parent might have two chromosomes of different origins, and there will also be recombination during meiosis (during spore production in the sporangia), which will alter the chromosomes. And even if all selfed offspring from the same prothallus will carry that same chromosomes, different prothalli from the same parent will carry different chromosomes, which means that all offspring will not be identical. So to label selfed ferns as clones wouldn't be accurate, since the offspring wouldn't be genetically identical to their parents and offspring from different prothalli would also not be genetically identical. The situation is similar to e.g. monoecious plants that lack self-incompatibility (especially those pollinated by wind), where selfing will be common. The difference in ferns is that all gametes on the same prothallus will carry the same chromosomes.
Also note that some ferns have mechanisms to avoid self-fertilization, and that many species have a mixed mating strategy that allow both selfing and outcrossing, usually with higher fitness in outcrossed individuals.

In ferns (and seed plants) the dominant, largest stage of life is the diploid sporophyte. Within the sporophyte, meiosis occurs producing haploid spores. These spores are dispersed and grow into the small haploid gametophyte, AKA the prothallium. The gametophyte produces haploid gametes - both egg and sperm coming from the same individual, usually. The sperm fertilizes the egg forming a diploid zygote, which grows into an adult sporophyte.
This image should help. Let me know if anything is unclear

I suppose what's confusing me is if the prothallium is if fertilizing itself, then it must have two identical copies of the its parent's chromosomes, which themselves are identical. So is there is no recombinant mixing of alleles? Are all ferns essentially clones of one another?

@BRZA The resulting zygote is not a clone. First off, the prothallium is not necessarily always fertilizing itself: sperm from one prothallium can fertilize an egg from a nearby prothallium (if the weather is wet to allow the sperm to be mobile). So, the prothallium does not have two identical copies of the parent's chromosomes. The prothallium has one recombinant copy of one of the sporophyte's chromosomes: by the time the prothallium has formed, meiosis and thus crossing over have already occurred. Even if the resulting gametes from the same prothallium fertilized each other [cont]

[cont] the resulting offspring would not be genetically identical to the parent due to the crossing over that has already occurred

It has already been mentioned that different prothalli have a different mix of chromosomes, and that in some (yet not all) ferns a single prothallus doesn't fertilize itself, e.g. because male and female gametes aren't produced at the same time.
I want to add that one prothallium usually only produces one sporophyte.
So even in cases with self fertilisation, you only get clones if the gametophyte produces several sporophytes.


text:
Length of dispersal flight of European spruce bark beetle?
I'm interested in length of dispersal flight of Ips typographus. I can barely find some information about dispersal distances, height of dispersal flight, but not at all information about how many days does it takes for one beetle to find suitable host in average? The only information I found is that it is highly variable (Forsse, E., & Solbreck, C. 1985. Migration in the bark beetle ips-typographus duration timing and height of flight. Z. Angew. Entomol. 100 (1). 47-57). I also know that it is weather dependent but this won't help me... thank you !!

You should check out this recent dissertation, which might contain useful information: Kärvemo. 2015. Outbreak dynamics of the spruce bark beetle Ips typographus in time and space.

thanks @fileunderwater! I didn't know about this one !

The number of days may still be unknown, and it is probably a large variation when they find a suitable host tree. The "pioneer males" might use "random-walks", when they try several trees before they chose the right one. Its also a large difference between endemic and epidemic periods regarding dispersals.
Anyhow, the flight distance of I.t. has been shown to be more than 8 km (see Botterweg, 1982), but during outbreaks when it can be pheromone sources everywhere most of them may disperse less than 500 m and maybe even less than 100 m. See:
Kautz. 2011. Quantifying spatio-temporal dispersion of bark beetle infestations in epidemic and non-epidemic conditions.
Whichmann and Ravn. 2001. The spread of Ips typographus (L.) (Coleoptera, Scolytidae) attacks following heavy windthrow in Denmark, analysed using GIS
and as mentioned above, the dissertation by Kärvemo and articles within.
I hope this helps.
cheers
Simon

Hi @SimonKärvemo, thank you very much for the answer and for the proposition of different papers. I hoped to obtain a type of answer as "10 days" or similar but I was sure that it will not be so simple... I am working with Kautz's paper but they simply establish that the flight  takes "several days". I also wanted to relate it to IT life cycle but this is highly variable too ( from 7 - 11 weeks - it is almost the double ! - to establish the threshold value). So, it still remains unknown... but I feel much more sure about this information now ! :)


text:
What is the proper format for genus and species names in latin?
When using the latin nomenclature for a fish in printed materials (such as Sander vitreus for walleye), what is the correct capitalization of each word?
In this example, should 'S' be uppercase only, or both 'S' and 'V' be upper/lower case?

The correct latin nomenclature is Sander vitreus, with the genus capitalized and the species name in lowercase.  This is known as binomial nomenclature.

Carl Linnaeus chose to use a two-word naming system [...] binomial nomenclature scheme, using only the genus name and the specific name or epithet which together form the whole name of the species. For example, humans belong to genus Homo and their specific name is sapiens.  The first letter of the first name, the genus, is always capitalized, while that of the second is not, even when derived from a proper noun such as the name of a person or place.

Some scientific naming conventions:

Classification example (for Homo sapiens):

Adding to it: If you abbreviate the name its the genus which is shortened. In this case it would be S.vitreus.

Awesome -- thank you both SO much for the quick and thorough responses!

