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How was the resemblance between apes and humans explained in pre-Darwinian biology?
Humans and apes have somewhat obvious similarities, these must have been apparent to natural philosophers before the possibility of a common ancestry was first proposed in the mid-1800's. These proposals were not formally made in Darwin's On the Origin of Species (1859), but his general ideas of common ancestry were built upon in Thomas Huxley's Evidence as to Man's Place in Nature (1863) and then Darwin's The Descent of Man (1871).
How was the resemblance between apes and humans explained prior to this shift in thinking?

The time before Darwinism, people believed life as an entity which is created rather evolved. But there were great biologists interested in the relationship between species, who deliberately thought of evolution ideas and some of them believed in ape-human similarities and placed humans and apes in same group.

In 1699, Edward Tyson, an English anatomist, dissected an ape specimen(chimpanzee) and showed that its anatomy closely approaches ours.But he didn't established any relationships between humans and apes. It was first done in 1738 by Swedish scientist  Linnaeus in his book Systema Naturae .After that in 1759, Lamarck, a French naturalist  who was Darwin's predecessor in general theory of evolution, stated that humans were derived from up-right walking apes.

In 1759, just half a century before Darwin was born and precisely one hundred years before he published his famous book , "Origin of Species", Linnaeus, the great Swedish scientist, discovered that man was a mammal. He then placed man in the Order of primates, which means literary the first, or the highest,order of mammals.It comprises all the monkey like forms, including the man-like apes.
  Reference

References
Primate Evolution and Human Origins - Russel L. Ciochon & John G.Fleagle
Human Evolution: A Guide to the Debates - Brian Regal

It seems Aristotle discovered this prior to Linnaeus: "The monkey, as has been observed, is furnished with a tail. In all such creatures the internal organs are found under dissection to correspond to those of man." (Historia Animalium II.9, courtesy this comment).

The concept of evolution was widespread even before Darwin. For instance, Linnaeus, Lamarck and Erasmus Darwin (C. Darwin's grandfather) all expressed evolutionary ideas.
Another interesting example is the German philosopher Immanuel Kant, which appears to have had rather well-developed ideas about evolutionary change, a common origin of life, that also included humans:

The agreement of so many genera of animals in a certain common schema, which appears to be fundamental not only in the structure of their bones but also in the disposition of their remaining parts,—so that with an admirable simplicity of original outline, a great variety of species has been produced by the shortening of one member and the lengthening of another, the involution of this part and the evolution of that,—allows a ray of hope, however faint, to penetrate into our minds, that here something may be accomplished by the aid of the principle of the mechanism of nature (without which there can be no natural science in general). This analogy of forms, which with all their differences seem to have been produced according to a common original type, strengthens our suspicions of an actual relationship between them in their production from a common parent, through the gradual approximation of one animal-genus to another—from those in which the principle of purposes seems to be best authenticated, i.e. from man, down to the polype, and again from this down to mosses and lichens, and finally to the lowest stage of nature noticeable by us, viz. to crude matter. And so the whole Technic of nature, which is so incomprehensible to us in organised beings that we believe ourselves compelled to think a different principle for it, seems to be derived from matter and its powers according to mechanical laws (like those by which it works in the formation of crystals).

(from: Kant. 1790. Critique of Judgment, MacMillian 1914 (translated by Bernard), https://www.gutenberg.org/ebooks/48433)


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Are there grass or fiber eating birds?
My understanding, that may be wrong, is that cellulose/fibre has little nutritional value to many animals because it's hard to break down thus making consumption inefficient. However, Ruminating mammals, other mammals such as black bears, and many insects such as grasshoppers digest grasses.
Are there any birds with the gut flora to break down fibre? Or even some that eat grass but digest it in another way?

The hoatzin has a digestive system that makes use of bacterial fermentation. Many other birds also consume grass, e.g. ostriches, ducks and geese.
There's also a large body of literature on how birds can digest cellulose.

+1 It could also be noted that the fact that Canada Geese eat grass is one of the reasons that they are thriving (i.e., a nuisance) in the human constructed suburban environment of lawns and ponds.

My society finch love to eat moist grass particularly orchard grass. Nibbling the whole strand they have chosen back and forth until they are satisfied with the texture and then proceeds to swallow it. They brake most grass into no bigger than an inch in length. I buy the orchard grass from most pet stores. problem with that is the grass has been dried. not very suitable for eating but Fantastic Four nesting. I grab a handful of dry grass and mist it with water then place it in a plastic sandwich bag, put it in the microwave for 30 seconds.
Do not completely seal the bag.
When i place it in the enclosure its like bird ice cream. fantastic treat!

Welcome to Biology SE and thanks for your interesting comment on your finches. However, while this answer would be more than suitable at Pets.SE, here at Bio.SE we expect a little bit more science behind answers. I have flagged it to be converted into a comment instead. Once you gain enough reputation you can place comments anywhere.

If possible can you add a picture or something.

source: Stack Exchange

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Simple Mendelian sex-linked chromosome fruit fly question
From my molecular biology textbook:

When red-eyed flies (dominant) were mated with white-eyed flies (recessive), most, but not all, of the F1 progeny were red eyed. Furthermore, when the red-eyed males of the F1 generation were mated with their red-eyed sisters, they produced about one-quarter white-eyed males, but no white-eyed females. In other words, the eye color phenotype was sex-linked.

First, wouldn't recombination scramble the eye color alleles among the sex chromosomes?
Secondly, even without recombination, the F1 generation will be heterozygous and all F1 flies will have white and red alleles. Some F1 males will have a white X and some F1 females will have a white X, in which case it should be possibly to have an F2 white fly.
Can someone explain this?

I think the text is slightly misleading. But before going into the detail genetics of eye color let's answer your first question.
First, wouldn't recombination scramble the eye color alleles among the sex chromosomes?
Two X chromosomes do recombine but one X and one Y chromosome do not recombine (to the exception of the so-called pseudo'autosomal region).
I am not sure why recombination would change anything here. I think the eye color of flies in determined by a single locus.
How is this possible?
Let's go through the text slowly because I think the text is a little misleading. I am suggesting the only scenario I could think of that would explain the observed pattern. Note that this scenario also depends on the interpretation of the text and I would need more info on the experience to make sure my interpretation is right.

When he mated red-eyed flies (dominant) with white-eyed flies (recessive), most, but not all, of the F1 progeny were red eyed.

Actually, only males are sometimes white eyed here. And to be more accurate, if sex was uncorrelated form eye color in the parental lines, then half of the males should have white-eyed.
What was happening here is that red is dominant, white is recessive and the locus for eye color exists only on the X chromosome. As a consequence, all F1 females are now heterozygous (and display the dominant red-eyed phenotype) and all males are hemizygous, half of them having the red-eyed phenotype while the other half have the white-eyed phenotype.

Furthermore, when Morgan mated the red-eyed males of the F1 generation with their red-eyed sisters, [..]

Let's forget about the white-eyed males from above, we will just cross the red-eyed males with their sisters.

they produced about one-quarter white-eyed males, but no white-eyed females.

By they produced about one-quarter white-eyed males what is meant is that a quarter of all individuals were white-eyed males. That is half of the males were white-eyed. The other three quarters of the individuals were red-eyed.
The males received their X chromosome from their mother only (as they can only receive the Y chromosome from their father). Half of the males have therefore received the white-eyed allele while the other half have recevied the red-eyed allele. For the females, they all received from their mother either a white-eyed allele from their mother or a red-eyed allele. As we selected only father that had red eyes in the previous step, all father carry exclusively the red-eyed allele. As a consequence, all females receive a red-eyed allele from their father. Therefore half the females are homozygous red-eyed or heterozygous. In any case, all females are red-eyed.

Wow, that was really clear and easy to understand! Just one question: doesn't crossing over occur between X-chromosomes in females?

Yes, crossing over occurs between X-Chromosomes in females.

In the first cross, if we talk of a single mating pair of flies, one parent is red eyed, one is white eyed. The ambiguity about sex leaves two options, 1) red eyed male crossed to white eyed female, 2) white eyed male cross to red eyed female. If it were the former (red eye male) then the mother must have two X chromosomes both of which have do not carry the dominant red eye allele, and all daughters would be red eyed and all sons white eyed (their X always comes from the mother).
If it were the latter (white eye male) that would leave two further possibilities, mothers are homo- or heterozygous for the dominant red eye allele. If the mother is homozygous for the red allele then all offspring should have red eyes, all will receive an X that carries the dominant red eye allele.  If the mother is heterozygous then half of the offspring will be red eyed and half white eyed, because both of the fathers sex chromosomes do not have the red allele (the X and the Y) and only one of the mothers carries it.
In the exercise, you have some white eyed flies in the first offspring, but not all, and most are red eyed. Given the wording of the question (that red eyed flies were mated to white eyed flies, and not a red eyed fly was mated to a white eyed fly) I would suggest that the first generation was produced by crossing multiple red eyed females to multiple white eyed males, and that the females were a mixture of hetero- and homozygotes. Therefore some of the offspring were white eyed. The point being, with the first cross it is impossible to tell whether the females used were each hetero- or homozygotes, you can't deduce their genotype.

In the second cross, both parents have red eyes. What this tells you is that the fathers have an X chromosome with the dominant red eye allele, and the mothers have at least one X with the dominant red eye allele. They produce sons and daughters, among which, 1/4 are white eyed males, and none are white eyed females. The implied/logical further outcome is then that 1/4 of the offspring were red eyed males, and 1/2 (2/4) were red eyed females. In the second cross the mothers must be heterozygous (have just one red eye carrying X chromosome). The key difference here is that you can establish the genotype of the parental flies.
The cross below shows this. The sons, who inherit an X from their mother and Y from their father, are white eyed half of the time because there is a 50% chance of inheriting a red eye X from the mother and 0% chance of inheriting a red eye X from the father. Females are always red eyed because the X comes from the father, and he has only one X (which carries the red eyed allele). Half of the daughters will be heterozygous, and half homozygous, for the red eye allele, but it is dominant so all have the red eye phenotype.

