The evolution of sexual dimorphism & Fisher’s fundamental theorem.

Sex differences in traits such as body size, morphology, behaviour, and life history – a pattern called sexual dimorphism – is a feature present in all dioecious species. The evolution of sexual dimorphism is the central theme of my work, more specifically, how sex differences can evolve when there is a shared genome. Most or all of the genome is inherited by offspring of both sexes in the vast majority of dioeceous species – humans only have sex-limited transmission of the Y-chromosome and mitochondria, all other genetic material can go from parent to offspring of either sex. Sexual dimorphism is most commonly driven to evolve by sexually antagonistic selection, selection for different phenotypes in either sex.


The only part of the Drosohpila nuclear genome not present in females is the Y-chromosome (green). 

Phenotypic traits are generally determined by a mixture of genetic, environmental, and gene x environment interactions. If we consider height in humans as an example, we can hypothetically state that both male height and female height are each determined by 100 equally influential loci in the genome, and that sexually antagonistic selection is occurring (for large males, small females). If these genes are sex-limited (the 100 loci determining male height do not affect female height and vice versa) then sexually antagonistic selection can easily spread mutations which make males larger and females shorter. Given enough time, mutations, and stable selection, then populations will evolve to reach their sex-specific phenotypic optima. A population where the genes affecting height are entirely sex-limited then the correlation of height between the sexes will be zero, the height of a female has no relation to the height of her father, and the height of a male has no relation to the height of his mother.


A correlation of ~0 means the sexes can evolve independently along any trajectory within the trait space.

Consider now what happens if the 100 loci affecting male height are also the same 100 loci affecting female height, but sexually antagonistic selection remains. The correlation between the sexes, intersexual genetic correlation (rmf), would be one (or minus one if there is an inverse relationship). Assuming an rmf of one, then tall mothers will have tall sons and daughters, so too will tall fathers, and short mothers will have short sons and daughters, again so too will short fathers. With sexually antagonistic selection acting on these shared loci a mutation which makes males larger will also make females larger, this moves males towards their optimal phenotype but also moves the females away from theirs – therefore the mutation will not spread through the population by selection (though it could still drift). The intralocus conflict that occurs causes a fitness depression in the population so sex-specific genetic machinery must evolve to resolve the conflict and allow the optimization of the sexes.



A correlation of 1 means male and female trait values are tightly connected and evolution can only occur along one trajectory.

According to Fisher’s fundamental theorem, the amount of variance in a trait determines the rate at which it can respond to selection. More genetic variance in a trait means a greater rate of evolution can be realized.This is related to the breeders equation where the response = selection x heritability (additive genetic variance). Simply looking at this you can see that variance will determine the rate of response, if heritability is zero then the response is zero, selection will have no effect. The same applies for genetic covariance between traits, such as male and female height. If the genome is entirely shared then there is a high covariance, selection affecting males will produce a large response in males. If a genome is sex-limited then there is no covariance so selection will produce no response in the other sex.

The conclusion of all this theory is that sexual dimorphism should be related to the intersexual genetic correlation, with sexual dimorphism only evolving when the intersexual correlation is not one or minus one, and being more extreme at zero rmf. This has been previously shown using 8 traits in waltzing flies (Bonduriansky & Rowe 2005), a meta-analysis by Poissant et al 2010, using multivariate breeders equations by both Lewis et al 2011 and Gosden et al 2012. My own paper in 2013 used gene expression data from multiple species of Drosophila and thousands of genes to demonstrate the pervasive and long-term constraint of a shared genome on the evolution of sexual dimorphism. A previous post of mine discusses in more detail the G-matrix, developed by Lande as a component of the multivariate breeders equation.



Phenotypic traits are determined by three components; genetics, environment, and the interaction between genes and the environment (when genes produce different phenotypes dependent upon the environment). The genetic variance underlying phenotypes can be further divided in to subcomponents, the additive, dominance, and epistatic variances.

Additive genetic variance of a trait is the amount of variance caused by additive loci – where the number of each allele at the loci determines the phenotype. For an illustrative example, imagine two loci determine height in a diploid organism and there are two alleles each A/a and B/b respectively. An individual with the genotype aabb has a height of 1 metre, and each copy of A or B adds 20 centimetres to the height. Therefore Aabb and aaBb genotypes are 120 cm, AAbb, AaBb and aaBB are 140 cm, AABb and AaBB are 160 cm, and AABB are 180 cm. In summary , in an additive locus the heterozygote is the intermediate of the two homozygotes.

Box: Additive genetic variance

The amount of variation in phenotype determined by additive genetic variance is also known as the (narrow sense) heritability, a measure of how much offspring will resemble parents. The value is constrained to be between one and zero where a value of one means the offspring will perfectly resemble the midparent value (be an average of both parents) and zero when the phenotype of the parents has no relation to offspring phenotype. Analysing additive genetic variance, for the purpose of heritability estimation, is central to quantitative genetics. Better estimations will allow greater insight in to the heritability of disease, improvements in breeding programs (useful for both commercial and conservation purposes) and the theory of evolution.

