When the age of the dinosaurs ended around 65 million years ago, mammals stepped in to fill the gap, and the age of the placentals began. However, whether early placental mammals were already present on Earth before the demise of the dinosaurs has been the subject of a long standing debate. Recent research in GEE used genomic data, in combination with fossil evidence, to show that the earliest placental mammals were indeed scurrying between the feet of dinosaurs.

The huge diversity of placental mammals on Earth today first appeared shortly after the mass extinction event that killed the dinosaurs. It is thought that the loss of the dinosaurs, along with much of life on Earth, freed up niches which placental mammals to evolved to fill. But were early placental mammals present, waiting in the wings, during the age of the dinosaurs, or did they appear rapidly after their demise? One recent study suggested that, based on fossil evidence, the placental mammals must have appeared after the cretaceous-tertiary boundary (KT) when dinosaurs and most life on Earth was wiped out. However, a recent paper by GEE’s Mario dos Reis and Ziheng Yang, in collaboration with Philip Donoghue from the University of Bristol, highlights flaws in the methods used in this study, and utilitsed a more thorough approach to show that early placental mammals likely predated the KT boundary.

Using genetic sequence data from over 14,000 genes, combined with fossil evidence, GEE researchers applied 3 alternative statistical methods to estimate the age of the earliest placental mammal; ancestor to all modern placental mammals. Although different statistical methods yielded slightly different estimates, and differed in their accuracy, they all agreed that placental mammals must have already been around before the dinosaurs went extinct. The adaptive radiation of mammals that occurred after the extinction of the dinosaurs was dramatic, but it was initiated by a few shrew-like species which had already evolved. This study highlights the importance of using statistical methods to estimate the true age of ancestral species; the age of the oldest fossils is not the same as the age of the ancestral species that gave rise to them, and statistical techniques must be employed to estimate this. Using both molecular and fossil evidence to inform estimates also provides more robust evidence for the true age of the first placental mammals, and the theory that the earliest ancestors of placentals predated the disappearance of the dinosaurs.

Original Article:

This research was made possible by funding from the Biotechnology and Biological Sciences Research Council (BBSRC).

In many species, males have special adaptations to attract females. From antlers to stalk-eyes, to bright plumage and beards, males across the animal kingdom work hard to look attractive to the opposite sex. In some species, looking good isn’t enough, though. Male wild turkeys need a less attractive ‘wingman’ to help him attract a woman. Wingman turkeys show less extreme sexual traits than the dominant males, and researchers from GEE have exploited this ‘intermediate phenotype’ to investigate how gene expression controls sexual traits. Subordinate male turkeys are physically demasculinised, and this is reflected in their gene expression. Whilst clearly male, these turkeys tend to express ‘male’ genes less and ‘female’ genes more, indicating that sexual phenotypes, at least in this species, exist upon a continuum. This has important implications for how we view sexual selection and sexual traits across the animal kingdom, as well as in our own species.

You might think this is a face only a mother could love, but to a female turkey, this guy is very attractive. Male wild turkeys have a number of physical traits that make them very, very sexy…. to female turkeys, at least. They are larger than females, their feathers are iridescent, their faces are bright red and adorned with caruncles, wattle and a snood. As they grow up, young male turkeys argue with their brothers for dominance. One brother wins, and the others become subordinate. These subordinate males rarely get the chance to mate themselves, but helping out their brother means passing on their genes indirectly. If, later in life, the dominant brother dies, the subordinate may get his chance in the limelight and develop a dominant phenotype. This shows just how plastic sex can be in the animal kingdom.

Differences in Gene Expression
Differences between the sexes form ‘sexual phenotypes’ that are largely the result of the differential expression of genes that are present in both sexes. Although sex chromosomes are also important in controlling the development of sexual traits, many genes on other chromosomes also contribute. Many genes show differences in expression between the sexes.

Theory suggests that genes expressed differently in different sexes are responsible for generating the sex-specific characteristics we observe. However, this hypothesis has been difficult to test in species where sex is binary. This is where wild turkeys come in handy – the existence of the subordinate male phenotype, with reduced sexual traits, provides a rare opportunity to decouple genetic sex and sex-biased gene expression. If sex-biased genes encode sex-specific phenotypes then the subordinate male phenotype should be expected to be the product of reduced expression of male-biased genes and increased expression of female-biased genes.