I assume that recombination cannot occur in males (D. melanogaster has no recombination in males) and therefore has nothing to do with the solution, but that depends which species of fruit fly the example refers to - could you clarify? It appears this is this book, and therefore it is D. melanogaster.

Wow, thanks so much for the thorough and illustrated answer.

The book is Molecular Biology 5th Edition by Robert Weaver, ISBN 0073525324, chapter 1.1 page 3.

And yes, the book says on the same page that this experiment involved Drosophila melanogaster.

@rg255 On a side note: What programming language or software did you use to make these diagrams? +1 Thanks

Im ashamed to admit I just used PowerPoint! I could have done it with R but didn't bother - I had power pint open to work on a presentation I'm giving next week anyway @remi.b

Ha ha no shame. I was curious as I never made these kind of diagrams and would not really know how to do with R (except eventually with iGraph).

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Why are people tired after surgery?
I had surgery when woke up I felt like I only had 20% energy & felt extremely tired. Is this a common sensation? Why do people feel so tired after surgery?

I think you were feeling the aftermath of the narcosis.

Of course this is common. You can account anesthesia to be responsible for this. Also if you were asked not to eat anything for some prescribed time before and after the surgery, as is usually done, the body is already in need for some energy and at the same time it is also trying to come back to the conscious state. It has to make good efforts. Surgery is a type of stress condition for the body!

Answers in comments are correct. The tail effect of hypnotic drugs combined to opiates given for pain relief will make you feel really tired just after surgery.
But if you are referring to a more long-term effect, such as feeling tired for several days after surgery, then several factors combine:

psychological stress
physical deconditioning: inpatients usually do not move much. And even a few days of immobility will have a huge impact on your physical abilities. That is why in modern medicine, every effort is made to make the patient move as quickly as possible. Intensive physical therapy, readaptation therapy, and fast-track pathways are a result of this effort.
physical stress: undergoing surgery is a physical effort. Your body needs to accommodate for large shifts in volemia, positive pressure ventilation, reaction to pain (which still takes place during anesthesia), etc. The physical abilities of the patient are evaluated by the anesthesiologist for that reason, using MET effort units (often measured in number of flights of stairs you can climb without stopping). People with angina pectoris or diagnosed atherosclerosis can also be submitted to an ergometric test (cycling) or stress echocardiography/scintigraphy to evaluate if their heart can tolerate the physical stress of surgery.


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Is it really detrimental to humans as a species to reproduce with one's own first cousin?
Tired of hearing of these urban legends and popular opinions, I ask this question here to see if there really is scientific merit to this belief. My questions is, is it really "harmful" for a person to reproduce with his/her own first cousin? Everyone, at least in America, seems to think that this is incest which I completely dismiss because incest is purely a religious concept. The next argument I get is that we want more genetic diversity and having offspring with a first cousin is detrimental to our survival as a species. If you have any genetic weaknesses then your cousin is likely to be carrying them as well and then the chances of your offspring carrying them increase and so on.
I don't really believe any of this. It is rather well known (or may be not so well known) that only a very small percentage of a human individual is different from another human individual's genome. Differences due to skin color, race, ethnicity, and such are literally skin deep. So one reproducing with her cousin or someone half way across the globe is only negligibly different.
Forgetting about religion, has this been scientifically systematically tested and/or proven? Has any research been done on this? Is it true one way or the other? I don't mean to spark any debates here. Opinions are of course welcome. But if anyone can point me to any reputable sources or published results/references, that would be ideal.


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Ecomorphs as evolutionary definitions
There have been demonstrations of ecomorphs in different taxa, where each morphology type is associated to a single environment. I know that it happens because special morphological characters increase the fitness and therefore will be positive selected.
My question is; if we find similar places (talking about natural pressures and climatic conditions) on earth and given enough time, can we expect to see more or less the same ecomorphs living in different places? Also, assuming that, could evolution be a regarded a non-stochastic process?

The phenomenon you describe, where the same result comes about in more than one time/location via evolution, is called "convergent evolution." It is when the same character, or trait, evolve independently of one another. One example is the wing, it has evolved (at least) several times independently, in bats, birds, and insects. Parallels can also be drawn with other traits like dispersion methods of seeds, or the evolution of fins in fish, dolphins, and whales. Here is a classic paper by Ernest Williams from 1972 which describes one of the earliest examples given of ecomorphs, the anolis lizard, also talked about on this site.
This is from a good article on the new scientist website that would be worth reading:

"Evolutionary convergence occurs at every level, from proteins to
  societies. An unusual antibody once thought to be unique to camels has
  a close equivalent in sharks, for instance, while naked mole rats form
  social colonies like those of ants and bees.
"What this means is that if we could wind the clock back and let life
  evolve all over again, life might take very different paths but still
  produce organisms that, in some ways, resemble the organisms alive
  today.
"There would almost certainly be streamlined swimmers in the oceans and
  winged creatures in the skies. In fact, some argue that the evolution
  of intelligence is also virtually inevitable, though intelligent
  organisms could be very different from us."

The answer to your question is yes, with enough time and the same selection effects we would not be surprised if there was a similar pair of independently evolved characters. However, selection acts on random mutations which is not a directed process, therefore for the same characters to evolve you would need mutations to occur that had similar effects. This is why given enough time we can see the same responses. Despite the non-random effect of selection, we could consider evolution to be a stochastic process, it only arrives at the same converged point by chance. This is because selection (the main driver of evolution) acts on randomly generated genetic variation thus the direction of the evolutionary trajectory is random.

"..often used to represent the evolution of some random value, or
  system, over time. This is the probabilistic counterpart to a
  deterministic process (or deterministic system). Instead of describing
  a process which can only evolve in one way (as in the case, for
  example, of solutions of an ordinary differential equation), in a
  stochastic or random process there is some indeterminacy: even if the
  initial condition (or starting point) is known, there are several
  (often infinitely many) directions in which the process may evolve." -
  wikipedia entry on Stochastic Processes

Following the quote above it may seem that evolution is a directed process, i.e. selection is aiming for a specific target. It is not, selection can only weed out the least fit genotypes and increase the frequency of the better ones, selection has no goal or pre-existing aim. Thus, when discussing stochasticity in evolutionary terms it is perhaps better to use evolutionary trajectories, to describe the randomly created paths they move along, instead of "directions."

As an example of convergent evolution we could use the peppered moth and a little imagination because this is purely a hypothetical illustration I am making up on the spot.
The peppered moth is famous for once being a white moth that turned dark during the industrial revolution, when towns and cities grew and pollution killed the light coloured lichens that helped the light morph hide. This meant, rather suddenly by evolutionary time-scales, the white morph of the moth was not very well camouflaged against the dark bark of the trees. This created a positive selection for darker morphs, as such, alleles which made for dark moths would have spread rapidly in the population.
Using a little imagination we can think about two different parts of the world where this same event occurred independently - e.g. Glasgow and Plymouth in Britain which are quite far apart but both grew expansively during the industrial revolution. In both of these locations we would have seen a simultaneous rapid loss of lichens and increase in the dark moth ecomorph. This would have been convergent evolution because it is likely that they were independent of each other, i.e. the dark moth probably did not evolve in Glasgow and then fly itself down to Plymouth.

@BrandonInvergo In my opinion evolution is stochastic because "there are several (often infinitely many) directions in which the process may evolve" because evolution can occur through drift or selection. Convergent evolution is when one identical or similar direction of evolution is achieved. It relies on random mutations, a stochastic process, which selection, a deterministic process, then acts upon, or the more unlikely possibility of genetic drift to the same result.

@BrandonInvergo I'm not sure I say evolution is directional, maybe I missed that, but I definitely agree, it is not a directed process. Where do you mean (I'd like to change it to make it clear)? Perhaps you mean "directions in which the process may evolve" - this is where evolution proceeds along a trajectory, it's motion along the trajectory is random (therefore not directed) but it is still a direction (away from the origin) nonetheless.

@BrandonInvergo ah yes, perhaps misleading, too late to edit the comment, future note: "similar direction of evolution is achieved" in my above comment better stated as "similar evolutionary trajectory and result is achieved". I'll also give the answer a tweak later to make it clearer that evolution is not directed.

Thanks @BrandonInvergo and GriffinEvo for your answers!, both where too much good and im gonna read the paper that Griffin suggested me. Returning to the discusion and looking only the results of evolution, ¿the achieve of ecomorphs in all the places under similar conditions makes the result predictable (high fitness), so we can say is directional (deterministic), even if the "process" is stochastic or deterministic?. ¿Could ecomorphs been the final result of the evolutive process?, ¿Can we expect homoplasy in all linages in enought time?

@CristianRomán No, the journey to two ecomorphs is not deterministic, it is merely the result of similar mutational effects occurring in scenarios with similar selection. Using the moths example, the selection is created when the camouflage is less effective and thus leaving them more prone to predation. Group A might develop mutations which make them darker which selection would then favour, whereas Group B might instead evolve mutations to fly quicker or see better, making them better at avoiding predators. In convergence they arrive at the same result by chance mutations, not determinism.


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Main mechanism of the evolution of sexual dimorphism
Sexual dimorphism is very common and (normally) requires the evolution of sex-specific genetic variation/regulation so the genetic correlation between the sexes can be <1. Is there consensus as to how this type of variation predominantly spreads?
I can see it could evolve by drift and selection and I expect it is predominantly via selection (sexually antagonistic selection for different optimal genotypes)- We typically associate sex differences in traits with sex differences in selection (ecological, sexual selection...).