Additive genetic variance has classically been estimated using experimental designs like full- and half-sibling breeding or pedigree analyses. One problem with these approaches, though I firmly believe they are still useful, is their limited power. For example a half-sib experiment might take a small number of males, each mated to just a handful of females therefore just capturing a small amount of the genetic variance within the population within each set of half-siblings. Further, while an individual in the offspring generation shares on average 25% of it’s genetic variance with its half-siblings (50% probability of having the same genetic material from one of the two parents), the same individual compared to one half-sibling selected at random could share anything from 0-50% of its genetic material. Therefore to get a good estimate of additive genetic variance from a half-sib design it is necessary to get large numbers of samples, both within half-families (many females per male) to maximise background genetic variation, and from many males to maximise the amount of genetic variance being measured. Obviously this is limited by feasibility – unfortunately money and time can be a huge constraint in science.


Half-sib experimental design: each father mated to multiple females

Hemiclonal analysis in Drosophila melanogaster, pioneered by the Rice lab in the 1990’s, offers a solution to this problem. I use hemiclones extensively for my PhD work and a recent paper by our lab demonstrates how useful they can be in quantitative genetic analysis. A hemiclone is analagous to taking one sperm, cloning it, and fertilizing many different eggs with them. All of the offspring produced from those crosses would share exactly half of their genetic material, a clonally amplified haploid genome, while the other half is random. This will give a very good precision in the estimate of additive genetic variance because it does away with one of the above problems (variance in the degree of genetic relatedness between relatives).

To make a hemiclone line we use genetic tools and take advantage of a lack of recombination in males.A randomly selected wild type male is crossed to a DXCG female, a female that has a double X-chromosome (two X-chromosomes fused together allowing her to also carry a Y-chromosome) and with both major autosomes translocated (one autosome is split and fused to half of the other autosome, leaving two chromosomes composed half of autosome 2 and half of autosome 3). This means three quarters of the offspring do not hatch (those with three X chromosomes, two Y-chromosomes, or 2.5 copies of either major autosome) and the surviving quarter are either brown eyed males or white eyed females (the translocated chromosomes are also marked with recessive and dominant eye genes which, when homozygous give white eyes, and when heterozygous give brown eyes). The brown eye males are then crossed to fresh DXCG females, and this cross can be repeated many times to maintain lines.



Hemiclone production: the first step shows how the line is produced, the second shows how it is maintained, and the final part is the production of many wild type focal flies each carrying the clonally amplified haploid genome.

By crossing the brown eyed males to wild type females, or females with a double X-chromsome (double X also gives a yellow body colour) and wild type autosomes, we can produce many offspring, female and male respectively. Because many fathers and mothers can be used to produce each line a high degree of replication can be achieved, and much of the standing genetic variance can be captured in the background genetic variance within lines. Furthermore, because lines can be maintained for many generations, many lines can be assayed in an experiment (using many small experimental blocks), enabling a better capture of genetic variation across the lines.

hemiclone diagram


Chromosome diagram of the hemiclone production process

In the ~20 years since the advent of hemiclonal analyses in Drosophila there was initially a slow rate in the use of this method, however in recent years the publication rate is on the rise. Over half of the 34 papers that reference the Drosophila hemiclone analysis pioneered by Rice were published in just the last six years. The growing trend is indivicative that finally this powerful tool is being utilised on a greater scale within evolutionary biology.

For more information about hemiclonal analyses see these links: Link 1, Link 2, Link 3, Link 4.


A lot of time has passed since I last posted anything, I’ve been virtually glued to my lab bench for the last 6 months but finally I’ve managed to break free. I was doing a huge project, collecting data for use in a G-matrix to show how shared genetic variance constrains the evolution of sexual dimorphism. I’m really excited to be getting on to the analysis and writing now, it’s seems like a lifetime since I’ve had the chance to read papers. My escape from the lab should also mean I will have more opportunity to post on here too!


The practical work I’ve been doing was a in order to collect data for what I hope will be the most central and defining paper in my PhD thesis – using multivariate methods to assess genetic constraint on the sexually dimorphic evolution of life histories. This involved two key phases of work. The first was  a large selection assay, collecting trait data for 400 flies, and comparing it to their reproductive output over their entire lives. This was a long process because measuring lifespan means an experiment can take 3,5 months (because all of the flies need to die naturally) plus all of the set up time, time taken to measure other traits (e.g. body size) and time to count lifetime offspring production. The second phase then had to generate genetic variance-covariance data for the same traits (including lifespan again!) within my 80 hemiclonal lines (there will be a future blog post about the joys of hemiclones). This was both long and intense, particularly during the set up, because the data comes from 200 flies of each sex per line so I needed to produce and measure lifespan in 32 000 flies.