Researchers in GEE and the Department of Zoology, University of Oxford, investigated gene expression patterns in females, dominant and subordinate males. Around 2000 genes were male biased and nearly 3000 showed female bias.

Unravelling the ‘Wingman’ Phenotype
The gene expression patterns of subordinate males clearly clustered with dominant males. So subordinates are not intersex. However, there were subtle differences between the subordinate and dominant males. Subordinate males tended to express male-based genes at lower levels than dominant males, indicating transcriptional demasculinisation. They also expressed female-biased genes at a higher level than dominant males, suggesting transcriptional feminisation. Expressionally, subordinate males were less masculine and more feminine than dominant males. This is consistent with their visual appearance.

Furthermore, genes that were more strongly sex-based showed a greater level of demasculinisation in subordinates than those that were less strongly sex-biased. This suggests that the genes we find to be most strongly sex-biased may contribute the most to generating the male or female phenotype.

These patterns were also true for genes found on the z chromsome – the sex chromosome in birds (analogous to our ‘Y’ chromosome). However, the patterns were no stronger for these genes than for those on other chromosomes, suggesting that the sex chromosome does not contribute disproportionately to the male or female phenotype. This might come as a surprise – surely the sex chromosome should control sex? There is now a great deal of evidence that this isn’t the case, and many animals get on just fine without a sex chromosome at all!

Dominant and subordinate males reveal a continuum of sexual characteristics physically, and this is mirrored by gene expression patterns. Whilst clearly male, subordinate males showed up-regulated of ‘feminine’ genes and down-regulation of ‘masculine’ genes across the transcriptome. This demonstrates for the first time that sex-biased genes are indeed important in generating the sexual traits we observe in nature. Physical sex is determined by the combined action of many genes, some male-biased and some female-biased, and intermediate physical characteristics are possible simply through altering the expression of key sex-biased genes. This result has clear implications for how we view sex and gender in our own species, and greatly enhances our understanding of sexual selection and sexual dimorphism across the animal kingdom.

Original Article:

This research was made possible by funding from the European Research Council

Across the animal kingdom, males have evolved fancy physical ornaments, songs and courtship rituals, all in an attempt to attract the opposite sex. Most of the male ornaments and sexually-selected traits biologists tend to study are large, elaborate and flamboyant. But mathematical models predict that sexual selection is just as likely to make an ornament smaller or more modest as it is to make it more elaborate. Recent research by Dr Sam Tazzyman and Prof Andrew Pomiankowski from UCL’s Department of Genetics, Evolution and Environment, in collaboration with Prof Yoh Iwasa at Kyushu University, investigates why male ornaments tend to get bigger rather than smaller.

Sexual selection is the process whereby traits are favoured because they increase an individual’s success at obtaining mates, often at the expense of survival or condition. Sexual selection is a special case of natural selection, where natural selection is concerned with increasing the overall fitness of an organism. Sexual selection may act in opposition to natural selection, when traits that make you more attractive to the opposite sex also make you less fit in other ways. In these cases, the form a trait takes may be somewhere between the most attractive (sexual selection optimum) and the most fit (natural selection optimum). Sexual selection has been the focus of a great deal of evolutionary research, both experimental and theoretical, because it has the power to generate extreme physical and behavioural adaptations: huge antlers, complicated courtship displays, brightly coloured plumage, etc. Most research has focussed on bright, bold, exaggerated traits like these. But theory suggests that sexual selection should be just as likely to drive traits to be less extreme (than the natural selection optimum) as it is to make them more extreme. So why don’t we see sexually reduced traits much in nature?

First, Tazzyman and collegues searched the literature on mate choice and sexual selection for examples of reduced sexual traits – that is, cases in which females prefer males with a trait smaller, duller or less elaborate than the natural selection optimum. They found that for many types of trait, reduction simply isn’t possible, or is extremely difficult to define. For example, when a sexually-selected trait is a particular colour of a patch of plumage, how can we define exaggeration or reduction in this trait? Is the size of the patch most relevant, or the hue or saturation of colour? Similarly, for many traits, the natural selection optimum might be zero – no trait at all. For example, in many species the male is brightly coloured while the female is dull, here the dull colouration can be considered no trait and is assumed to be the natural selection optimum. Likewise, in many species the males carry physical adornments such as the red crests (or combs) of many gamefowl, which are totally absent in females.