Sexual dimorphism evolves, as you suspect, via natural selection, specifically sexual selection (which I view as a form of natural selection).  Genetic drift, by definition, is random. Random changes of allele frequencies are extremely unlikely to lead to the consistent evolution of phenotypic differences between males and females.
Sexual selection on the other hand can lead to rapid evolution of secondary sexual characteristics (sexual dimorphism). If you consider natural selection in the broad sense, an organism's traits affect survivorship but do not guarantee reproduction. Individuals that live longer have an increased chance of reproducing more frequently but this does not mean the organism actually will reproduce more often than any other individual. In contrast, sexual selection acts directly on mating success. If a female chooses a male based on his secondary sexual characters, then that male will mate. His fitness (offspring produced) will be increased relative to males that are not chosen and do not mate. This can lead to runaway sexual selection for male traits and even speciation.
You are correct that sexual selection results from sexual conflict. Such conflict can arise because females invest considerable energy into relatively few eggs. Thus, it benefits her to be selective for her mates. If she chooses poorly, her fitness can be decreased quite a bit. On the other hand, males can produce copious quantities of sperm rapidly and with little energy cost. If a male wastes sperm on a genetically-poor female, his fitness is not really reduced. He can quickly mate with other females at little cost.
References
Any evolutionary text. They cover the basics of sexual selection in some detail.
Gavrilets, S. 2000. Rapid evolution of reproductive barriers driven by sexual conflict. Nature 403: 886-889.
Hosken, D.J. and P. Stockley. 2005. Sexual conflict. Current Biology 15: R535-R536.
Lande, R. 1981. Models of speciation by sexual selection on polygenic traits. Proceeedings of the National Academy of Sciences USA 78: 3721-3725.


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More extreme phenotypes when parents are from diverged populations
In quantitative traits we have many loci affecting a trait. If we took a bunch of parents where all mothers and fathers were of a certain value at the upper end of a trait range, and then looked at the offspring would we expect offspring from pairs of parents from more divergent populations to be even more extreme variance in their traits?
For example: if we look at 2 men from East Africa, both 190 cm tall. They each have children with women who are 180 cm, one of whom is from East Africa and the other from Canada. We could assume that the Canadian woman is probably more unrelated to her male than the East African woman. I would therefore expect that it is quite likely that the East Africans in the example are tall because of "tall-alleles" in many of the same loci, whereas there is a greater probability that the Canadian female is tall thanks to mutations at different loci. Therefore would it be reasonable to expect greater variation in the offspring of the Canadian woman?
Is there any evidence of this phenomenon?
Note: Ignore environmental and gene * environment interaction variance, just go with a simple additive model, and assume populations have had some barriers to migration for some time

If I get you right, you might be looking for something like heterosis (http://en.wikipedia.org/wiki/Heterosis)? Although mostly described for animals and plants, the principle should basically apply to sufficiently distinct human lineages as well.

Yes, the MHC example there is quite relevant @Hav0k

If being tall is beneficial, the "tall" loci are probably (partially) dominant and therefore, two tall parents from different origin may be expected to have taller offspring than two parents from the same origin. It seems hard to me to draw such general conclusion as it really depends on the number of loci under consideration, on the pattern of dominance and on whether the parents are homo or hetero zygous (and on epistasis).

If we assume that the parents are both heterozygous (for all loci under consideration) and all loci are bi-allelic and allele are additive, and parents are of any size, then indeed I would expect that the offspring from the parents form different origin will have higher range o possible genotypes. I am not sure my comments can help :) The question is very interesting +1

Yes, it would be reasonable to expect greater variation in the offspring of the Canadian woman.
Human genetic variation is the genetic differences among populations. Populations have access a pool of genes and over-time polymorphisms may arise to create greater variation.
Human populations within a species are defined by, divergence times and rates of gene flow - From mitochondrial, X and Y chromosome re-sequencing data.
Genetic Distance is the genetic divergence between species or between populations within a species (as in your example above). Populations with many similar alleles have small genetic distances. This indicates that they are closely related and have a recent common ancestor.
E.g. Height as you use for your example is a polygene. The inheritance of many genes alter phenotypic height of offspring.
Thus, it would be reasonable to expect a difference in allelic variations pertaining to height from the Canadian woman. The offspring may have a different height profile of alleles, and thus a different phenotypical height.
I should mention that:

"individuals from different populations can be genetically more similar than individuals from the same population"

But the above example - should not be expected.

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Additive genetic variance components from LMER in R
I've set up some dummy data in R which makes 40 genetically related lines, they are all siblings within a line so are genetically related by a factor of ½ thus additive genetic variance should be twice the variance explained by line. For the lines there are 200 individuals being measured, for three characters/traits. The first trait has low phenotypic variance, the second has high environmental variance, and the third has high genetic variance.
rm(list=ls())
re = 200 # replicate individuals per line
li = 40  # lines

# setup
set.seed(5)
data = data.frame(rep(1:li, each = re))
colnames(data)="Line"
library(nlme)
library(lme4)
par(mfrow=c(1,3))

# trait 1: little variance (Va or Ve)
data$Trait = rnorm(li*re,10,1)
boxplot(data$Trait~data$Line, ylim=c(0,20), main = expression("Low V"[A]*"& Low V"[E]))
var1 = var(data$Trait); mean1 = mean(data$Trait); m1 = lmer(data$Trait ~ (1|data$Line))

# trait 2: high enivronmental variance, little Va
data$Trait = rnorm(li*re,10,1); data$Trait = data$Trait + rnorm(re*li,0,3)
boxplot(data$Trait~data$Line, ylim=c(0,20),main = expression("Low V"[A]*"& High V"[E]))
var2 = var(data$Trait); mean2 = mean(data$Trait); m2 = lmer(data$Trait ~ (1|data$Line))

# trait 3: high additive genetic variance, little Ve
data$Trait = rnorm(li*re,10,1); data$Trait = data$Trait+rep(rnorm(li,0,3),each=re)
boxplot(data$Trait~data$Line, ylim=c(0,20), main = expression("High V"[A]*"& Low V"[E]))
var3 = var(data$Trait); mean3 = mean(data$Trait); m3 = lmer(data$Trait ~ (1|data$Line))

Plots of the three traits,

Then to estimate additive variance ($V_A$) I extract the line variance ($V_L$) from the lmer model and double it,
# line variances (variance in additive effect of each haploid genome)
m1_line = unlist(VarCorr(m1))[[1]];
m2_line = unlist(VarCorr(m2))[[1]];
m3_line = unlist(VarCorr(m3))[[1]]

# additive variance (double the line variance because it is a hemiclone)
m1_add = 2*m1_line;
m2_add = 2*m2_line;
m3_add = 2*m3_line

Residual variances should be (assuming perfect experimental design, no measurement error etc.) the estimate of environmental variance ($V_E$) and phenotypic variance ($V_P$) should be the sum of $V_L$ and $V_E$,
# residual variance
m1_res = attr(VarCorr(m1), "sc")^2
m2_res = attr(VarCorr(m2), "sc")^2
m3_res = attr(VarCorr(m3), "sc")^2

# phenotypic variance
m1_phe = m1_line + m1_res
m2_phe = m2_line + m2_res
m3_phe = m3_line + m3_res

Heritability is additive variance divided by the phenotypic variance
$h^2 = V_A / V_P$
But I think it is correct in this case to use line variance rather than additive variance (if someone could explain in an answer that would be useful), so I've done,
# heritability (line/ (line+ residual))
m1_h2 = m1_line/ m1_phe
m2_h2 = m2_line/ m2_phe
m3_h2 = m3_line/ m3_phe
m1_h2; m2_h2; m3_h2

My question(s):
Is it appropriate to use the lmer function in R to extract variance components in this manner?
Have I calculated $V_A$, $V_E$, $V_P$, $h^2$ correctly? I think $V_A$ and $V_E$ are correct, $V_P$ could perhaps be the sum of $V_A$ and $V_E$ rather than $V_L$, and subsequently $h^2$ may be $V_A/V_P$.

Can you add a flowchart or just methodology instead of/in addition to the code.

I deleted my answer. I am too unsure of what I was saying! Sorry. I might give another try thinking about that later when I'll have the opportunity to use R.

From what I understood of your code and what you are asking I am guessing that you do the following:
Generating a virtual set of 40 individuals (lines) of which you have 200 measurements (repetitions). You say that they are full siblings, so they share both parents. Then you use the lmer function (which I am not familiar with) to give you the total variance, within-group variance and between-group variance, ($V_{T}, V_W, V_B$ respectively). What you call $V_L$ would be the $V_W$.
We know that $V_P=V_A+V_D+V_E$
In full siblings we also know that $V(A,A')=\frac{1}2V_A+\frac{1}4V_D$ where $A$ is the additive value and $D$ is the dominance value because they share a quarter of their gene combinations.
If you are treating with full siblings the $V_W$ should be then the $V_E$ and the $V_B$ would be the $\frac{1}2V_A+\frac{1}4V_D$ as you are seeing the variance between siblings.
So no, you are not calculating correctly the $V_A$ because you are missing your $V_D$ on your counting. The code itself looks fine for what I understood, but maybe you should take that to corssvalidated with the R tag

Thanks - I actually use Hemiclone lines, which are like full sibs (related by a half) but have no dominance effect, I just wrote siblings rather than having to explain hemiclones. If then half sibs were used, the code I use would correct except for $V_A = 4V_L$ right? And likewise if there was no dominance then for full sibs $V_A = 2V_L$

I could check it thoroughly but my gut says that $V_A=2V_L$ in this case as there would be no dominance effect then, but in the rest of the effects it would be full sibs.


text:
Does mixing alcoholic drinks really make you more drunk?
There is plenty of anecdotal evidence ("beer after wine and you'll feel fine, wine after beer will make you feel queer") that mixing alcoholic drink types leads to a stronger effect, but I can't find any true studies.
In fact the only studies I found are looking at mixing energy drinks and alcohol (mixing with energy drinks increases motivation for more alcohol (in college students) [1]), and discussed mixing caffeinated beverages with alcoholic ones [2].
Are there any studies specifically looking at mixing alcoholic drinks? They would have to compare people drinking the same amount of alcohol, but some people mixing, others drinking the same thing. Maybe even a cross-over study design? Same people do both, one after the other? The only way to get an unclouded answer!
I am also interested in the follow-up why question: Why does mixing some drinks make you more drunk? Presumably it is something in wine (for example) that interacts badly with something in beer at the chemical level (the metabolites maybe)?

