Archive for July, 2013

The Battle of the Sexes:
Sexually Antagonistic Genes in Small Populations

By Claire Asher, on 18 July 2013

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

Male and female Red Deer
(Cervus elaphus)

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 fruit fly,
Drosophila melanogaster

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).

Summer Science Events

By Claire Asher, on 17 July 2013

July has been an exciting month for science shows – The Royal Society Summer Exhibition ran from the 2nd to the 7th at Carlton House in London, and on Friday 5th July, Soapbox Science took to the south bank for it’s third annual event celebrating women in science.

DSC03524 DSC03626

Technology for Nature. Dr Robin Freeman (UCL, ZSL) demonstrates Mataki technology

At this year’s Royal Society Summer Exhibition, Technology for Nature, a joint project between UCL, Imperial College London, Microsoft Research and the Zoological Society of London, held a successful stall demonstrating a number of applications of technology to ecology and conservation. A particular highlight was the demo for Mataki, a new tracking technology which can detect behavioural information as well as locational information from a small tracking device attached to an animals back. This technology is being used to monitor the movement and foraging behaviour of sea birds. Professor Kate Jones and Dr Robin Freeman were amongst demonstrators during the week, talking to the public.

“We have a pressing need to better assess the behaviour, distribution and status of many species, and new technologies provide new ways to achieve this. From recording the dynamic behaviour of animals in the wild, to better assessments of distribution and diversity – within the Technology for Nature unit we’re developing and using new technological innovations to understand the natural world on which we rely.”
– Dr Robin Freeman (UCL CoMPLEX, Zoological Society of London)

Now in its 10th year, the Royal Society Summer Science Exhibition is an annual event showcasing cutting-edge research from around the UK. Each year, teams of scientists congregate in London hoping to demonstrate and communicate their science to the public, to students and fellow scientists, to policy-makers and the media. With interactive demonstrations, along with evening events and talks, the Royal Society Summer Science exhibition is a highlight of the year. This year, 24 Universities were selected to bring their scientific innovations to the exhibition, covering topics as diverse as dark matter, glacial melting, antibiotics and ecological monitoring. UCL’s Technology for Nature, in collaboration with Imperial College, ZSL and Microsoft Research, demonstrated three of their innovative projects aiming to apply technological advances to ecological problems.


One of the highlights of the Technology for Nature stand was the Mataki demonstration, that had members of the public step into the shoes (wings?) of seabirds to test out the revolutionary technology that can not only track animals, but also monitor behaviour. The small, light weight, economical tracking device produces data that enables different types of flight and foraging behaviour to be identified.

Robin Freeman, a research fellow in UCL’s CoMPLEX and head of the Indicators and Assessments unit at ZSL, helped develop the technology: “The Mataki platform provides an open, low-cost tool that researchers can use to record animal movement and behaviour in the wild. By providing a powerful tracking technology in a small, low-cost package, I hope that more researchers are able to gather the rich data that we need to understand the changing behaviour of animals in the wild.”

DSC03624 DSC03515

Professor Kate Jones (UCL, ZSL) and Dr Robin Freeman (UCL, ZSL) engage with the public to demonstrate Technology for Nature

Professor Kate Jones, from UCL’s Center for Biodiversity and Environment Research, has been working on a number of projects aimed at improving the ease of detecting and identifying bats, and utilising crowd-sourcing as a means to tackle large data sets generated by such technology.

“Developing easily accessible tools with which to identify wild species is critical to engage more people with the natural world and to monitor any changes. Imagine a world where you could hold up your smartphone when you hear a bird call and it would identify the species – like a Shazam app for biodiversity. We are still a way from that point yet but we are progressing with such tools for bats where the first stage is to develop an online tool that can identify bat echolocation calls. We are now developing that into a smartphone application”
– Professor Kate Jones (UCL CBER)

Find out more about the Technology for Nature project.

Soapbox Science


Julie Dunne (Bristol University)
talking about the history of dairy

As the long awaited summer finally arrived in London, so did 12 of the UK’s top female scientists, ready to communicate their science to the public in one of London’s most unusual science events – Soapbox science. Here, scientists are challenged to enthuse, entertain and educate a diverse audience about their research, without the aid of powerpoint slides and scientific jargon. Armed with nothing more than a few props, a Soapbox and a lot of enthusiasm, this years inspiring female scientists were challenged to explain their research to the public.

Soapbox science is a collaboration between the Zoological society of London and L’Oréal-UNESCO For Women in Science, which aims to highlight the struggles faced by women pursuing a career in science and challenge the public’s view of women in science. Soapbox science was created by Dr Seirian Sumner and Dr Nathalie Pettorelli, hoping to inspire a new generation of female scientists.


Professor Laura Piddock talks about antibiotic resistance, and Dr Emily Cross demonstrates how the human brain perceives complex movement.

Co-organiser, Dr Nathalie Pettorelli (Zoological Society of London) says: “Now in its fourth year, Soapbox Science is a platform to showcase the most eminent female scientists in the UK, and to highlight some very serious issues that we have witnessed as mid-career scientists: the disappearance of our female peers”. Dr Seirian Sumner (Bristol University) adds “Through events like Soapbox Science and our Campaign for Change, we want to actively bring women of all career stages together and promote that women can have a career in science”.