Certainly, these issues with definition occur most frequently for colour, pheromone and behavioural traits. Morphological traits tend to lend themselves more readily to being classified on a simple scale, in which both exaggeration and reduction of that trait is possible. There are a few cases of females showing a preference for a smaller trait, but these examples are few and far between. Of 40 sexual traits for which both elaboration and reduction could be defined, 34 were found to be subject to sexual selection for exaggeration.

This imbalance may be partly explained by our own observation bias – smaller traits may be more difficult to detect and so tend not to become the subject of study. But, it is unlikely this is the full explanation. However, it seems that females may suffer a similar problem; if biologists aren’t noticing small ornaments, maybe the females aren’t either. This is one of three possible hypotheses that Tazzyman and colleagues tested to explain the apparent asymmetry in the direction of sexual selection. Male ornaments are signals, aimed at attracting a female – if that trait cannot easily be seen or detected by the female, then it cannot serve it’s purpose. Consistent with this, a mathematical model of sexual selection assuming asymmetrical signalling efficacy (where smaller traits are less effective at conveying their message) showed that exaggerated traits were more likely to undergo the ‘runaway’ selection characteristic of sexually-selected ornaments.

Their models also ruled out two other possible explanations – that it is more costly for a female to prefer a small trait than a large one, and that is it more costly for a male to carry a small trait than a large one. Neither of these models resulted in a bias towards exaggeration. Only models including an asymmetry in the efficacy of signalling produced results that mirror what we observe in nature.

Sexual selection acts upon traits that make one sex more attractive to the other, and can favour characteristics that are otherwise detrimental to survival or condition. Sexual selection has the power to generate the bright, flamboyant, exaggerated characteristics such as antlers that we see in many animals. Although many theoretical models predict both exaggeration and reduction in sexual traits, in wild populations, we rarely see this – almost all documented sexual traits are more extreme than their natural selection optimum. Sexual traits act as signals to the opposite sex, and this may explain why in the wild, sexual selection tends to exaggerate and elaborate traits which are more visible to females and so more effective at communicating their message.

Original Article:

This research was made possible by funding from the Natural Environment Research Council (NERC), and the Engineering and Physical Sciences Research Council (EPSRC)

Every living cell, whether solitary or part of a larger multicellular organism, is an extremely complex system, involving a multitude of simultaneous chemical reactions regulated by proteins and RNA. Keeping this machine running relies upon a careful balance of gene expression and protein degradation, and cells must be prepared to modulate these processes in response to environmental variation (both internal and external). Homeostatic mechanisms can be an efficient way to regulate gene expression, however one key mechanism – negative autoregulation – is rarely used in organisms like flies and humans. Mathematical modelling by GEE’s Max Reuter and Andrew Pomiankowski shows that evolutionary constraints in the evolution of negative feedback may exist for species who carry multiple copies of each chromosome in their cells.

A Eukaryotic (Animal) Cell and a Prokaryotic (Bacterial) Cell

Homeostasis: From Radiators to Cells
One of the simplest ways to regulate any system is through negative feedback, whereby a particular process is inhibited by the products of that process. This is the system employed by central-heating systems, which use the temperature to regulate the action of a radiator. The radiator pumps out heat, and when the thermometer detects too much heat in the room, it signals the radiator to stop. Negative feedback systems can be highly efficient, stable and responsive.

Negative feedback, or homeostasis, would also be a sensible way to regulate the expression of genes within a cell – a particular gene would continue to be expressed and produce its protein product until there is enough of that product in the cell, at which point expression would stop. This system would be sensitive to the demands of the cell – if the product was being used up quickly, then expression would continue as long as demand was high. In fact, many simple, single-celled organisms, such as E. coli, use this system to respond quickly to changes in their environment.

Around half of all genes in Escherichia coli are regulated by this kind of negative feedback loop, known as negative autoregulation. However, when we look at other organisms such as yeast (Saccharoymyces cerevisiae), fruit flies (Drosophila melanogaster), and humans, we find a very different picture – almost no genes show signs of negative autoregulation (around 2%). If negative autoregulation is such a neat solution to apparently common problem, why aren’t humans and flies using it?