Marczinski CA, et al, (2012). Mixing an Energy Drink with an Alcoholic Beverage Increases Motivation for More Alcohol in College Students. Alcohol Clin Exp Res, epub. doi: 10.1111/j.1530-0277.2012.01868.x
Touyz LZ, (2011). Mixing drinks and concocting troubles. Curr Oncology, 18(6):262-3. PubMed; FullText.

There are some very general answers to your question.

Definitely, there is a lot of magical thinking. We as humans are very prone to anecdotical evidence and extrapolations from incomplete data, even more so when we are drunk.
As an interesting "proof" is the fact that the German counterpart of the saying "beer after wine and you'll feel fine, wine after beer will make you feel queer" is "Wein nach Bier, gönn' ich Dir, Bier nach Wein, lass es sein" -- which means the exactly opposite of the English saying (beer after wine is bad, wine after beer is fine).

Many kinds of alcohol contain unwelcome additional substances, for example fusel alcohols. Definitely, "mixing" broadens the range of these additions.

Mixing can lead to a misperception about the actual amount of alcohol that was taken in. Many people who would not drink a vodka and drive have no problem driving after a half a liter of beer (which contains same amount of alcohol two shots of vodka).

That is very interesting about the saying in different languages! Many thanks.

Mixing of alcohol and energy drinks can be detrimental to ones health as both alcohol and the caffeine in energy drinks are both stimulants which can cause adverse effects on the heart especially if one has a natural sensitivity to caffeine.  One also has to be careful as both caffeine and alcohol are diuretics which when combined can cause even greater risk of dehydration.  And some studies suggest that taurine, which while naturally occurring (and even quite necessary in the developmental stages of humans) may cause adverse affects on kidneys and combine that with two diuretics all tied together...it could cause serious potential for health risks.  At least in some individuals. [ 1 ] [ 2 ]
I conducted a non-scientific experiment one night when friends were discussing the merits of 'alcohol before liquor' and vice versa where I decided to mix a pint of beer and three shots of Bacardi 151 in stein and consumed it as I would a straight beer.  Personally I felt no ill effects but I also had a hell of a tolerance for alcohol.  I agree that mixing alcohols can 'confuse' someone regarding just how much alcohol they have consumed and should be watched carefully.  Although vigilance is often not one of the virtues displayed by people who consume such drinks.

Kristen Kirkpatrick M.S., R.D., L.D. - http://www.doctoroz.com/blog/kristin-kirkpatrick-ms-rd-ld/energy-drinks-demystified
Time Magazine Online - http://time.com/3677044/alcohol-energy-drinks/

Welcome to Biology and thanks fore your answer. We appreciate scientifically sound answers and the first paragraph needs sources to back it up in my opinion. The second part is anecdotal and is better of as a comment.

Thanks, but you have not actually provided an answer for the question asked: "Does mixing alcoholic drinks really make you more drunk?"

"both alcohol and the caffeine in energy drinks are both stimulants" - alcohol is a depressant, is it not?


text:
Why is gynodioecy common and androdioecy rare?
Gynodioecy is when a population features individuals that produce both male and female gametes and individuals that produce just female gametes. Androdioecy is when a population features individuals that produce both male and female gametes and individuals that produce just male gametes. The former is "not uncommon" and the latter is "virtually unknown."
Charlesworth 1991 states that this is common because cosexual populations would normally evolve a male sterile mutation first, causing gynodioecy, and then female sterility mutation(s) will build up leading to dioecy.
Why should it be so much more common for male sterility mutations to evolve first?
(I think the answer lies within articles cited in the above paper, Charlesworth & Charlesworth 1979 Proc R Soc B, and 1987 Evolution which I'll try to read this weekend, if it is I'll post a self-answer but in the mean time...).

I think the short answer is along the lines of: Because ovules represent the limiting factor while there are plenty of pollen grains. Males have a hard time surviving in a androdoiceous population while female might be able to survive in a gynodioceous if it spares enough energy (by not producing any pollen grains) to create ovules. One advantage for a female of not being hermaphrodite compare to other individuals in the population is that it won't lose ovules to produce inbred offspring by selfing.

That's what I had interpreted it as


text:
Evidence & discussions of hard polytomy
Phylogenetic trees with >2 branches on a node are polytomic, and polytomy can appear on trees for two reasons. Firstly a lack of information in the data prevents proper resolution within a clade, called soft polytomy. Alternatively, hard polytomy may exist, this is when there truly is a simultaneous split from one lineage (species) in to more than two. Yang states that "it may be argued that hard polytomies do not exist" but makes no citation or attempts at theoretical discussion. Are there any papers which discuss the theoretical possibility of hard polytomy and any evidence of it occurring?

Image from http://biology.fullerton.edu/biol404/phylo/polytomies.html

I think that changes in features that determine a node may happen in parallel or close together in a sequence. If the fossil record is not complete enough then the cladogram has to contain these stars. From a stochastic statistic point of view, although unlikely, it could actually happen that 2 or more  characteristics develop exactly during a similar time frame, so from a philosophical point of view, I disagree with yang.

I think Yang's wrong too, divergence is not an instantaneous process so it's possible that two (or more) divergence events may be occurring at once within the same population, but it is probably quite unlikely

@GriffinEvo "but it is probably quite unlikely" - I think rare would be a better word in this case...

@GriffinEvo Technically one event of mutation can give rise to only one mutant. But as Chris Stronks said, it is possible that in a given time frame, due to lack of evidence such a result is possible (especially if intermediates perish — perhaps as in case of LUCA). However, it is almost improbable for trees based on molecular phylogeny (Unlikely that a given nucleotide position has more than two polymorphs and there are no  differences elsewhere).

One may imagine the following scenario: different unlinked mutations occur in the germline of a single individual, this individual has at least three offspring, each carrying a different mutation, and each being the ancestor of a new clade. Even if said offspring are not born simultaneously, in terms of cladogram, there will be a single splitting event.

You might want to have a look at some of these: Patterns of speciation and limits to phylogenetic resolution, Molecular polytomies, Problems with "soft" polytomies, and Polytomies, the power of phylogenetic inference, and the stochastic nature of molecular evolution.

Thanks, Do you have time to expand on these links?

Sorry, no. Besides, I'm not knowledgeable in this area; I just read some abstracts found via Google Scholar. I suspect that essentially all "hard" polytomies are just soft polytomies where evidence to resolve them is hard to acquire.


text:
Mechanisms of genotype*sex interactions
I'm looking for suggestions of the mechanistic level at which genotype*sex interactions can occur. These give different phenotypes from the same genotype dependent on the sex they are expressed in. For example, cis-acting sex-specific modifiers can affect gene expression.
What other mechanisms can create a gene*sex interaction?

I am a little unclear about what you mean by gene*sex interaction

genotype*sex interaction in determining the phenotype, so a single allele could produce different phenotypes depending on which sex it is in, I am trying to find some known examples of how these sorts of things occur (e.g. known sex-specific gene expression regulation pathways) @WYSIWYG

Something like this and this ?

Are you talking about genomic imprinting?

So you want to know about the specific molecular mechanisms (e.g. interactions between gene products), and not just examples of gene*sex interactions?

Yes @fileunderwater


text:
Does unequal dominance mean the X-chromosome should be a coldspot for antagonistic variation?
Sexually antagonistic genetic variation, in a simple model, will persist if the benefit to one sex is (near) equal to the cost in the other, otherwise the polymorphism will be selected out of the population.
[Rice's theory][1] suggests that sexually antagonistic genetic variance should be over-represented on the X-chromosome, because males are hemizygous (thus express male beneficial alleles more often than females) and females have the X-chromosome 2/3rds of the time (thus female benefit does not need to equal male cost for persistence). This model expands the range of conditions under which SA variation can persist.
[Fry argues here][2] that unequal dominance means the conditions under which sexually antagonistic variation can be maintained in the autosomes. Because of dominance the mean population fitness is increased under conditions of polymorphism (cost of a new allele to one sex < the benefit to the other). This model also expands the range of conditions under which SA variation can persist.
I think Fry concludes that the X-chromosome should therefore be expected to, not only not be a hotspot, but to be a coldspot (a dearth of SA variation on the X).
Conceptually, why does the hypothesis of unequal dominance make the autosomes more permissive to genetic variation than the X-chromosome? (Therefore making the X- a coldspot for SA variation). This is what his abstract says, it seems to suggest that...