@Sbechet When you like the answer (and it answers your question) you can upvote it and also accept it. This way the person who answered it get the reputation credit for it and it is a nice way of saying thank you on the Stackexchange network.


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What does the Gini index mean in a biochemical context?
What is the meaning of the Gini index, as specificed in this link, which describes the Gini index of beta-glucopyranose bound to hexokinase?
Is this true that if Gini index has a very low value that means it doesn't interact much? If Gini index is high for a compound, it will interact?

they had a heature called gini index, wanted to know what that was

+1, thanks for the clarification. Edited answer to make more sense to me, feel free to roll back if that was wrong.

The paper by Graczyk (2007) is probably relevant for you. It says that the Gini index is a measure of reactive selectivity of kinases, with values close to zero indicating no selectivity and values close to one indicating high selectivity, and it is created in direct parallel to the Gini index in economics, which is used to describe economic inequality. In its basic form, the Gini coefficient is a measure of statistical disperson. Also see Anastassiadis et al. (2011) for a more recent example where the index is used.

Abstract
  A novel application of the Gini coefficient for expressing selectivity of kinase inhibitors against a panel of kinases is proposed. This has been illustrated using single-point inhibition data for 40 commercially available kinase inhibitors screened against 85 kinases. Nonselective inhibitors are characterized by Gini values close to zero (Staurosporine, Gini 0.150). Highly selective compounds exhibit Gini values close to 1 (PD184352 Gini 0.905). The relative selectivity of inhibitors does not depend on the ATP concentration.

References:
Graczyk. 2007. Gini coefficient: a new way to express selectivity of kinase inhibitors against a family of kinases. J Med Chem. 50(23)
Anastassiadis et al. 2011. Comprehensive assay of kinase catalytic activity reveals features of kinase inhibitor selectivity. Nature Biotechnology 29: 1039–1045

"expressing selectivity of kinase inhibitors against a panel of kinases is proposed" what does this line mean, please explain

@user3237995 I assume that it means that the gini index is calculated in relation to a specific set of kinases. Biochemistry is not my area though, but I'm interested in the Gini index in general. If you look at the paper they show e.g. that the Gini indices calculated from a set of 20 kinases are very similar to the indices calculated using an expanded set of 85 kinases.


text:
Value of r (intrinsic rate of natural increase)
What is the current value of 'r' (instrinsic rate of natural increase) in India? How do we calculate it?
My book says that In 1981, the r value for human population in India was 0.0205. But this link (https://www.google.co.in/amp/knoema.com/atlas/India/topics/Demographics/Population/Rate-of-natural-increase%3fmode=amp) says it was around 22.50 in the year 1981. Such big discrepancies are a query.

Perhaps you should check the census report. You should add details to your question and be clear about what you are asking. [Edit] the question to add all necessary details. Comments should be used for asking clarification.

About the value of 22.5 (in your question); that is referring to a growth of 22.5 persons per one thousand population. So a growth of 2,3% (22.5/1000= 0.0225).

From the UN database (this info is also reported on wikipedia), the growth rate in India in 2016 was $r=1.019$.
It is computed as $r = \frac{N_{2017}}{N_{2016}}$, where $N_{y}$ is the population size at year $y$. This estimate is based on the total number of residents (regardless of their legal status).
More explanations
$r$ is simply defined as $r = \frac{N_{2017}}{N_{2016}}$. Often, you will read statistics in the sense of percentage of increase. Let's call this value $x$. $x$ is then defined as $1+x = r$.
It is just like when you put money in a bank account. If your interest rate is $x = 2\% = 0.02$, then if you had $N_{2010} = 1000$ dollars in 2010, in 2011, you'll have $$N_{2011} = 1000 + 1000 * 0.02 = (1+0.02) * 1000$$. Note that $1+0.02 = 1 + x = r$. Over $k$ years, you'll have $$N_{2010+k} = N_{2010} (1+0.02)^k$$.

My book says that r is calculated as birth rate minus death rate, and calculating it through the values mentioned on the internet, it shows big discrepancies!

https://en.m.wikipedia.org/wiki/Demographics_of_India Considering Wikipedia, the birth rate minus death rates comes out to be 11.

Per 1000 individuals, yes. Divide 11 by 1000 and you get $0.011$, which means $N_{2016} = N_{2017} + N_{2017} * 0.011$, which can be rewritten $N_{2016} = (1 + 0.011) \cdot  N_{2017}$, hence $r = 1.011$, which is pretty close to $r=1.019$. Does it make sense to you?

Do we always take the original population size as 1 for a year, while calculating this rate?

I don't really understand this follow-up question. But please see edit.

You calculation is of lambda ($\lambda$), not $r$ (instrinsic rate of increase), where $r$ is $ln(\lambda)$.

NCERT shows per capita value is divided by 1000, not hundred (%). So the data you see is 22.50 per thousand! So, the per capita rate is 22.50/1000 = 0.02250 that is almost equal to 0.0205 given in book!
To make you understand better, remember that GDP and per capita GDP is different, the same way birth rate or death rate is calculated per 1000 but when we ask per capita we have to actually divide it by 1000.
Now in 2016 , it is 0.01019 i.e. 0.0102
I hope you understand!!