A Matter of Ploidy
One of the key differences between humans and E. coli (although probably not the one that springs to mind!), is that E. coli carry only a single copy of each gene in each cell. They are haploid, with a single circular chromosome in each cell that carries a single copy of each gene in the E. coli genome. By contrast, humans, yeast and fruit flies are all diploid, meaning that they carry two copies of each gene in every cell. Our genes are split up into many, straight chromosomes, and we have two copies of each chromosome. Recent research in the department of GEE has used a mathematical modelling approach to investigate how diploidy (having two sets of chromosomes) might constrain the evolution of negative autoregulation.

In a paper in PLoS Computational Biology in March this year, Dr Alexander Stewart, Professor Rob Seymour, Professor Andrew Pomiankowski and Dr Max Reuter from UCL’s GEE produced a mathematical model of how gene regulation might evolve differently in species with one or two sets of chromosomes. Their model focuses on mutations in the promoters of genes, which alter how other protein molecules interact with and repress the expression of those genes.

In haploids, with a single copy of each gene, negative autoregulation produces very tight regulation of gene expression, giving a very rapid response to changing demand. Likewise, in a diploid species with two identical copies of a particular gene, negative autoregulation tends to be beneficial and achieves very efficient gene regulation.

Constraints in the Evolution of Regulation
The problem arises when the diploid carries two different variants of the same gene. This would be the situation whenever a new mutation arises – new mutations appear in a single copy of a particular gene. For a new mutation to be favoured and spread through the population, it must be able to do well, at least initially, as a single copy. The mutated gene must be able to work well alongside the original version. And this is where the problem arises. Stewart, Seymour, Pomiankowski and Reuter (2013) found that mutations that altered the negative autoregulation of a gene didn’t tend to play well with others. Their model considered mutations that alter the strength of the binding site – essentially how strongly regulated that gene is. An individual carrying one strongly regulated gene and one weakly regulated gene actually did worse than an individual with two weakly regulated genes. These heterozygote individuals responded more slowly to changes in demand, and there was more noise in the system. This situation, known as underdominance, where a genetic variant has a lower fitness in the heterozygote form, could be a major constraint to evolution.

Underdominance in negatively autoregulated systems arises because of the disparity in binding site strength between the two different copies of a gene. As each gene pumps out gene product, the stronger binding site is quickly suppressed by the product produced by both genes. It takes much longer for the weaker binding site to be suppressed, as it requires more product to be activated, and most of this is being used up by the stronger binding site. Compared to a haploid, the strong site shows faster response times but the weak site shows a much slower response time, and this averages out to an overall slower response.

Stewart et al (2013)’s model showed that the extent of underdominance depended on how different the two genetic variants were. Large differences in the strength of their binding sites reduced response time and created more noise than smaller differences. Slower response times and increased noise in heterozygotes mean that the maximum strength of regulation achievable in a diploid may be as much as ten-fold lower than in haploids.

Because very small differences between genetic variants in their binding site strength did not experience such a strong effect of underdominance, they were more likely to lead to the evolution of autoregulation. Evolution in diploids could proceed through many very small changes, however there is also likely to be lower limit on the size of mutations – very small changes cannot be ‘seen’ by natural selection and are unlikely to spread. Likewise, multiple binding sites, each relatively weak but which act together cooperatively, were also more likely to overcome the issue of underdominance in the model. However, in general, diploids had a much harder time evolving negative feedback as a mechanism for gene regulation. This evolutionary constraint might have forced diploids such as fruit flies and humans to develop alternative mechanisms to achieve rapid responses, such as increased rates of protein degradation or alternative regulatory mechanisms.

Original Article:

This research was made possible by funding from the Natural Environment Research Council (NERC), the Engineering and Physical Sciences Research Council (EPSRC), and the McDonnell Foundation

By definition, males and females are physically different. In some cases, these differences are restricted to the sex organs, but in many species males and females also differ in their physical appearance and behaviour. What makes you a good male does not necessarily make you a good female, and the benefit of some genes depends upon which sex they find themselves in. These antagonistic genes have sex-dependent fitness effects, and can be a source of genetic variation in natural populations. Research in GEE shows that in small populations, chance events can alter the frequency of antagonistic mutations, and alter the balance of fitness between the sexes. Small populations tend to produce either good males and poor females, or good females and poor males, but not both. This phenomenon could have interesting implications for dispersal and fitness, especially in fragmented populations.