"..such polymorphisms are expected to be more common on the
  X-chromosome... here I show that there are plausible assumptions under
  which the reverse is expected to be true."


text:
What are the common methods to estimate additive genetic variance?
Additive genetic variance can be estimated in a number of ways, and is a key concept in evolutionary biology and quantitative genetics.
What are the typical methods (experimental designs) used to estimate this variance? How are they done?
I found papers such as this, which use paternal half sib breeding designs and the fit a model to estimate genetic variance and then multiply the values by 4 to estimate the G-matrix.

Of particular importance is the sire-level covariance matrix because, when multiplied by four, it provides an estimate of G.

I am interested in this because I am working on hemiclones and want to think about the differences, strengths, and weaknesses of classical methods compared to hemiclonal analysis.
*note, I mean to estimate the standing additive genetic variation within a population

I think for that you have to first establish the additive nature of the set of genes (i.e their independence).

The question is very much related to how we can estimate heritability and an answer will probably talk about regression of parents on offspring, identical twins, common garden and response to selection. The response to selection experiment intuitively seems to me is the most accurate and straightforward solution in order to measure the additive genetic variance.


text:
Additive genetic variance $V_A= 2pqa^2$ ... what is $a$?
Reading Falconer and Mackay looking at equation $V_A = 2pqa^2$ (equation 8.5, page 126).
I am trying to write a clear explanation of how additive genetic variance is defined and calculated, but I keep getting twisted up in the books I am working from.
Just what is the term $a$ and how is it calculated?

can you add a little context or provide a link to that article?

there's not much more context one can add, but I've linked to the book

Actually I could not access the book. Though you got an answer, I would suggest that you put up a snapshot of the page so that other users may find the question useful.

This information is given in p.118.
In essence $a$ represents the deviation from the population mean due additive genetic effects.
Say a trait is controlled solely by locus X with the effect alleles X impacting the phenotype Y in an additive manner (no dominance and epistasis effect), then we can calculate the effect size of carrying the X allele, called $a$, and representing the distance from the population phenotypic mean of homozygote XX. Based on this definition, the distance from the mean for individual with the following genotype is given by:

XX: $a$
Xx : 0
xx: $-a$

This makes more sense using the genetic model:
$P=G+E=BV+I+E=A+D+I+E$ (parameters listed at the bottom)
In the example, the locus has only an additive effect then D=0 and assuming there is no epistasis then I=0 as well which gives $P=BV+E=A+E$ therefore $BV=A$
In this case $a$ can be computed directly from the BV, with p=f(X) and q=f(x), as:

$BV(XX)=2qa$
$BV(Xx)=(q-p)a$
$BV(xx)=-2pa$

Now for the complete case of both additive and dominant effects, i.e. $BV=A+D$, you can refer to table 7.3 in p.118 which describe that XX individuals are given the value $a$, Xx -> $d$ and xx -> $-a$ with the corresponding relationship to the BV given by (care here it's not $a$ but alpha $\alpha$):

$BV(XX)=2q\alpha$
$BV(Xx)=(q-p)\alpha$
$BV(xx)=-2p\alpha$

with $\alpha=a+d(q-p)$

P=phenotype
BV=A+D=Breeding value
G=Genotypic effect
E=Environmental effect
A=Additive genetic effect quantified by $a$
D=Dominant genetic effect quantified by $d$
I=Epistasis effect

Thanks @cagliari that is a really good way of explaining it - are you studyin quantitative genetics? (I am in the chat room)

@rg255 Thanks! Yes and no, just finished a pop gen class where we used Falconer & Mackay intensively so this is still very fresh in my mind but my main research interest is actually in RNA/DNA structure prediction.

Cool the I'm stuck firmly in a popgen group - Hartl & Clark only, I had to do my own Q.G book clubs... I've realised where I was getting stuck too, it was $a$ becoming $\alpha$ that was throwing me off, but seeing equation 7.5 I see that $a = \alpha$ when $d = 0$.


text:
Imperfect dosage compensation
Dosage compensation is used to make up for different copy numbers of the major sex chromosomes in males and females (One X or Z chromosome in one and two in the other). Two main mechanisms of dosage compensation exist, inactivation and upregulation.
But dosage compensation is not entirely perfect, the amount of gene product from an upregulated X/Z-linked genes in the heterogametic sex is not exactly that of the two in the homogametic sex.

"In Drosophila, the male-specific lethal (MSL) ribonucleoprotein
  complex mediates dosage compensation by upregulating transcription
  from the single male X chromosome approximately twofold."

On average how well is dosage compensation performed? What is the variance like:

within a single chromosome (between genes)?
within species?
between species?

You mean Y chromosome?

@ChrisStronks no. there is one X in males, two in females. To compensate for this males either upregulate their X or females down regulate (or silence) one of theirs.

Note that there are several sources of variation. There may be stochastic, environmental and genetic among individuals, within individual and within chromosomes variations. For example, in the pseudo-autosomal region (PAR) were the genes are present in two copies in both males and females, you may have much lower change in expression as there is nothing to compensate for. It may (or may not) depend on the protein beeing made and how a shift in the concentration of this protein influence the rate of chemical reaction according to a Michealis-Menten dynamic.

I may have too a selectionist view though and I may overlook how complicated is the question. It is a very interesting question +1

@remi.b selectionist views are more exciting that neutralist ;)

@GriffinEvo I understand but it says X and W chromosomes in your question body, I thought the male chromosome is called Y.

@ChrisStronks ah now I see what you mean. It's in reference to zz/zw systems (and should be a z not a w)

Related, and a partial answer on the inactivation of X-chromosomes and genes that escape silencing can be found here: http://biology.stackexchange.com/a/27743/3624


text:
Non-fatal / low-harm measurement of Drosophila traits
I am trying to generate some candidate traits to measure in a fitness assay of wildtype outbred (lab population) flies. The key trait I will measure is lifespan.
I am looking for some additional traits which can be measured from the same flies as those in the lifespan assay without harming or killing the fly in the process. For example, I could measure wings using a technique devised by the Houle Lab called WingMachine. I think I could also do some other measures with the same equipment, leg length etc.
The traits should also be present in both sexes (can be monomorphic or dimorphic) and quick to measure; I'm aiming for 200-250 measures/collections/images a day. Traits that can be measured properly in a fly which has died of old age would also work. Traits can be morphological, behavioral etc..
What other traits can be done like this?

You could do negative geotaxis (climbing) assay, (larval or adult) locomotion assays, % brain vacuolisation (after the flies die), maze tests. There are probably much more but these are all I can think of that are no-lethal and can be applied to males and females and some larval work too.
You could maybe consider doing starvation assays and longevity in some of your populations.


text:
Comparing gene expression levels between control and disease at different time points
I have a data set with expression levels of a list of genes, measured in replicate at two different time points between two groups; a control group and a disease group.
I want to identify the changes in expression between the two groups, however I'm having some trouble on formulating how best to do this. For example, if I have $[C_0]$ and $[C_1]$ as the control group measured at $t=0$ and $t=1$ respectively, and $[D_0]$ and $[D_1]$ as the disease group, I had tried to do:
$$\frac{([D_1] - [D_0]) - ([C_1] - [C_0])}{[C_1] - [C_0]}$$
I feel like a fold change would be appropriate, however it doesn't seem to make any sense logically for the genes where $[C_0] = [C_1]$ or $[D_0] = [D_1]$.
Could anyone suggest an appropriate ratio or measurement? This is straightforward enough when it's simply comparing between C and D, (e.g. you just find $\frac{D}{C}$), however I'm not sure how to treat the different time points.

The gene expression profile may change at different time points between the two groups; you should decide what you actually want to measure. If you want to see if the diseased group is different from the control then you should compare them at every time point. For most situations you would need to compare just their steady state behaviour.
Imagine a diseased individual who shows some physiological differences at certain developmental stages compared to the control but in the end turns out to be perfectly normal. So what matters in most cases is the steady state and not the transients.
However if you are interested in the change in expression then you should compare ([D1] - [D0]) with ([C1] - [C0]). This will tell you if the dynamics of the diseased and the control samples are similar or not.
There are issues with fold changes. Though they are decent measures, you cannot really apply a t-test with fold changes (normalizing to 1 is a different thing).
You can do another t-test between [C1] and [C0] (similarly for D). This would tell you if the diseased or control population changes its expression at time t=1 or not.
AFAIK you cannot compare the dynamics and the values simulatenously. What you should test depends on what you are interested in.


text:
What are parental antagonism & parental conflict?
I've been reading the chapter by Haig et al in The Genetics and Biology of Sexual Conflict. I think this chapter has them quite unclearly defined. Could anyone describe these two phenomenon more clearly than the chapter does? Real or hypothetical examples would be good to give clarification, and clarification of how they are distinct from sexual conflict and antagonism.

"Parental Conflict will refer to phenotypic interactions in which
  matrigenes and patrigenes prefer different outcomes"
"Parental Antagonism occurs when an allele has a relative advantage
  when inherited from one sex but a relative disadvantage when inherited
  from the other."

Do you know about genomic imprinting? This seems very linked to your question.

You may inherit a gene, which is actually detrimental to your (most efficient) functioning and hence has a cost (eg. gene for being small when food is available from tall trees). On the other hand, you may inherit a gene which has a benefit for you (gene for being tall with food available from tall trees).
Sexual Antagonism:

What’s good for the goose may not be good for the gander. Thistwist on
  an old proverb captures the notion of sexual antagonism.Traits that
  confer high fitness on geese (females) may confer lowfitness on
  ganders (males), and vice versa.