So that’s just a little update on what I’ve been up to, and an explanation for my absence, I promise I’ll be more active over the summer! (I’m also happy to finally have time to get out on the bike, enjoy some summer, and watch the Tour de France & World Cup!)

Happy Birthday Charles Darwin.



February 12th is the day evolutionary biologists (and evolutionists) celebrate every year as Darwin Day. On this day in 1809 one of the most important influences on the world of evolutionary biology was born. After years of travelling and study, including a five year voyage on the HMS Beagle, he published the infamous book On the Origin of Species in 1859 which featured his theory of evolution supported with compelling evidence. Without his work, and interactions with the Alfred R. Wallace, it is likely that the field would be much less advanced than it is.

Happy Darwin Day, thanks Charles Robert Darwin.

Nye/Ham debate: Historical science.

In the creation story, found in the book of Genesis in the bible, God separated light from dark in one day, the next day he created the sky, and on the third day land and vegetation. On the fourth day came the sun, moon, and stars to marks seasons, night, and day, all by God’s hand. On the fifth day God created living creatures of the sea and skies and on the sixth he created the animals of the land. Those land animals included the humans to care for, rule over, and cultivate all other animals.


This is the proof that biblical creationists such as Ray Comfort and Ken Ham will cite as the way in which life came in to existence. The evidence they turn to is a written account of the events leading up to, and including, the creation of man. It’s an interesting choice. Here is a quote from Ken Ham in the recent creation debate with Bill Nye (04-02-2014, Creation Museum, Kentucky).

 “…there’s aspects about the past that you can’t scientifically prove because you weren’t there.” – Ken Ham (view the debate here, quote taken from around 1:59:00)

horse fossil evolution

Rough schematic of horse evolution constructed using fossil evidence, past (~50 MYA, left) to present (right)

It’s an argument often used by the creationists to rebut the use of evolutionists arguments that go along the lines of “you can prove evolution by looking at the fossil records because they are the fossils of organisms that once existed.” Creationists say that, because no one saw dinosaurs roaming the earth 200 million years ago, evolutionists cannot say there were dinosaurs 200 million years ago. It’s a distinction that they term “historical science” – a term which carries no meaning beyond the Creationist circles and requires direct human observation of an event for it to be admissible as evidence in the debate. Ray Comfort repeatedly uses this argument to shut down evolutionists in the 2013 video Evolution vs God (see ~3:20 for example in the EvG video).

“Historical science” is analogous to the use of evidence other than direct witness accounts in a crime. Clues are used to piece together the story so that a conviction can be brought without the need for witnesses. Imagine how few crimes would be punished if Ken Ham made the rules.

My question to creationists is if God did not create man until the 6th day, how do we know what he did in the preceding 5 days? No one was there to see it. I feel that creationists should be able to answer this seeing as it is there description of evidence that it must be directly observed, otherwise their use of the argument is hypocrisy (and hypocrisy is a sin). However, I personally think that direct observation of an event is not the only way to prove an events happening (I’ll perhaps post something on that in the future).

Nye/Ham debate: The orchard of creation.

 “…from such low and intermediate form, both animals and plants may have been developed; and, if we admit this, we must likewise admit that all organic beings which have ever lived on this earth may be descended from some one primordial form.” – Ken Ham quoting Charles Darwin.

This quote describes the evolutionary tree of life. It proposes that every organism has a common ancestor, and, logically more closely related species have more recent common ancestors. According to Ham this suggests that we do not need to find every species of dog (Canidae), every species of cat (Felidae), and every species of elephant (Proboscidea) on Noah’s Ark.

Based on the accounts of the bible, creationists have described an orchard of creation which stipulates that we only need two dogs, two apes, two birds, two dinosaurs, two lizards, two of each “kind” to lead to all of the species we have. Because there is great variation in genetics of any creature the new species, such as every Canidae species, can develop from the two individuals of the kind found on the ark. Ham also states that because lineages do not switch “kind” that evolution must not be true, species do not evolve by descent with modification.

creation orchard

An illustration of the Orchard of Creation

Now I may be wrong, but, Ham has just massively contradicted himself hasn’t he? The orchard of creation he describes is, by definition, and example of evolution. Is the descent from one species to many not the perfect manifestation of “descent with modification,” Darwin’s definition of evolution? Furthermore, I am aware of no theory that says lineages can or do switch kinds (or family) on the tree of life. No credible evolutionary biologist suggests that birds evolve in to apes, or dogs in to cats. Evolutionary theory proposes that these species share a common ancestor on the tree of life (and the orchard of creation) but evolution does not suggest that they will ever share a common descendant. The tree of life is a tree, on a tree the branches do not split in two and then rejoin later in life. One branch descends in to many.