Differences in physical appearance between the sexes is known as sexual dimorphism, and occurs because characteristics that make you good at being male are often different from the characteristics that make you good at being female. A brightly coloured male may get more females because he is more visible or attractive, but a brightly coloured female doesn’t lay more eggs, she just gets eaten.

Sexual dimorphism allows males and females to independently adapt to different optima. The problem is dimorphism is actually quite hard to achieve. Males and females of the same species share, more or less, the same genome. Some species, such as birds and mammals, have sex-specific genes and chromosomes (e.g. the Y chromosome), but these represent a very small proportion of their genes, and many species achieve sexual dimorphism without any sex chromosomes at all. For the most part, traits that differ between males and females are generated from the same set of genes. The evolution of dimorphic traits such as body size, plumage colour and antlers proceeds not through changes to gene function, but changes in gene expression.

Gene Expression and Sexual Dimorphism

A gene that codes for a trait that is beneficial to males but detrimental to females can become sexually dimorphic if it is expressed only when it appears in males (or vice versa). This same gene, when it finds itself in a female body, simply isn’t expressed and does not exert its effect. So a female red deer carries the gene for antlers, but never grows any because the gene is silent.

Sex-specific gene expression is an elegant solution to the problem that males and females face different challenges in life. However, the road to sexual dimorphism is not that straight forward. For a new sexually dimorphic trait to evolve, it must first appear as a novel mutation in a pre-existing gene. At first, it will be expressed just like most other genes – equally in both males and females. This mutation might do great when it finds itself in a male, allowing him to produce more offspring, but when it appears in a female, it would be harmful, reducing the number of offspring produced. For this new mutation to be successful and spread through the population, it needs to avoid the negative fitness effects that come from being expressed in a female. At this stage, a second mutation altering gene regulation – so that the gene is expressed only in males – would be hugely beneficial, but this mutation may take time to arise by chance.

There are many examples in nature of sexually dimorphic traits – genetic variants expressed in one sex but not another. But scientists are increasingly finding mutations that haven’t made it to this happy equilibrium yet – their fitness effect is sex-dependent but they are still expressed in both males and females. These genes are known as ‘sexually antagonistic’ and are thought to be a major source of genetic variation within populations.

Generating Variability
Normally, a gene that has a detrimental effect (i.e. reduces how many offspring you produce) is quickly removed from the population by natural selection. Sexually antagonistic genes are different because their detrimental effect is only seen by natural selection when the mutation appears in one sex. Half the time, the mutation is beneficial, and half the time it is harmful. Overall, the effect of the gene can even out to be essentially neutral. Neutral mutations can stick around in a population for ages, although they may be lost, or spread, by chance.

Chance, also known as genetic drift, can change the frequency of mutations in a population irrespective of their fitness effects, and the effect of chance is much greater in smaller populations. Sexually antagonistic genes may be particularly susceptible to genetic drift because their effect is, on average, neutral. Most theoretical and empirical studies of sexual antagonism use very large populations with high genetic diversity, where the influence of genetic drift is very small. Researchers in GEE have been investigating the evolution of sexual antagonism in small populations to see how chance might influence their frequency.

The Role of Chance
In a recent paper in Evolution, Jack Hesketh, Kevin Fowler and Max Reuter from GEE looked at how small populations of the fruit fly Drosophila melanogaster evolved, and how sex-specific fitness changed under the influence of genetic drift, through the random spread of sexually antagonistic genes. Four populations of 100 flies were maintained for 80 generations, and the fitness of both larvae and adults was measured in terms of survival (larvae), fertilisation success (males) and egg-laying (females).

Over 80 generations of evolution in the lab, the four fruit fly populations diverged in terms of fitness. Average fitness across the sexes didn’t differ significantly between populations, but there was a strong interaction between population and sex – some populations produced very fit females and unfit males whilst others produced fit males and unfit females. This effect was not present for larval fitness however, which makes sense since larvae are primarily concerned with growth and not reproduction. In the original source populations, some individuals carried mutations beneficial to females, whilst others carried mutations beneficial to males. In this experiment, through the process of genetic drift, different populations ended up with a different selection of these mutations – some populations kept hold of the genetic variants favourable to females and consequently produce very fit females but relatively crap males (and vice versa).