In sexually dimorphic species (like all common complex life), the evolution of males is usually decoupled from females. This is not as bad as it seems, as females and males may have different patterns of selection, different phenotypes of mutations all at the same time dodging pleiotropic effects. Hence mutations benefiting one sex will sometimes be deleterious to the other (i.e. their fitness effects are ‘sexually antagonistic’)
Sexual Conflict:
Males and females have divergent interests in reproduction that are rooted in anisogamy and lead to distinct roles, due to sexual antagonism. Sexual conflict occurs between the same or different genes,  when there are different optima for a trait expressed in both sexes (intralocus conflict) or when there is conflict over the outcome of a male–female interaction (interlocus conflict).
Intralocus sexual conflicts are potentially very common. Researchers have found a strong positive genetic correlation between male and female fitness at the larval stage in the fruit fly (when interests of the males and females are essentially the same -> survive and grow), but a strong negative genetic correlation between adult male and female reproductive success (when the sexes are expected to have different genetic interests). This is possibly due to sexual antagonism.
Interlocus conflicts occur when there is conflict over the outcome of male–female interactions, so that the optimal outcome is different for the two sexes,as occurs in yellow dung fly mating behaviour. In a rare instance, wikipedia does a good job of explaining the example:

In the yellow dung fly Scathophaga stercoraria, females can be injured
  in the battles between males suitors. Males are selected to evolve
  traits for competitive ability that would increase their reproductive
  success, but females would evolve a set of antagonistic adaptations to
  reduce their chances of being injured in battles between the males.
  Therefore, there is an interlocus sexual conflict in males and females
  that could possibly lead to an "unresolvable evolutionary chase" when
  a novel trait in males increases their competitive ability while
  harming the females

[5,6]
.
Parental Antagonism:
An allele in a gene is said to be parentally antagonistic if it has an inclusive fitness benefit when derived from one parent (say the mother), but an fitness cost when derived from the other parent (in this case the father)
There are many different theories out there, but the gist of it is essentially some process creating an asymmetry between the genes that you inherit from your father and mother (patriGENIC and matriGENIC), that causes differential expression of alleles (silencing the other copy) [2]
Parental Conflict:

When parent-offspring relations in sexually reproducing species are
  viewed from the standpoint of the offspring as well as the parent,
  conflict is seen to be an expected feature of such relations. In
  particular, parent and offspring are expected to disagree over how
  long the period of parental investment should last, over the amount of
  parental investment that should be given, and over the altruistic and
  egoistic tendencies of the offspring as these tendencies affect other
  relatives. In addition, under certain conditions parents and offspring
  are expected to disagree over the preferred sex of the potential
  offspring. In general, parent-offspring conflict is expected to
  increase during the period of parental care, and offspring are
  expected to employ psychological weapons in order to compete with
  their parents. [7]

Reading:
[1] Haig, David. "Parental antagonism, relatedness asymmetries, and genomic imprinting." Proceedings of the Royal Society of London. Series B: Biological Sciences 264.1388 (1997): 1657-1662.
[2] Patten, M. M., et al. "The evolution of genomic imprinting: theories, predictions and empirical tests." Heredity 113.2 (2014): 119-128.
[3] Patten, Manus M., and David Haig. "Maintenance or loss of genetic variation under sexual and parental antagonism at a sex‐linked locus." Evolution 63.11 (2009): 2888-2895.
[4] Normark, Benjamin B. "Perspective: maternal kin groups and the origins of asymmetric genetic systems—genomic imprinting, haplodiploidy, and parthenogenesis." Evolution 60.4 (2006): 631-642.
[5] Connallon, Tim, and Andrew G. Clark. "Evolutionary inevitability of sexual antagonism." Proceedings of the Royal Society of London B: Biological Sciences 281.1776 (2014): 20132123.
[6] Chapman, Tracey, et al. "Sexual conflict." Trends in Ecology & Evolution 18.1 (2003): 41-47.
[7] Trivers, Robert L. "Parent-offspring conflict." American zoologist 14.1 (1974): 249-264.

This reply may be overly scientific and jargon riddled. If so give me a shout, and I'll try and make it more easier to understand. And also note that I have lifted out paragraphs from papers and stitched them together, and have duly supplied the references for further reading.I did this, because the seminal papers which these ideas have been published in are the best way to learn the same.

No worries on that front - about defend a phd about intralocus sexual conflict! Thanks for the excellent looking answer, I'll give it a proper read tomorrow to see if I get it clear! (Expect either 15 points or a comment looking for clarification tomorrow!)

Just noticed did I just necro this thread from last year...?


text:
Defining dominance and selection in these formulae
This paper uses two equations to explain the different conditions under which sexually antagonistic genetic variance is maintained in a population, while allowing for unequal dominance, for autosomally linked loci:
$h_f / 1-h_m + h_fs_f   <$ $ $ $   s_m/s_f   <  1-h_f/h_m(1-s_f)$
And X-chromosome linked (X-linked) loci:
$2 h_f / 1+h_f s_f < $ $ $ $ s_m/s_f < $ $ $ $2(1-h_f)/1-h_f s_f$
where $s_m$ and $s_f$ are the selection coffecients against the less fit homozygote (or hemizygote) in males and females respectively where the most fit genotype has a relative fitness of 1. Similarly $h_m$ and $h_f$ represent the dominance of the less fit allele in males and females, and $h_m$ is not applicable in the X-linked equation because there is no dominance (due to hemizygosity it can only be homozygote).
I'm having a little trouble understanding how $s$ and $h$ are defined here.
For $s$, is it the fitness of the deleterious homozygote or the difference in relative fitness between the two homozygotes? Such that either $s$ = the relative fitness of the homozygote, or, $s$ = 1 - relative fitness of deleterious homozygote, where one represents the fitness of the fittest homozygote thus giving the fitness differential.
For $h$, is the dominance defined as the fitness difference between the less-fit homozygote and the heterozygote, or the most-fit homozygote and the heterozygote? Or is it the deviation from the average fitness of the two homozygotes?
Going from the graph (see below for values of fitnesses), what are the values of $s_m$, $s_f$, $h_m$, and $h_f$ where the dashed line is Females and solid line is Males. I see possible values of either $s_m$ = 0.2 or 0.8 (fittest genotype - fitness of weakest), likewise $s_f$ is either 0.3 or 0.7, $h_m$ is either 0.1 (deviation from most-fit genotype), 0.7 (deviation from least-fit) , or 0.3 (deviation from average) and $h_f$ is either 0.3, 0.4, or 0.05.

The values here are, as fitnesses for genotypes A1A1, A1A2, and A2A2, for males, 1.0, 0.9, 0.2, and for females 0.3, 0.7, 1.0.

Fry (2010) borrowed his variables from Kidwell et al. (1977).  Kidwell defines the fitness of each genotype as,
$w_{m1}$, $w_{f1}$ = male and female fitness of the A$_1$A$_1$ genotype.
$w_{m2}$, $w_{f2}$ = male and female fitness of the A$_1$A$_2$ genotype.
$w_{m3}$, $w_{f3}$ = male and female fitness of the A$_2$A$_2$ genotype.
Kidwell then establishes the following parameters for each fitness variable for opposing additive selection,
$w_{m1} = w_{f3} = 1$,
$w_{m2} = 1-.5s_m$,
$w_{f2} = 1-.5s_f$,
$w_{m3} = 1-s_m$, and
$w_{f1} = 1-s_f$.
Therefore,
$s_m = 1-w_{m3}$, and
$s_f = 1-w_{f1}$.
$s_m$ and $s_f$ are the relative fitness differences between the two homozygous genotypes of each gender. The heterozygotes are assumed to have half of that differential. This is what Fry refers to on page 2 (page 1511 of the publication):

In Kidwell et al.’s notation ... the most fit genotype in a given sex has a relative fitness of 1, and $s_m$ and $s_f$ are the selection coefficients against the less-fit homozygote (or hemizygote) in males and females, respectively.

For opposing selection with arbitrary dominance, Kidwell parameterizes the heterozygous fitness components as
$w_{m2} = 1-h_ms_m$, and
$w_{f2} = 1-h_fs_f$.
Notice that $h$ is modifying the fitness difference $s$ in the heterozygotes. This is due to incomplete dominance of one allele over the other. If both alleles in a heterozygote contribute equally to the phenotype, then $h = 0.5$, and you have the additive fitness described above ($w = 1-.5s$).
If one allele is incompletely dominant over the other, the selective difference $s$ will be modified by some amount, $h$. If A$_1$ is only slightly dominant over A$_2$, (say, $h=0.6$), the effect on $w$ won't be much different than if $h=0.5$. Both alleles will affect fitness but the more dominant allele will have a slightly greater affect on fitness than the other allele. If one allele is much more dominant, then $h$ becomes larger and the more dominant allele contributes more to the overall fitness than the other allele.
Finally, if $h=1$ then one allele is completely dominant so the other allele will not contribute at all to fitness. When $h=1$, the equations reduce to $w = 1 - s$ (for the respective genders), remembering that $h$ is based on the dominance of the allele with maximum fitness in the other gender.
Consider a female. Her maximum fitness is the A$_2$A$_2$ genotype.  If A$_1$ is completely dominant over A$_2$, then a heterozygous female would have fitness equal to the A$_1$A$_1$ genotype which, for females is defined as $w = 1-s_f$. On the other hand, if A$_1$ is not completely dominant over A$_2$, then the heterozygote will have some reduction in fitness but not as much as for complete dominance.
To answer your final question about your figure, given the following values for A$_1$A$_1$, A$_1$A$_2$, and $_2$A$_2$, respectively:
$w_m = 1, 0.9, 0.2$, and
$w_f = 0.3, 0.7, 1$, then
$s_m = 1 - 0.2 = 0.8$, and
$s_f = 1 - 0.7 = 0.7$.
For the heterozygosity effect ($h$), given that
$w = 1 - hs$, then
$h = \frac{1-w}{s}$, therefore
$h_{m2} = \frac{1 - 0.9}{0.8} = 0.125$.
A$_1$ is nearly completely dominant over A$_2$ in males, so the presence of A$_2$ is the male is not reducing his fitness by very much. For females,
$h_{f2} = \frac{1-0.7}{0.7} = 0.429$.
The presence of the dominant A$_1$ allele in females has stronger heterozygous effect so her fitness is reduced more, compared to heterozygous males.
Citations
Fry, J.D. 2010. The genomic location of sexually antagonistic variation: some cautionary comments. Evolution 64: 1510-1516.
Kidwell, J.F. et al. 1977. Regions of stable equilibria for models of differential selection in the two sexes under random mating. Genetics 85: 171-183.