It the most basic form, the intrinsic rate of increase, $r$, is defined as:
$\frac{dN}{dt} = rN = (a-b)N$
where $a$ is the birth rate per unit time and $b$ is the death rate per unit time. So $r$ is the birth rate minus the death rate. The modell can naturally also be extended to e.g. include carrying capacity or to make $r$ (or underlying parameters) functions of time or environmental variables.
However, from census data (taken at fixed points in time), you can calculate lambda ($\lambda$), the discrete-time per capita growth rate (also called the finite rate of increase), as:
$\frac{N_{t+1}}{N_t} = \lambda$
This shows the growth across a fixed, discrete time intervall. $\lambda$ can  be converted to an instantaneous instrinsic rate of increase as $r = log(\lambda)$. Using the values in Remi.b's answer (from https://esa.un.org/unpd/wpp/DVD/), this yields and $r$ of 0.0188 (i.e. log(1.019)). For a bit more background see https://en.wikipedia.org/wiki/Population_dynamics and http://www.zo.utexas.edu/courses/thoc/PopGrowth.html (or any textbook on population dynamics).

Population growth curved à when responses are not limitting the growth , plot is exponential , b when response are limitting the growth , plot is logistic , k carrying capacity

Please provide additional details in your answer. As it's currently written, it's hard to understand your solution.

this doesn't answer the OP's questions, which is specifically about the value of r for a particular population (humans in India)

Welcome to Biology.SE. If you can address the problems noted in the above comments, please also provide a citation/source for the image you are using — images should be credited to their creators just like quotes are to their authors. This is generally considered good practice in scientific communication and will help other users by providing context. ——— If you are unwilling or unable to fix these issues, please delete your post. Please take the [tour] and then consult the [help] pages for more advice on [Answer] effectively on this site.


text:
Relation between heterozygosity and allelic diversity in founder effects/bottleneck?
Can someone try to explain me why allelic diversity falls faster than heterozygosity, reminding you that we're talking about bottleneck or a founder effect? Look at this graphic:

It's clear to me that both are related, so both have to decrease.
It is clear that allelic diversity has a huge fall because there was lost of alleles (specially the rare and uncommon ones that, despite contributing less to allelle frequencies, each one has the same weight to allelic diversity, take a look at the other graphic to understand what I'm talking about).

Now, heterozygosity is specifically related to allele frequencies, and since the most rare/uncommon don't contribute much to this, the only alleles that will have a large impact on the decrease of heterozygosity are the more/most common.
Since that after a bottleneck, (probably) the alleles remaining are the most common, heterozigosity will decrease less than allelic diversity.
I'm aiming for some complementary ideas about this, specially when it comes to statistical models that describe heterozygosity. It's hard for me to understand the relation between allele frequencies and heterozygosity when it comes to this case - in what manner do allele frequencies influence H?

What is the source of the graphs?

Unfortunately, I don't know. It was provided to me without references.

So this is part of a homework/course work question?

Well, yes. Is there a problem?

No, not really. We just normally add a tag to homework questions (which I've now done). However, it is a bit unclear to me what your specific question is, since you seem to understand/explain why allelic diversity should decrease more than heterozygosity. Are you looking for a mathematical relationship between heterozygosity and allelic diversity?

Yes! I've an idea but I would like to complement it with a mathematical relationship.


text:
Importance of knowing GC Content of an organism
I was looking at the GC content percentages of few organisms. I also know calculating the GC content percentage. But, what I want to know is, what information would we get., let us suppose if human genome has 40% of GC in the genome.
Does it help us compare the number of genes between different species, for example, a bacteria has less GC content than human, so does it mean Human produce more genes than bacteria?
or Is it that the 40% of the genome,has coding regions in them and more genes are found in those regions? What is the number "40%" actually indicate us?
Please help me understanding the concept. Would be thankful your answers and suggested reading.
EDIT: My question is what does knowing percentage of GC content help us knowing? If the GC content is 40%, does it correlate to number of genes in the genome?
Regards,
Prakki Rama.

I don't understand your question. Do you want to know the function of the different GC-contents of different genomes?

Hi, Please check my edit.

Interesting question. The GC-content seems to evolve over time and it also seems that the GC-content of coding regions is higher than for the surrounding non-coding regions (see reference 1). If there is a specific function for this higher GC-content or not is (if I understand this right) debated among the groups which do research in this field. Have a look at the references (and probably also their references) to decide on this:

Both selective and neutral processes drive GC content evolution in
the human genome.
Integrating genomics, bioinformatics, and classical genetics to
study the effects of recombination on genome evolution.
Recombination Drives the Evolution of GC-Content in the Human Genome
GC-Content Evolution in Mammalian Genomes: The Biased Gene
Conversion Hypothesis
Contrasting GC-content dynamics across 33 mammalian genomes:
Relationship with life-history traits and chromosome sizes

Thanks for the references. So, is it that the number "40% GC content" is just a statistic to know about the organism and there is not much information associated with the number?

As far as I understand it, yes.


text:
Why do insectivorous birds migrate?
Living in northern latitudes, I have always wondered why do migratory birds invest so much time and energy to travel twice a year the vast distances between their breeding grounds and wintering areas. The most commonly found explanation, and the one I am grown accustomed to, is the scarcity of resources, resources meaning food and nesting places.
For years I have considered this a quite convenient explanation but recently I came to rethink it.
As you know, many of the longest migrating birds are insectivorous such as European Pied Flycatcher that breeds in much of Europe and western Asia but spends winters in western Africa. While it is easy to see the scarcity of food (insects) in northern breeding areas during winters, it is more difficult for me to see the scarcity of food in southern wintering areas during summers. - Take, for example, ants, that I expect, are abundant in those places all year around. Considering their total biomass, they would seem to hold a potential for a stable food source for masses of insect eaters with minimal food gathering effort required. So why migrate?
Is it that ants (or any other seemingly overly abundant invertebrates such as termites and mosquitoes) are not nutritious enough? Or are they too stingy and poisonous perhaps?
As for nesting places, I am aware that many birds defend their home range (thereby setting an upper limit for population density), but I imagine that such behaviour could be subject to change (or never had emerged in the first place) if there was no need to compete for other resources (mainly for food).
Or are the primary constraining factors disease and predation that would follow from a larger population density?
So in short, my question is, what is (/are) the primary reasons(s) for insectivorous birds to migrate instead of staying in their wintering areas and feeding on (seemingly abundant) local resources such as ants?