This study shows that in real populations, genetic drift may lead to population-divergence in sexually antagonistic genes. This could have interesting repercussions for fragmented populations where different fragments may diverge differently in terms of sexual antagonism. Dispersal in this situation could be extremely favourable – a fit male in a population full of fit males would be faced with stiff competition, but if he wandered over into a neighbouring population full of unfit males, he would presumably have his pick of the ladies. Max Reuter and colleagues in GEE hope to continue to investigate this phenomenon and its consequences in natural populations.

Original Article:

This research was made possible by funding from the Natural Environment Research Council (NERC) and the Biotechnology and Biological Sciences Research Council (BBSRC).

Every cell in our bodies is a collaborative effort. A collaboration that dates back to just after the dawn of life itself, and marks one of the deepest divides in the tree of life. This symbiosis has had remarkably far-reaching effects, and is now thought to be key to understanding sex, ageing and death. The symbiotic entity in question is the mitochondrion; the power house of the cell. Biologists are increasingly realising the centrality of energy in understanding life, and a special issue of Philosophical Transactions of the Royal Society, introduced by Nick Lane, focuses on the synthesis of energy, genes and evolution.

Around 1.5 billion years ago, a simple, single-celled bacterium engulfed another one. But it didn’t eat it. Instead, the two cells started working together, and over the following millennia developed a cooperative relationship that laid the foundation for multicellular life and for diversification on a scale never seen before. This symbiotic relationship founded a new type of life – the eukaryote. Unlike their prokaryote ancestors, the eukaryotes had a special advantage: they now had internal membranes. This enabled them to generate energy more efficiently, utilising a force generated across a membrane, known as the proton-motive force. This allowed them to support bigger cells, a wider variety of diets, and ultimately led some eukaryotes to group together into multicellular, sexual organisms such as plants and animals.

Hand Over Your Genes!
Since mitochondria originated as free-living single celled organisms, they came complete with their own genetic information. As the cooperative partnership between the eukaryote host and its mitochondrial partners developed, the majority of these genes were transferred to the nuclear (host cell) genome. Bizarrely, though, a few genes remained with the mitochondria. In fact, the same few genes stayed put in almost all eukaryotes, even though this process happened many times independently. So what is so special about these genes? Why keep them in the mitochondria when it is costly to do so?

A Rapid Response System
It is thought these genes remain in the mitochondria because they are needed there to allow individual mitochondria to respond rapidly to changes in the energy demands of the cell. When mitochondria are out-of-sync with their surroundings, they start generating dangerous ‘reactive oxygen species’ (ROS), also known as free radicals. Free radicals are famous for causing cancer, and this is because they act as mutagens, causing changes to DNA they encounter. Mutations caused by ROS can cause all sorts of problems, not just cancer, and many of the diseases of old age are thought to be caused by ROS mutations.

So, we need to keep a small set of genes – those that code for key components of the respiratory chain that generates energy in mitochondria – in close proximity to their site of use so that they can quickly respond to the ever-changing cellular environment. This is also true for chloroplasts in plants, and recent research by Puthiyaveetil and colleagues in GEE lends support for this explanation. They have found evidence for a chemical partnership, unique to eukaryotes, which may be important in regulating chloroplast function to minimise ROS production.

Both mitochondria and chloroplasts have held onto a few genes in order to allow a rapid response to changes in demand. Trouble is, by keeping those genes there, they are vulnerable to attack from any free radicals that are generated. Mutations in these genes can often cause the production of more free radicals, causing a downward spiral that eventually leads to the death of the cell.

Unusual Inheritance

Mitochondrial genes are not inherited in the same way as normal nuclear genes. The majority of our genes (residing in the nucleus) are inherited biparentally, that is, we inherit half from our mother and half from our father. Mitochondrial genes, on the other hand, are inherited only in the maternal line, through the egg. Mitochondria are also present in sperm cells – they have to be, since they are crucial for providing energy to power all that intense swimming – but sperm mitochondria are killed shortly after fertilisation. Recent research by John Allen in GEE suggests that uniparental inheritance of mitochondrial genes relates back to those pesky free radicals.