Hi @MikeTaylor Thanks for the answer, I've just edited a couple of the annotations which I think were incorrect, could you check the edit history to proof them for me please

also should "Therefore,
sm=1−wm1, and
sf=1−wf3." read as "Therefore,
sm=1−wm 3 , and
sf=1−wf 1 ."

@GriffinEvo Thanks for your careful proofing. I also added a bit more to answer your question about your figure.

Thanks again, I had gotten myself tangled - I knew how to define a selection coefficient but got spiralled out by self doubt when reading the paper and getting tangled in the math of it all! It's all cleared up for me now (and I've managed to recreate fry's results, using dummy data in R I have managed to duplicate figure 3a and 3b)


text:
Sexually homologous traits
When papers refer to traits as being sexually homologous do they refer to traits which are:
a) present in both sexes but can be dimorphic (e.g. body size is sexually homologous because both sexes have a measurable trait which has the same criteria in either sex, but this is frequently dimorphic)
Or
b) present in both sexes and not different between the sexes
I have always thought it is a, but I'm now using the term in a paper and want to check. I would have thought the latter would be "homologous homomorphic traits" or something like that.
If an answer could have an example of the use(s) which make it obvious from published work that would be great!

By traits do you mean gross phenotypes (something that you can measure without using molecular techniques)?

yes @WYSIWYG ...

Innate immune response, vision (Not too sure. Will look for references)

@WYSIWYG I'm not looking for examples - im checking use of terminology :)

Without any doubts a), i.e. a trait present in both sexes but the phenotype can be different. Here an example.

Your first definition is correct: a homologous trait is one that can be mapped unambiguously between two samples. What establishes the homologous relationship depends, of course, on the trait or feature being mapped.
For example, one way sexually homologous traits can be identified is by tracing the physical development of a male vs. a female organism. If precursor x becomes y in a developed male and z in a developed female, then y and z can be referred to as homologues.


text:
Falconer & Mackay population mean calculation & genotypic values
I am reading chapter 7 of Falconer and Mackay where they give a formula to calculate the population mean as a deviation from the heterozygote genotypic value.
As an example, imagine a one locus two allele trait, with alleles $A_1$ and $A_2$, with respective frequencies $p$ and $q$, and genotypic values ($\theta$) of $A_1A_1 = \theta_{1,1} = 0.5$, $A_1A_2 = \theta_{1,2} = 0.4$, and $A_2A_2 = \theta_{2,2} = 0.3$.
The mean is given by
$ M = a_1(p-q) + 2pqd$
where $a_1$ is the deviation between the genotypic value of $A_1$ homozygotes and genotypic value heterozygotes, and, because $d=0$ (the dominance deviation), this equation reduces to
$ M = a_1(p-q)$
For my above example, if $p = 0.7$ then $M = 0.04$ and the population mean should be
$\frac{1}{2} \theta_{1,1} + \frac{1}{2} \theta_{2,2} + M = 0.44$
$\frac{1}{2} \theta_{1,2} + M = 0.44$
Is this correct?
What is the correct term and notation for the genotypic values (which I termed $\theta$)

You can't ping a user that hasn't participated on the post, they simply won't get the ping


text:
Sex biased gene expression in the X chromosome
It has been shown that the X chromosome is frequently enriched for female biased genes, and has a deficit of male biased genes. For example in this paper, and this one.
However, I'm struggling to find papers which test the general distribution sex-biased genes. I am trying to find out if the X is enriched for sex biased genes, e.g. if the X hosts 20% of all protein coding genes, it would be enriched if it carried 30% of all sex-biased genes.
Are there any such studies?

I think I found an answer tucked in the methods section at the back of the Allen paper where 15% of sex-biased genes were X-linked, I'd suggest this means that 15.55% ($100 \times (\frac{1075}{1075 + 4938 + 4323})$) of sex-biased genes are X-linked - other examples are still sought:

"Genes associated with chromosomes 2 (4,323 genes, 37%), 3 (4,938
  genes, 43%), and X (1,705 genes, 15%) were used in the analysis; these
  chromosomes accounted for 10,967 (95%) of the genes... a further 547
  (4.7%) of the genes ... were omitted"

You can answer this question for yourself using the modMine data warehouse for modENCODE datasets.  All you need is a list of female-specific genes (using your identifier of choice, although FlyBase FBGxxxxxxxx are the simplest). You can use their list tools to upload your own list of identifiers, and then there are a bunch of widgets that will tell you things like GO Term enrichment, PubMed references, and one is a histogram plot showing the chromosomal distribution of your genes, and a second histogram showing the "expected" distribution. Access to many modENCODE sites can be found at www.modencode.org
Okay, I went and did this myself.  modMine was quite slow, but fortunately the intermine server at FlyMine is working fine.  I downloaded Supplemental table 25 from Graveley et al., Nature, 2011 and cut and pasted all of the "Female Biased" IDs for those rows that had FlyBase Gene Identifiers.  This figure shows the chromosomal distribution of the 928 genes:

The Labels on the X-axis do not line up properly (for some reason), so here is a table with the Chromosome names and the counts:
Chrom     Actual    Expected
2L:     157      169
2R:     176      186
3L:     143      173
3R:     174      217
4:       0       10
X:     264      150


text:
How to interpret the breeders equation?
The univariate breeders equation is defined as,
$\ R = h^2 s$
where $\ R $ is the response, $\ h^2 $ is the heritability (additive genetic variation), $\ s $ is the selection differential. The multivariate equation is similar to this in principle but includes a multiple trait variance-covariance matrix and multiple selection differentials.
Essentially the breeders equation tells us how strong the response to selection will be as a result of the additive genetic variance within a trait (and between traits in the multivariate) and the selection applied to that variation ($\ s = cov (w,x) $ = the covariance between fitness ($w$) and the trait $x$).
For example, in trait $x$, $s$ = 0.8 and $h^2$ = 0.5 the value of the response for $x$ is $R$ = 0.4. Compared to another trait, $y$, where $s$ = 0.8 and $h^2$ = 0.1 and thus $R$ = 0.08.
My question is, if we look at a trait in a population, measure it's population mean and define $h^2$ and $s$ values, can we then predict the change in the population? IE. can we predict (with the values of $s,  h^2$  and the population mean) what the mean population mean trait will be in the next generation directly from the result of the breeders equation? Does the value of $R$ give us anything of use?
Following from the example above, I examine a trait (wing length in chickens) and find the mean to be 24 cm. I select birds to start my next generation in a way that causes $s$ = 0.8. The additive genetic variance for the wing length is quite high, $h^2$ = 0.5. The predicted response is $R$ = 0.8 x 0.5 = 0.4. What does this tell me about the next generation?

The breeder's equation as you wrote it:
$$R = h^2S$$
The heritability that is the ratio of additive genetic variance over the total phenotypic variance is called the heritability in the narrow sense and is noted $h_N^2 = \frac{V_a}{V_P}$, where $V_A$ and $V_P$ are the additive genetic and phenotypic variance respectively. In contrast the heritability that consider the total genetic variance is called the heritability in the broad sense and is noted $h_B^2 = \frac{V_G}{V_P} = \frac{V_A + V_D}{V_P}$, where $V_G$ is the total genetic variance and is equal the sum of the additive genetic variance $V_A$ and the genetic dominance variance $V_D$. We can rewrite the breeder's equation using the standard notation for the heritability in the narrow sense:
$$R = h_N^2S$$
The so-called response to selection $R$ is the mean deviation of the trait in the next generation. In other words, $R$ is the difference between the mean trait of the parents and the mean trait of the offspring, So to answer your question, yes, the breeder's equation gives the value of the mean trait in the following generation. It does not give any information about the frequency and number of alleles though.
$S$ is the the mean trait of the individuals which reproduce weighted by their reproductive success minus the mean trait of the parents. In other words, it is
$$S=\frac{1}{\bar w}\sum_{i=1}^{\text{nb inds}}m_iw_i - \bar m$$
, where $m_i$ is the trait measurement and $w_i$ is the fitness of this individual, $\bar m$ is the mean trait of the parents and $\bar w$ is the mean fitness.
The mean trait of the parent generation does not appear in the breeder's equation but only their mean trait weighted by their reproductive success. In the standard case of truncated selection (common in artificial selection programs) all $w_i$ are equal and $S$ becomes the mean trait of the individuals that we allow to reproduce in the parent population. And it is exactly the same thing for the multivariate case except that the variance-covariance matrix should be taken into account.

@GriffinEvo Let me know if I answered your question or if I missed your point.

Following on from @Remi.b and @Ell :
z score = (x - μ)/ σ from https://ncalculators.com/statistics/z-score-calculator.htm
Z score (predicted response in standard deviations) = X - adult population mean / standard deviation of normal distribution
0.4 = (X) - 24 cm/ (1)  solve for X
X= 24.4 cm, which would be the expected value of the mean trait in the following generation.