Reason for Migrating Birds:
Migrating for a Meal
Food scarcity: If birds will stay and eat all the bees they find, there will be no bees to feed on for the next generation. So, they fly away to take advantage of these places where there is abundance of food. And when the insects or replenish they come back.
Migrating for Family
Flocks of bird can be easy prey as they are small and are in a huge number. Also for the young ones who can't fly it is very dangerous. (Though they abandon the young one as soon they can fly)
Migrating for better Climate:
Some of the species fly away to sustain the temperature and come back when it is suitable for them. So, Northern birds migrate to tropical places for the winter and come back to north for the summer to lay eggs.

There are too many other theories for bird migration. It had been confirmed that migration is often due to genetics than any other reason.
Further Reading: THEORIES OF BIRD MIGRATION
Sources:
[1] http://birding.about.com/od/birdbehavior/a/Why-Birds-Migrate.htm
[2] http://en.wikipedia.org/wiki/Bird_migration

Just want to mention, not all insectivores are abandoned once they can fly. Specifically Magpies are still fed by their parents for 3-4 weeks after they learn to fly.
http://www.rspb.org.uk/discoverandenjoynature/discoverandlearn/birdguide/name/m/magpie/life_cycle.aspx
They fledge after 26 to 30 days, and are fed by the parents for a further four weeks after leaving the nest.


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Implications of what the discovery of Naia means
Recently a discovery was made of a ~12,000 year old girl in Hoyo Negro in Mexico.
This has been covered by many different news agencies.
I'm confused however by many of the reports.  Does it strengthen the hypothesis that the ancestors to the Native Americans came over the Bering Strait?  Or is there still some doubt on the matter?
Additionally, what are the arguments against the Bering Strait migration?

As far as I can remember from skimming the published paper, it does provide support to the hypothesis that the first Americans probably migrated over a Bering Strait land bridge sometime during the last ice age. Remember, individual scientific findings rarely "prove" anything, they just support or refute a certain hypothesis (what a layman would call a "theory", a word which has a rather different meaning when used by scientists).

I would rather call it hypothesis for this reason instead of theory.

@MattDMo, updated to reflect your and Chris' suggestions.

The discovery strengthens the bering strait land bridge hypothesis because if I remember right they did genetic analysis and her ancestors were almost certainly east asian. As for opposing migration models, they involve boats. Some evidence exists for polynesians reaching the west coast of south america, but probably in small numbers and not before humans walked in from the north. There is more information here: https://en.wikipedia.org/wiki/Models_of_migration_to_the_New_World


text:
What is the connection between exercise and muscle growth
From a physiological perspective, all that is done during exercise is the expending of energy in the form of ATP to fuel muscle contraction and extension.
When I looked up why muscle grow due to exercise, there is the claim that recovery of micro lesions formed during exercise enables slight growth of muscle. I am not sure how micro lesions are formed and intuitively, these micro lesions should cause atrophy of the muscle rather than strengthening of the muscle fibers.
Further there is no logical connection as to why muscle fibers would be strengthened rather than just restored to its previous form during rest.
Can someone help me make the mental leap from the consumption of ATP through exercise to muscle growth?

Muscle growth and development is mediated by "trophic factors" not biochemical reactions (ATP) or muscle contraction directly. The best method of releasing tropic factors is exercise and not electrical stimulation or biochemical reactions (ATP) or biomechanical contraction.
Nerve ending release growth or tropic factors which stimulate muscle growth and for example if the nerves die off either due to injury or disease (ALS) the muscles will atrophy.
Not all of the tropic factors are as of yet known, but it is these tropic factors that stimulate muscle growth, not the biochemical or biomechanical reaction of the muscle (contraction). One can not as of yet stimulate muscle growth by delivering electrical energy to the muscle, for example (it has been tried to in an effort to maintain muscle mass in critically ill patients).
There is a review of the trophic factors here - http://neuromuscular.wustl.edu/lab/trophic.htm
And a review of electrical stimulation - http://www.medword.com/MedwordStore/PCP/EMS_truth.html
There are many claims of benefit for electrical stimulation, such as regeneration of the facial nerve in facial paralysis, such as Bell's palsy.
The "problem" is that the prognosis in Bell's palsy is very good, even without electrical stimulation, and so it is difficult to "prove" benefit with electrical stimulation:

With or without treatment, most individuals begin to get better within 2 weeks after the initial onset of symptoms and most recover completely, returning to normal function within 3 to 6 months.

http://www.ninds.nih.gov/disorders/bells/detail_bells.htm

Statistically, the natural history without treatment was described in a study of 1011 patients in 1982 [8]. One-third had an incomplete paralysis, and two-thirds had complete paralysis. Overall, 85 percent showed signs of recovery within three weeks, 71 percent had complete recovery, 13 percent had slight sequelae, and 16 percent had residual weakness, synkinesis and/or contracture. Patients with incomplete lesions had a 94 percent rate of return to normal function, while only 60 percent of those with clinically complete lesions returned to normal function.