In sperm cells, mitochondria are working overtime to make sure the sperm has the energy to swim and find the egg. In the process they are churning out free radicals, and damaging the mitochondrial DNA. The mitochondria inside sperm start to suffer from the ravages of old age. But we don’t want to pass on old mitochondria to our offspring. It seems evolution has found an elegant solution – switch off the mitochondria in egg cells and pass these young mitochondria on to your offspring. De Paula and colleagues looked at the mitochondria in eggs, sperm and the bell of moon jellyfish (Aurelia aurita) and found egg mitochondria were largely inactive and simple in structure. Egg mitochondria also showed reduced levels of gene expression, an almost non-existent membrane potential and produced no free radicals, indicating that they were not actively generating energy. Eggs don’t need that much energy compared to sperm, and they can borrow what they do need from other cells. By switching off the mitochondria in eggs, and making sure these are the only ones passed on to the next generation, eukaryotes can reduce the build-up of harmful age-related mutations in mitochondria from generation to generation.

Energy, Mitochondria and the Meaning of Life
The generation of energy is central to life. Mitochondria generate energy in all eukaryotic cells (animals, plants, fungi), and the symbiotic event that brought them into the eukaryotic cell changed life on Earth forever. Mitochondria proved massively beneficial, allowing eukaryotes to try new things, and ultimately produce the huge diversity of multicellular life we see today. However, housing another genome inside the cell came with nuances of its own, which led us to have sex, to age and die. Recent research in GEE highlights one way in which evolution has overcome one of these nuances – by switching off mitochondria in egg cells, offspring can inherit an undamaged copy, and because of this, ageing is not heritable. Other research in plants is broadening our understanding of why these genes are stored inside the mitochondria and chloroplasts in the first place. Throughout a plethora of different disciplines, mitochondria are proving crucial to understanding the fundamentals of life.

Original Articles:

Introduction to the Special Issue:

This research was made possible by funding from the Natural Environment Research Council (NERC) and the Leverhulme Trust

The tree of life is a vast tangle of branches and twigs representing around 9 million species. Understanding the patterns and processes by which these species originated is a fundamental topic in evolutionary biology. Previous studies have suggested that the generation of new species may not be uniform over time, often with an initial burst of speciation, slowing as the lineage expands to fill the available niches. However, recent research in the department of GEE suggests this may not always be the case, and a previous focus on island species may have skewed our perspective of species accumulation.

When a new lineage begins to diverge, adapting to exploit new habitats or lifestyles, this often leads to an adaptive radiation, with many new species appearing over a short space of time. This initial rush of new species eventually begins to slow, as all the available niches become saturated, and slowly speciation grinds to a halt. This is the traditional view of how lineages have diversified to produce the vast array of species we see today (as well as many who have long since gone extinct). However, much of the research in this area has focussed on species confined to islands and lakes, where different processes may influence the appearance of new species. Continental species have a larger area to expand into, and a wider array of climatic conditions to cope with, providing a different set of parameters which may influence speciation. Recent research in the department of Genetics, Evolution and Environment suggests the pattern of species generation in continental lineages may differ from that of islands.

Tree of Life image © 2007 Tree of Life Web Project. Image of rose © 1999 Nick Kurzenko. Image of annelid worm © 2001 Greg W. Rouse

In their recent paper in Systematic Biology, Day and colleagues determined species relationships for 81 species of squeaker catfish from Africa in order to investigate the patterns of species generation and diversification during their 35 million year evolution. Using genetic data along with fossil evidence, they constructed a squeaker catfish tree and estimated divergence dates and historical geographic distributions. This tree revealed an almost constant rate of species generation over time. Across 35 million years of evolution, through major climatic and environmental changes, the squeaker catfish have been churning out new species at approximately 1 every 8 million years, and look set to keep going for another 90 million years, or so.

Syndontis ‘squeaker’ catfish . Photograph by Roger Bills

So why don’t the continental, river-dwelling catfish follow the same rules developed through years of studying island and lake-dwelling species? Continents are, of course, generally much larger than islands, and rivers provide more opportunity for movement than lakes. Continents allow for more constant species generation, as there is more space and habitat diversity available for species to move into and exploit. The climatic changes in Africa over the last 30 million years may have also helped the catfish maintain constant production of new species – creating a variable environment which is much less likely to become saturated with species. The squeaker catfish have survived through major tectonic activity in the East African Rift valley, including volcanoes and earthquakes, as well as huge climatic changes that influenced sea level and temperature. By combining phylogenetic and biogeographical data, Day et al suggest these environmental variations may have played an important role in African catfish diversification.