See this example as well: https://math.stackexchange.com/questions/1318981/z-score-and-stats


text:
Book suggestion on computational molecular evolution
I'm currently reading Computational Molecular Evolution by Yang. Can you recommend alternative books?
I am finding it to be lacking on conceptual discussion (it's more focussed on the mathematics and statistical intricacies). I'd like to find something which discusses why we do the things, and the strengths and weaknesses of the ideas, which are presented in the Yang book whilst not being overly specialist - more of an introductory text to the field.
Any introduction to phylogenetics books??

I would suggest the course of Coursera.org:
Computational Molecular Evolution
By Anders Gorm Pedersen
Technical University of Denmark (DTU)
PS: Do tell us if you found a better book!


text:
How far in evolutionary distance is the P-distance estimator "accurate"?
I'm reading Yang's computational molecular evolution and in the very first chapter it says the P distance is a "simplistic distance measure" between two sequences. It is the number of different sites / the total number of sites.
However, because back mutation and multiple hits cause inaccuracy it become weak over longer distances (large number of generations to most recent common ancestor, MRCA, I guess).

"The raw proportion p is usable only for highly similar sequences,
  with p <0.05 (5%, approximately)."

How far back in divergence time do we have to go for this p<5% to be violated? I assume it has to do with the mutation rate right? I'm trying to get a sense of scale on this for myself. Are we talking a distance of just a few generations (within species), the distance between two closely related species, or an even greater distance?

Yes, obviously it depends on the mutation rate, which in turn depends on the locus you are dealing with and is organism-specific.


text:
Drosophila melanogaster eclosion
Is there any published data which shows the number of Drosophila melanogaster fruit flies eclosing (hatching out of the pupae) against time since egg oviposition? I'm thinking there should be something like a "cumulative flies eclosed" plot showing the cumulative number of flies emerging per time interval after the eggs were oviposited (something like this dummy figure).

I expected to find this in the Ashburner et al Drosophila book but there was nothing. I am trying to see how much variance there is around the mean for an experiment design. It may be helpful to know (though I am not necessarily after specifics to this set up) we keep our flies at 25 degrees, 12:12 light dark cycle, 60% humidty on a yeast and sugar based food source. The flies are an African lab adapted population (Dahomey ca ~1970's?) and eggs in the experiment would be kept at low density so resource competition is not an issue.

Although I found this study, where mean and 95% CIs of median time to
eclosion (h) are provided for some strains of D.m. (with a resolution of 12 h) (in table 3), the moment of eclosion seems to be under circadian control: "in Drosophila melanogaster, the emergence of adults from their pupal cases (eclosion) is gated by the circadian clock such that it occurs during a window of approximately 8-10 h starting 1-2 h before lights-on in 12-h light:12-h dark cycles (LD)". In that particular study Canton-S flies eclosed within 4-5 days after pupation (LD 12:12, 25°C) with the following distribution over day (digitized from Fig. 1A [numbers are approximate, percents don't sum up to 100]):
Hours   % eclosed
Dark
12-14   0.5
14-16   0.4
16-18   0.6
18-20   1.1
20-22   1.4
22-24   5.6

Light
0-1     20.4
1-2     9.3
2-3     13.7
3-4     12.0
4-5     10.3
5-6     11.3
6-7     6.6
7-8     4.9
8-9     2.1
9-10    0.8
10-11   0.8
11-12   0.4

authors: محمد عبدالله دفع الله الجعلي


text:
What kind of bird species is this?
Every now and then I got a glimpse of this bird which I'm pretty sure is not native to Northern Germany where I live. There are at least three of these birds around but I usually only see something quick and green somewhere in the trees. I finally managed to get some decent pictures so I'm hoping someone can tell me what kind of bird this is. I'm curious what biological niche this bird is likely to fill and which native species it might compete with.

Almost definitely (I'm not a regular birder) European Green Woodpecker (latin name: Picus viridis) and it is native to your area according to its species distribution map.

"Green woodpeckers are the largest and most colourful woodpeckers
  native to Britain. They are easily recognised by their laughing
  ‘yaffle’ call, which they use to demarcate their territory. They also
  drum on trees, though the sound is not as resonant as that made by the
  other two British species (the greater and lesser spotted
  woodpeckers). Green woodpeckers survive on a diet of insects and have
  a particular fondness for ants. They return day after day to their
  favourite ant hill to feed." - BBC nature

I confirm rg255's answer: it is a Picus viridis.
Additionally we can see it is a young male (immature).
Young because the spots; picture of an adult here and young here.
Male because the red spot under the cheeks, the females get this part only black.


text:
Can we identify an individual from their palm lines
Can we identify an individual from their palm lines. Is there any uniqueness for palm lines among family members ?

Studies show correlations between palm primary lines and lip lines and palatal rugae patterns.Familial uniqueness should be there.

Welcome to Biology Stack Exchange.  This isn't really a full answer at the moment, however you can [edit] it to add more details - for example which studies show this?


text:
Would it be possible/plausible for a type of spider to fly by weaving web between it's legs to create bat-like wings?
I've been thinking about this lately.  Would it be possible for a type of spider to gain the ability to fly freely by weaving its web between it's legs and creating wings much like those of a bat?
Is there anything like that in nature currently?
Is it plausible at all?

It might glide, but not fly, for the same reason that you can't even if we give you wings, the size is all wrong and you don't have the necessary muscles.

Over time, could the spider evolve the "muscles" and movement in order to sustain flight with these web-wings?

Perhaps but it would no longer be a spider. Your question asks whether a spider could fly without changing its morphology, just by spinning webs between its legs. If you allow it to change form then sure it could, just make it morph into an eagle.

I gotcha.  In the short term the most a spider could do with this is possibly glide.  In the long-term it could gain flight but would be very different than any spider you see today.

They might not fly, but some spiders can "balloon".

It takes more than wings to fly, just look at the poor penguins. The first problem is that simply weaving webs between a spider's legs would probably not generate enough lift to keep her airborne. Flying creatures have a specific body plan that allows them to fly, if you just add a couple of wings to a hippopotamus it won't be able to fly.
On top of that, the spider would not have the necessary muscles to enable it to flap these wings even if they were capable of producing sufficient lift.
While it is theoretically possible (I stress theoretically) for a spider species to adapt over time (long long time) into a flying form, then it would no longer be a spider. So, in answer to your question, no, it is not possible.

Great answer.  I guess with all the changes it would need to undergo, it would be too different from any current spiders.  But it's really interesting to think about!

probably permitted by the laws of physics and biology...
almost anything is possible, jumping spiders move extremely quickly for their scale, and you could easily imagine an evolutionary pathway... spiders already use parachutes: the parachute gets bigger, the line get shorter and controlled by the rear most legs...
maybe it has already happened, there likely wouldn't be any fossil record of it, and spiders have been around for a long time (compared to apes).

Very unlikely as spiders don't have direct muscle/exoskeleton connections like insects, it would be a more complicated mechanism for powered flight...
imagine replacing a radial engine in an airplane with and engine that powers a hydraulic pump that then has a mechanism that converts that force to a force usable for flight.

Why have you posted two contradictory answers?

@terdon I had not one, but two theses; and they didn't agree very well, I wrote it as one answer, but it was self defeating.


text:
Do all cells produce the same proteins?
If DNA is more or less the same in all cells, and DNA is used to produce proteins from aminoacids, then do all cells produce the same proteins or are they specialised/controlled by something?

Close-voters - I can't straightforwardly answer this question - what determines the expression profile of a cell? I mean, let's say it's different transcription factors (?), what determines the expression profile of those? I think this is actually a great question. +1

Direct yourself here, there's quite a robust survey of the topic.

@Christiaan In that case the question would be too broad. You have to start from maternal inheritance, morphogen signalling to the structure of the gene regulatory network. I guess question need not be closed and can answered in a very few lines but it is quite trivial (unless you go to the how of it, in which case it would be broad).

Each cell will indeed have the same DNA sequences and ability to produce any given protein. However, there are certain factors (transcription factors) and cellular conditions within a cell that dictate which proteins are produced. If the conditions are right then only certain proteins will be produced depending on what type of cell it is. This process by which a cell continues to express selected proteins and becomes specialized for a specific function, is called differentiation. Expression of proteins that are not required can be prevented by transcriptional repressors (or by epigenetic mechanisms such as methylation of DNA sequences). So to answer your question, while cells contain the instructions (DNA sequences) to produce potentially any protein, not every type of protein will always be produced.
Keep in mind that my answer is very basic; the answer isn't as simplistic as I'm making it out to be.

Could you add some references & supporting material to your answer please?

I didn't use any references per se.. everything was straight from memory from what I learned in college. I have two science degrees, one in Biomedical Sciences BS and the other in Medical Laboratory Sciences BS. If you give me a little time I could probably find some supporting data.

It seems someone edited your post since, just FYI here is a useful meta thread about why citations/external material are requested here. Welcome to biology SE!

I noticed the edits and I like the additions, I think they definitely add to my answer and provide more clarity. I'll definitely include references next time. I quickly answered while I had some free time at work and didn't think to do so.

if you sequence deep enough and add single-cell sequencing you will also find cell to cell differences in the DNA which will add an other layer of heterogeneity in protein expression between cells.

Protein expression in cells is majorly governed by a concept called RNA splicing. This also forms the basis of different types of cells which has different proteins expressed at different levels, but from the same nuclear material: DNA, which can be visually seen here. Differential splicing leads to various isoforms of the mRNAs, which are precursors of protein expression in cell. So, based on how the splicing occurs in different types of cells, different proteins are expressed at different levels, which constitute to the different phenotypes. This is just a brief introduction to these concepts following the previous comments, but I thought it would be a good time to mention these as these are pertinent.
I am new to this site, so may be not giving the best and most comprehensice answers, but I hope this is useful.