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Does the human hand have 27 degrees of freedom?
I have counted the degrees of freedom in my hand over and over and I keep getting the number 19.
Suppose each finger has 3 degrees of freedom. Then 5 * 3 = 15. The wrist can rotate around or back and forth so that contributes to 4 degrees of freedom. In total the hand has 19 degrees of freedom.
From a cursory google search, I can notice that it is commonly agreed upon that human hand has 27 degrees of freedom. Can someone provide a good reference and explanation for this?

The first link in that search is a paper which says this: "The human hand has 27 degrees of freedom: 4 in each finger, 3 for extension and flexion and one for abduction and adduction; the thumb is more complicated and has 5 DOF, leaving 6 DOF for the rotation and translation of the wrist."

@canadianer is there a video or some sort that I can visually see how this is the case?

Why is this flagged as "unclear"? Hasn't @canadianer already provided the answer in the comment? Can't you answer it canadianer? Better to answer a question than have it deleted. Admittedly, it's quite a poor question but I am happy to edit it a bit after an answer is put forward

@AliceD I didn't answer because I don't know anything about it and the OP seems to want a better explanation. I don't think the question should be closed.

@canadianer - yes I see his video comment. Personally, I think you should answer, you have my upvote :) But I understand your position. It won't result in an accepted answer I guess. Up to you!

IMO a degree of freedom allows movement in all co-ordinates along that direction. Fingers, wrist and elbow have restricted movement. I think that should bring down the DOF (https://www.cs.cmu.edu/~rapidproto/mechanisms/chpt4.html#HDR52B)

Keeping in mind that I know nothing about this, I will try to explain why the hand can be modelled with 27 degrees of freedom. This is just my interpretation of this paper, which says:

The human hand has 27 degrees of freedom: 4 in each finger, 3 for extension and flexion and one for abduction and adduction; the thumb is more complicated and has 5 DOF, leaving 6 DOF for the rotation and translation of the wrist.
To accurately model the hand, a complete model of the muscles, tendons, bones and a neurological control structure is necessary. The dynamics of such a complex model are still poorly understood, forcing the use of simplified models. Current models are too simplified for our purpose so we turn to recent work from the medical community to motivate assumptions used in a new model that we propose here. We use a 27 DOF model of the hand with the following sim- plifying assumptions:
  1. The thumb is independent of the other fingers.
  2. Adduction/abductionofthefingerjointsareindependent.
  3. Motion frequency does not affect joint interdependence.
  4. Both hands have the same interdependence model.
  5. The posture of the wrist and the rest of the arm do not
  affect the underlying interdependence structure.

Incidentally, this implies to me that there are different models of the hand with different assumptions that use a different number of degrees of freedom.
Anyways, take a look at this hand:

[source]
And now, follow along with your own hand!

finger (4 DOF): each finger has 2 interphalangeal joints between the distal, middle and proximal phalanges that allow for flexion/extension (2 DOF); each finger also has a metacarpophalangeal joint between the proximal phalanx and the metacarpal that allows for flexion/extension as well as abduction/adduction (2 DOF)
thumb (5 DOF): an interphalangeal joint between the distal and proximal phalanges allowing flexion/extension (1 DOF); a metacarpophalangeal joint between the proximal phalanx and metacarpal allowing flexion/extension and abduction/adduction (2 DOF); a carpometacarpal joint between the metacarpal and trapezium allowing flexion/extension and abduction/adduction (2 DOF)
wrist (6 DOF): between the carpals and radius allowing flexion/extension, abduction/adduction and supination/pronation (3 DOF); I think when the authors refer to translation of the wrist, they are simply saying that hand can be moved in all planes of 3D space (ie up/down, side to side, forward/backward - 3 DOF)

Since we have 4 fingers, they give 16 DOF. Adding the 5 DOF of the thumb and 6 of the wrist, we get 27. Please nobody question my reasoning. Thank you.

By the last 6DOF, the article just means the placement of the whole hand as an object in 3D space. They don't care about the radius, it's not a part of the hand.

An observations based on my hands: I think there are 3 more degrees of freedom, bringing the total up to 30DOF. I actually am able to move my metacarpals up and down independently, even quite noticably and somewhat easily for the pinky and ring fingers. Taking one as the reference, the other 3 add 1DOF each. The easiest way to observe it for me is to make a fist and alternate between squeezing these two fingers shut and trying to extend them while also resisting extension by trying to keeping the joints between metacarpals and phalanges at 90°. Or you can just move them with the other hand.

Note that my goal here was to find all visible degrees of freedom, not just "practical" ones, to make hand poses look more natural. The extra 3 I described above allow the knuckles to be in an almost straight line or in a very noticable curve, so I count them even if they are "useless". And I might as well give the joint between thumb's metacarpal and phalange just 1DOF instead of 2, for me it bends sideways about as well as all inter-phalangial joints.


text:
Help understanding the word 'glycosaminoglycan'?
In my biochemistry course I have to know about various polysaccharides and variants, and I am struggling with remembering them. I think it would help if I could break down their names.
For 'glycosaminoglycan' i think
-glycan just refers to the fact that it is a polysaccharide. Some, but not all polysaccharides have glycan in their name, e.g. glycogen vs amylase and amylopectin
-amino means there is an amino group somewhere in there?
That's all I can think of...