The processes shaping species diversification are varied and complex, and differ markedly between geographically isolated lineages (island / lake ecosystems) and wider ranging ones (e.g. continental rivers). Continental groups may take longer to reach species saturation, with environmental fluctuations facilitating continued species generation at a relatively constant rate. Moving beyond ‘model organisms’ and well-studied systems has the potential to reveal new processes and patterns, and illuminate old ones.

Original Article:

This project was made possible by funding from the Natural Environment Research Council (NERC)

Attracting a female can be expensive, and females may use this cost to weed out poor quality males. Male ornaments such as antlers are a reliable indicator of nurture, but what about nature? Recent research into in male ornamentation in stalk-eyed flies reveals a key role for genetics, and highlights the importance of mate choice in species survival.

Males throughout the animal kingdom go to some weird and wonderful lengths to try and attract females. This might involve an elaborate dance, a carefully wrapped gift, or an ornate head-dress, and these adverts are often costly to the male who performs them. A peacock’s tail makes him conspicuous to predators; a red deer’s antlers require food and energy to grow. And a female finds all of this very sexy, because it informs her about the quality of the male; only the highest calibre males can afford the handicap.

Stalk-Eyed Flies
This phenomenon isn’t limited to birds and mammals, of course, even flies need to attract a mate, and stalk-eyed flies have a rather odd form of ornamentation: their eyes sit on the end of long stalks that protrude out horizontally from their head. Clearly this makes their lives difficult; long eye stalks take more energy to grow, and make the males more cumbersome during flight. So why do males grow these impractical eye stalks? Because, despite the costs, males with longer stalks have more luck with the ladies.

A male Stalk-Eyed Fly (D. meigenii)
Photography by Alison Jameson

Females are thought to be attracted to males with longer stalks because they are reliable indicators of the quality of the male. Males with good genes, who grew up in plentiful environments, produce the largest ornaments and consequently get their pick of the ladies. In other words, these traits are strongly dependent on environmental conditions (e.g. food availability, temperature) and genetics. Or so the theory goes. There is good evidence that the appearance of male sexual traits is influenced by the environment in which the male grew up, but few empirical tests have been conducted to see whether ornaments also reflect genetic quality. And until recently, we had little idea of what impact this might have at the population level.

Nature and Nurture
Recent research in GEE has taken a major step towards answering these questions. Bellamy and colleagues conducted a long-term inbreeding experiment with the African stalk-eyed fly (Diasemopsis meigenii) to investigate how eye stalk length is influenced by genetic stress. Inbreeding is known to be harmful to populations, causing inbreeding depression by increasing the frequency of rare and damaging mutations, and thereby reduce the fitness of individuals. If long eye stalks are a sign of high genetic quality, then we would expect inbreeding to reduce the size of eye stalks over time. And this is just what 11 generations of mating with siblings: eye span decreased significantly during the experiment, more so than other traits such as wing size, which are not considered sexy. Thus, male traits important for attracting a female are more sensitive to genetic quality than non-sexy traits, supporting previous theory about why females are attracted to these traits in the first place.

Surviving the Genetic Storm
One rather unexpected result, however, was that male eye span at the start of the experiment was also a strong predictor of whether the line went extinct or not before the end of the experiment. Less than half the original lines survived the entire 11-generation experiment, and those who did survive were descended from males with longer eye-stalks. This again supports the idea that male eye span in stalk-eyed flies is linked closely to genetic quality; males with long eye stalks carried fewer deleterious mutations when the experiment began and so were more robust against inbreeding depression and less likely to go extinct. This result may have intriguing implications for conservation and for population dynamics in general. It shows that individual decisions such as mate choice may influence the fate of a whole population. Conservationists should take mate choice and sexual selection into account when designing programmes to conserve species, especially those with small or declining populations.

Original Article:

This project was made possible by funding from the Natural Environment Research Council (NERC), the Biotechnology and Biological Sciences Research Council (BBSRC) and the Engineering and Physical Sciences Research Council (EPSRC)