This is not what happens in Evolutionary theory. There is no change of “kind.”

Thanks Ken Ham. All you’ve done is prove you do not understand the theory of evolution. It would be great if people challenging the theory of evolution could get the definition right. Creationists are ignoring the real argument because of the confused understanding of evolution. The views of creationism (those accepting the orchard of life) and evolutionary biologists differ, not forward of the division of new lineages, but prior to the division of phylogenetic families.

where evolution differs

Hint… this is where the true debate lies

Creationists must refocus themselves or face losing significant ground in the debate over the origins of life on earth. Move on from attacks on the character of atheists and attempts to promote a false interpretation of the views of evolutionary biologists (creationists can be scientists as long as they are objective about their research). I think it is a debate which should continue and one which evolutionary biologists should not ignore because many people still do not accept evolution to be true. Eventually one side will produce such compelling evidence that it can no longer be debated, until then the discussion is bound to continue.

I will deal with the issue of “observable” evidence in new blog post soon because apparently we can’t observe fossils, my eyes must be deceiving me…

Evolution can only be true.

This entry is based on a short public talk I saw by a former lecturer of mine last year (Professor Tom Tregenza). He put across a simple way to argue that evolution is a process that cannot be denied. I chose to write about it because of it’s simplicity and elegance. I start by defining evolution and then expanding on the points made by Tom.

The theory of evolution was defined by Darwin as “Descent with modification.” That is, characteristics descend along a lineage (from parent to offspring) and, between generations, can become different from the ancestral characteristic. It is, in my opinion, only a theory by scientific definition, just like the theory of gravity. I know that if I stand on the surface of the earth and drop an apple, without applying any other forces, it will fall to the ground because of gravity. The existence of evolution is equally as certain, yet many do not accept it.

The aim of Tom’s talk was to provide a logical basis, supported by fact, upon which the only outcome that makes sense is to accept evolution. All of the following questions can only be answered with “yes” and thus irrefutably support evolution. I do not provide hard evidence for many of these points because the answers are so obviously true.


1. Do living organisms reproduce?

The very definition of life states that all living organisms reproduce. Every single species on the tree of life reproduces in some capacity. Right from simple clonal reproduction of single celled organisms through to the sexual reproduction found in many eukaryotes, and all sorts of weird and wonderful variations in-between and beyond. The answer to this question is undoubtedly yes.

2. Do some individual organisms have more offspring than others?

There is high variation in reproductive success even within species. Looking to humans we know that some people die before reaching a reproductive age, some are infertile, some chose not to have children, and some chose to have many. Looking across species we see even greater variance from very few offspring per parent to many thousands. Again, the answer to this question is yes.

3. Do individuals vary in their characteristics?

Look around you, there is variance in height, hair color, eye color, between species there is variance in the number of legs used to walk, the number and type of limbs species have, body size, shape, senses, color, behavior, and much more. So, is there variation between individuals? Yes.

4. Are characteristics heritable?

Again look at humans. We more often see that the characters of offspring resemble their parent’s characters more than the homologous character of a random organism. Tall people tend to have tall children. Short people tend to have short children. Humans tend to produce offspring that look more like humans than an elephant, and elephants tend to produce offspring that look more like elephants than humans. Obviously there is heritability in traits (and much of this is due to the passing of genes along a lineage) so the answer is thus yes.

5. Are traits causing variance in reproductive success heritable?

An example of this would be the genetic inheritance of disease. Some diseases kill people before they have reached the end of their natural reproductive window, the point where they can no longer viably reproduce. Cancer has been linked to genetic mutations which can be passed from parent to offspring (for example the BRCA1 gene is linked to high incidences of breast cancer). If a cancer, passed along the lineage, stops an individual from producing as many offspring as possible then a heritable characteristic has affected the variation in reproductive success. Traits affecting reproductive success need not be detrimental, a mutation might arise that increases may fertility for example. In such a case the male would be expected to sire more offspring in the next generation, thus there will be an increased proportion of the population with that mutation. Therefore the answer to this fifth and final question is also yes.

These five points are nothing pioneering or controversial, they just simply support the definition of evolution by showing that heritable changes can occur in a population and as a result the population may become different over time. *Technically, excluding point five, we can still say that evolution can only be true. Combing the evidence from points one to four, shows that traits are transmitted from one generation to the next in such a way that could cause a change over time – this is via genetic drift. Point five simply invokes selection for adaptation as a mechanism of evolution.*

The discussion over the truth of evolution is largely fuelled by religious groups who see it as opposing their beliefs, but eventually I am sure that religions will come to accept the theory of evolution. In the face of growing evidence, just as when we realized that the earth was round and not at the centre of the universe, those religions will be forced to adapt, to evolve.

* This section has been added after initial publication