Find a booklet about chemical nomenclature, I used to get one for free as a scientific bookshop. https://en.wikipedia.org/wiki/Chemical_nomenclature I am sure there are also plenty websites with catalogs of this.

There is a specific method for drawing a molecule based on it's named components. Organic Chemistry generally requires that you understand the main nomenclature, look for videos on it if you need different infos.

Glycosamines (or amino-sugars) are monosaccharide derivatives with an amino group substituting the hydroxyl group at second carbon. Glycosaminoglycans (GAG) usually contain repeats of a disaccharide unit one of the component of which is an amino sugar. GAGs are not strictly polymers of amino sugar monomers as the name might misleadingly suggest.


text:
NCBI EUtils. Get Homolog infromation using Gene ID
How to retrieve homologs information in xml or json format from NCBI using gene ID?
I tried one URL:
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=homologene&geneid=9&WebEnv=???&query_key=???

I dont know what to add in question mark regions

I'm voting to close this question as off-topic because it is a pure programming question better suited for BioStars.

I think the default format is xml. See more about EUtils here.

From Entrez Programming Utilities Help [Internet]:

Input: Any Entrez text query (&term); Entrez database (&db);
  &usehistory=y; Existing web environment (&WebEnv) from a prior
  E-utility call

To avoid the error messages, web1, and key1 can be used as terms (these are usually being used to associate with other searches), however this returns no data, probably because the ID you supplied was simply "9", and it remains unclear exactly what you're searching for in the context of other queries.
For example:
esearch.fcgi?db=<database>&term=<query>&usehistory=y

# esearch produces WebEnv value ($web1) and QueryKey value ($key1)

esummary.fcgi?db=<database>&query_key=$key1&WebEnv=$web1

So whilst view-source:eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=homologene&geneid=9&WebEnv=web1&query_key=key1 is a valid query, it's not pointing to anything.


text:
Chromosomes are of different size but why do all chromosomes have similar GC percentage?
When I browsed NCBI I saw a pattern: even if the chromosome sizes, number of genes, and number of proteins are different, GC% in chromosomes tend to be similar. The examples are linked below.
Yeast,
Plasmodium falciparum
If you see Mitochondria genome it is not very similar to chromosome. Why all chromosomes tend adjust their GC% near to the average of total GC%
Is there a specific reason related to metaphase of meosis?
to further clarify I have some images to help

The chromosome size or genes in an organism are not adjusting near the average of their total but GC% does. It has only 3-2% (falciparum) or 3-4% (vivax) variation in GC%. It feel like its balancing like equalizer. Why?

Just to clarify: are you asking why chromosomes of very different sizes each have an average GC content that is similar to the average GC content of the genome?

Yupp you got it... I just want to know why and how at any stage of evolution an organism like [plasmodium vivax] (http://www.ncbi.nlm.nih.gov/genome/genomes/35?details=on&) (43-47%) and faciparum (18-20%) (2 evolved types) try to maintain similar GC% in all chromosome (look a the links given the it feels all chromosomes are maintaining their GC% percent in chromosomes and they dont care for amount of genes or chromosome size)

As @dd3 points out, average GC% indicates a need for stability and coding regions or structural regions of the genome may need to be more stable.  But the largest %GC in genomes are found in thermophiles - organisms which live in high temperature water - in hotsprings and undersea geothermal vents. This review mentions how some thermophiles can be found with 50% GC.  The extreme thermophile Thermus thermophilus can have a GC% content of 69.4%.
But you are asking how does GC content get averaged out over the length of a large genome.  The answer is variation and selection.  When a gene needs to be more stable because of genomic function or because its trying to live in a hotter environment mutations that convert A/T to G/C base pairs will convey an incremental advantage to survival and will tend to be retained in the gene pool as long as no greater disadvantage to the mutation results.  Over time and as the stability creates a greater advantage, GC % will migrate further and further away from the mean.
This works for both thermo-tolerance and because of the biofunctional constraints of being a telomere, centromere or a coding region - stability and coding constraints play against each other to converge on an optimal GC content in any given stretch of the genome.
Conversely most genomes have a GC content below 50% are migrating there because too much stability can have a cost as well.  Breaking up the DNA helix for transcription and other cellular processes must go smoothly as well for example.
Coding regions are significant for bacteria (E coli is 89% coding sequence).  For coding sequences, the genetic code is logically 50% GC on the average, but if you look at the actual codons in the diagram below you will see that except in the case of a single codon case (tryptophan, methionine) the third base always has a GC option, allowing for a GC content in the mid 60 percentiles.  The constraint of allowing coding sequences to freely vary is only an approximation - in some cases substitutions to amino acids with GC rich codons might move the cieling up a bit. And the more frequent amino acids have the possibility of making 2 or 3 bases of their codon GC bases.  Overall it would be remarkable to find a bacteria with GC% greater than 72%.  Mutations and the requirements of proteins being coded for would simply not allow it.

So: over evolutionary periods these GC mutations accumulate where they are helpful, even to the extent of 2/3 of the genome being GC pairs.  The strongest selective force to accumulate a high average GC% for a genome is exposure of the genome itself to a high temperature environment.
Note that this thermo-stability argument doesn't count for many animals because they do regulate their body temperatures.

I liked your line "stability and coding constraints play against each other to converge on an optimal GC content in any given stretch of the genome." It feels more suitable to my question.  Can I get a reference journal please

Thanks.  That thought is a commonly known idea and its rederivable in practice. Let me add to the answer above..

There is significant variation in genomic GC content, both between species and within an individual genome. An average GC content in the range of 35%-45% is common, although there are definitely organisms that fall outside this range. The plasmodium species you link to above is an example of extreme AT richness (low GC content), whereas some bacterial genomes have as much as 70% GC content or more.
For eukaryotic genomes, nucleotide composition is not uniformly distributed. Just because a genome has an average GC content of 40% does not mean you can select any 10kb region in the genome and expect that region to have +/-40% GC content. Rather, eukaryotic genomes are a mosaic of large regions which internally have a very uniform composition, but whose composition is quite different from flanking regions (isochores).
So although all the chromosomes of a particular organism may have similar average GC content, realize this is just an average and that nucleotide composition varies significantly throughout the genome.

Thanks, I truly get nucleotide composition varies significantly (A:T:C:G changes) but still HOW GC% remains similar throughout all chromosomes. To further clarify vivax (V)(43-47% range) and faciparum (F)(18-20% range) are of same plasmodium family. Eg chr 11 of both have almost same size but their GC% percent fall in particular given range(V: 45:1%, F:19%). It feels like differently evolved organism are trying to maintain particular range of GC%. HOW? And journal reference would be much appreciated.

Good answer from Daniel. I'd also add that there can be significant differences between chromosomal or nuclear DNA GC content and that of extra-chromosomal entities like mitochondrial and chloroplast genomes or (naturally occurring) plasmids. These DNAs have different constraints on them (replication, sub-cellular location, eg) and that may be reflected to some degree by a GC content different than that of the nuclear chromosomes.

To begin, one might ask "What is the advantage of higher GC content?"
Higher GC content is associated with higher stability of the DNA, and accordingly, people have suggested that this is important for protein-coding regions.  It has been found that there are quite a few protein-coding regions in GC-rich regions, but I am not sure whether the converse is true, which is the important part.
If the converse is true, then one might look at the distribution of protein-coding regions across the chromosomes and correlate it with GC-content. If also the size of the protein-coding regions in a given chromosome is proportional to the size of the chromosome, then you would have a reason as to why the average GC content of each chromosome is similar.
However, I recognize that this is all very speculative.  Does anyone have better ideas?

I liked the idea of proportionality of chromosome protien coding size and genes.. thanks. Why this question made me think it is important to ask because evolution is with random mutation process and with new environmental conditions the orgamism evolves to form new genes & this will cause random huge variations but by looking at GC% information, though there might be huge variation in sequences of chromosomes, a life is conspiring to maintain an equilibrium in AT:GC ratio. life doesnt thinks It has to keep ATG at beginning and poly A tail end for gene. life just checks the equilibrium


text:
Conclusions from hybridization results
A double stranded DNA was denatured in a mixture that included mRNA from a gene in the segment. The mixture was then cooled to promote RNA and DNA hybridization. The following figure the results.

Which strand is DNA/RNA?
What is source of the genetic material (Prokaryotic/Eukaryotic)?
Which segment is exon/intron?

Give us at least a try of your thoughts. The answer is not very complicated.

I thought P is exon and Q is intron. I is RNA and II is DNA from bacterial cell

You are almost right. I modified you picture a little bit to answer it:

Structure I is indeed DNA, structure II is processed RNA.
This is because in I you see loop structures which have no complementary part in the RNA anymore, these are introns (structure Q and the flanking loop regions to P). P is an exon flanked by two introns.
The end of the RNA is not complementary to the DNA because the poly-A tail has been added here.
The DNA is eukaryotic since you have introns and exons (which are not present in bacteria) and since the processed RNA contains a poly-A tail (which is also not present in bacteria).

Everything is fine except that from this figure you cannot conclusively say that RNA is poly-A tailed.

This is the 3' region in which DNA and RNA can not hybridize. Additionally you could also think about a 3' untranslated region there.


text:
Clarification on Hatch and slack pathway
The following is a minor clarification that I want to make, since it is rarely addressed directly in most of the texts I have gone through.
In C₄ pathway, the chloroplasts are dimorphic, that is, the bundle sheath chloroplasts contain RuBisCO, but lack grana and can hence perform only the light-independent reactions. The mesophyll chloroplasts lack RuBisCO but contain the granal apparatus to perform light reactions for synthesis of ATP and NADPH. The bundle sheath cells are impervious to gaseous transport (to prevent the entry of O₂), but recieve the required CO₂ by the intake of an organic acid produced by CO₂ fixation by the mesophyll cells.

But, to effect the Calvin cycle in the bundle sheath cells, it
  requires a high concentration of the light reaction products, i.e.,
  ATP and NADPH. Since they themselves lack grana, they must obtain the required share from elsewhere. Where do they obtain it
  from?

My guess is that NADPH enters the bundle sheath cell with the organic acid primarily produced in the mesophyll cells where light reaction occurs. ATP is met by a similar uptake plus the utilisation of the ATP produced by respiration. I need to confirm this as it is usually never addressed in texts.

I guess they go via plasmodesmata.

I am not sure about the source of ATP but I can tell you something about NADPH.
The conversion of malate to pyruvate and CO₂ by malic enzyme is carried out in the bundle sheath cell. This process produces NADPH.

See the very 1st thing is bundle sheath cell shows very less concentration of Grana, hence we say Grana is absent,  the required amount of ATP & NADPH₂ are also transported from mesophyll cell to bundle sheath cell via plasmodesmata.


text:
Assembling DNA fragments with ~10kb overlap in vitro
Let's say I have two fragments of bacterial DNA (~50kb in length each) that overlap on the ends by roughly ~10kb; the overlap sequences are unknown. I would like to assemble these into longer fragments (in vitro) in some way, but the methods I've found so far rely on 24-40bp known overlaps (e.g., the isothermal assembly process in DG Gibson et al., Nature Communications 2009).
Anyone have any idea? I'm kind of new to this molecular biology stuff, so if this is an open problem, I apologize. I'm mainly just making sure I'm not overlooking something obvious. For all I know, there could be a standard protocol for this. Thanks in advance!

As far as I can see, typical overlaps are between 20 and 100 bases. These extreme long overlaps may generate some "funny" results which may result in a DNA that you don't want. What do you know about the bacterial DNA you are working with? Can you sequence the ends to find out how big the overlap is?

Thanks for your comment! My problem is essentially that I need fairly long DNA fragments from cells, but the extraction process tends to break them apart more than I would like. I'm just wondering if there exists some method to re-assemble them after extraction without sequencing. The overlap may be anywhere from nothing to several kilo-bases.

Can you use a different extraction method? Look into methods to prepare BACs from bacteria, they are several hundret kB in size and need to be prepared intact in order to use it further.

Good point. I currently get the DNA already-fragmented from a collaborator and could request a different method for future purposes. I thought if there were some way to easily assemble the ones I already have then it would be worth a shot, and if there wasn't a method already, then it would at least be interesting to think about :)


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Getting xyz co-ordinates from a .map file (CCP4 format) in VMD
I have a .map file which contains x-ray crystallography data of a bacteriophage. The format of the file is CCP4. I can open the file using VMD. However, I am unable to get the xyz co-ordinates. It shows the following error when I click on the option of saving data in xyz format:
`No timesteps selected; trajectory file will not be written.'
It is a big file of 64MB.
The file I am referring to may be downloaded at:
ftp://ftp.ebi.ac.uk/pub/databases/emdb/structures/EMD-1086/map/emd_1086.map.gz
Can't we save xyz co-ordinates for CCP4 files? Or is it possible to extract any other form of data?
I am new to VMD and these formats.
Any help would be appreciated.

It's an electron density map. What xyz coordinates do you want to extract?

Just Download and Install: CCP4: Software for Macromolecular Crystallography

CCP4 is a suite of 200+ programs, just installing it won't solve any problem.


text:
What's the physical meaning of Svedberg unit?
Sedimentation coefficients, using a centrifuge, are expressed using Svedberg unit (symbol S, sometimes Sv). Wikipedia states that $S = 10^{-13}$ sec but I also saw in a book that actually $S = 10^{-13}$ sec/$\text{rad}^2$. Which of these is correct?
I know that a 50S ribosome has higher molecular weight than a 30S ribosome and for that reason the 50S would travel faster (on a test tube placed in the centrifuge) than a 30S, but if substitute S by $10^{-13}$ sec, for me it's a little bit-non intuitive, because 50S would be $50\cdot{10^-13}$ sec (and that is greater than $30\cdot{10^-13}$ sec), which means it takes more time to travel? Obviously not, so what's the physical meaning of time in this situation?
In response to Alan Boyd:
"In other words, at 1x g a 1S particle will travel at $10^{-13} m\cdot s^{-1}$" or $10^{-12}$?
Indeed 5.5h is a reasonable value but I still cannot understand the significance of the ratio between velocity and acceleration which corresponds to Svedberg units (in seconds).
Maybe $50\cdot{10^-13}$ sec is the time that our ribosome takes to reach the terminal velocity in the fluid? That would make some sense, for example, if I drop an unfolded A4 paper to the ground the time it will take to reach terminal velocity will be lower than the time a A4 folded paper will take to reach it's specific terminal velocity, which is higher than the velocity from the unfolded A4 paper, because the area is larger (the friction force acting on it will be very high) which is consistent with the observations that are made (in centrifugation objects with larger surface area will travel at a slower terminal velocity). What do you think ?

Wikipedia:

The sedimentation coefficient is the ratio of the speed of a substance in a centrifuge to its acceleration in comparable units. A substance with a sedimentation coefficient of 26S (26×10−13 s) will travel at 26 micrometers per second (26×10−6 m/s) under the influence of an acceleration of a million gravities (107 m/s2). Centrifugal acceleration is given as rω2; where r is the radial distance from the rotation axis and ω is the angular velocity in radians per second.

In other words, at 1x g a 1S particle will travel at 10-13 m s-1 = 0.1 pm s-1
Particles with higher values of S will travel proportionately faster, and increasing g force will also increase sedimentation rate.
Let's look at the example of a 50S ribosome at 100 000 g:
rate of sedimentation = 10-13 x 105 x 50 m per sec = 50 x 10-8 m s-1
So how long to travel 10 cm = 10-2 m?
=10-2/(50 x 1010-8) s
= approximately 5.5 h, which seems about right.

I edited my question, in response to your answer because my comment was too large.

You are overthinking. Our ribosome is in circular motion so is experiencing a constant acceleration, which is why the WP quotation goes on to define centrifugal acceleration. http://en.wikipedia.org/wiki/Circular_motion

I'm asking for the intuition to compare the value of 50S and 30S in seconds. I can go to the formula and say that the centriptal acceleration experienced from both objects is the same therefore to have a greater S the terminal velocity must be greater and obviously 50S expirience a greater terminal velocity, but what does that quotient mean? What does the time indicate?