This year’s Soapbox scientists covered topics ranging from gut bacteria to the neuroscience of dance, from computing to antibiotics. Find out more about Soapbox Science

DSC03617 DSC03552

Soapbox Science in Gabriels Wharf. Dr Zoe Schnepp (University of Birmingham) explains superconducting seaweed and green nanotechnology.

Go with your Gut:
How Gut Bacteria Influence Health and Ageing

By Claire Asher, on 9 July 2013

Inside the human gut is a thriving community of bacteria, many of which provide nutrients in exchange for a safe place to live. But they are not merely passive inhabitants – these microbes can also impact upon our metabolism. GEE researchers in the Institute of Healthy Ageing have been investigating how gut bacteria interact with medicinal drugs to influence lifespan and health.

The Nematode Worm,
Caenorhabditis elegans

There are 100 trillion microorganisms inhabiting the human gut – outnumbering human cells ten to one. These microorganisms are generally harmless, and in fact many are beneficial, forming a symbiotic relationship with their host. Occasionally, this relationship is less friendly, however, and gut bacteria can sometimes cause illness. Whether beneficial or harmful, gut bacteria can alter metabolic processes and chemical signalling pathways in the host, and recent research by Filipe Cabreiro, Catherine Au, David Gems and colleagues suggests gut microorganisms may interact with medicines to effect health and ageing.

Metformin: Beneficial Side Effects in Diabetes Treatment
A drug called Metformin is the most commonly prescribed treatment for type 2 diabetes, but it has long been noted that Metformin has some positive effects beyond those it is prescribed for, including reducing the risk of cancer. Metformin has also been found to slow the ageing process in rats and the nematode worm, Caenorhabditis elegans. This is partly mediated through Metformin’s effect on an enzyme, AMP-activated protein kinase (AMPK), which is important in influencing several key signalling pathways which have a knock-on effect on the ageing process. However, this is not the whole story – in nematodes Metformin also influences health and ageing through an interaction with microbes in the gut.

The Bacterium, Esterichia coli

Using a combination of techniques, including liquid-chromatograph mass spectrometry (LCMC) to visualise folate composition, and mutant E.coli strains and nematode worms lacking key metabolic cycles, Cabriero et al showed that E.coli are a critical aspect of the anti-aging properties of Metformin. The nematode, C.elegans, usually feeds on E.coli, but some of their microbial diet manages to avoid digestion and stick around in the nematode’s gut. Although the microbes aren’t really welcome there, and ultimately contribute to the worm’s death, they inadvertently have some beneficial effects during their stay. Worms reared on an E.coli-free diet do not show the usual positive effects of Metformin – in fact, without E.coli, metformin is toxic to the nematode. The researchers were able to track this bacteria-drug interaction to the B-vitamin, folate. Metformin substantially altered the folate content of E.coli, and when the researchers created a mutant strain of E.coli that lacked the ability to metabolise folate, nematode hosts experienced the same toxic effects were seen as when nematodes lacked the gut-bacteria entirely.

Interactions Between Host and Guest
So, metformin alters the folate cycle in the gut bacteria of nematode worms, and this in turn influences ageing in the worm. But how? There were no changes in the folate levels of the nematode worms treated with Metformin, indicating there must be another step in the process. This step appears to be mediated by methionine, an amino acid which is an important part of the nematode’s diet, obtained almost entirely from its gut bacteria. Metformin, by altering the folate cycle, reduces methionine production in E.coli, and this seems to be responsible for the anti-ageing effects on the worm host.

Metformin, Dietary Restriction and Ageing
Metformin, in interaction with the gut-bacteria, seems to mimic the effects of dietary restriction – the well-documented but still relatively poorly understood phenomenon by which reducing food intake increases lifespan. Anti-aging effects of dietary restriction have now been documented in rats, worms, and monkeys, and some people have even made the decision to reduce their food intake in the hopes that it will extend their lives. Research into the mechanisms by which dietary restriction is able to increase lifespan is on-going, and is a major focus of research in UCL’s Institute of Healthy Ageing. It is currently thought that dietary protein (and amino acids) may be important in controlling the effects of dietary restriction on ageing, and several chemical signaling pathways, including those regulated by AMPK, have been implicated in this process.

Thus, the anti-ageing properties of Metformin appear to be two-fold. By activating AMPK, Metformin may mediate life extension through its influences on key signalling pathways, essentially mimicking dietary restriction. Secondly, Metformin alters folate metabolism in microbial symbionts, reducing methionine production and again mimicking a restricted diet. Importantly, in the absence of the gut microbes, the drug showed strongly toxic effects, indicating that in some way, E.coli is able to ameliorate the drug’s toxicity. The effect of the drug Metformin is the result of a complex interplay between both toxic and beneficial effects on the host and the gut microbiota. Finally, all of this appears to interact with the diet of the nematode – feeding nematodes on a high-sugar diet eliminated the positive effects of Metformin.

Our gut bacteria are not passive hitch-hikers, but instead interact with our metabolic processes and dietary intake in complex ways. The effects of medicine can be strongly dependent upon our gut microbiome, and understanding this may help us to understand why the same drugs have different effects on different people. Drugs chosen for one beneficial effect may also have other, unintended effects (both positive and negative), but the extent and type of these may be heavily dependent upon our diet and gut bacteria. By viewing our bodies as a complex ecosystem of human cells interacting with a large and varied microbial population, we can gain greater insights into the workings of our bodies, and how to improve our health and lifespan.

Original Article:

() Cell 153: 228 – 239

This research was made possible by funding from the Wellcome Trust, The European Union and the Medical Research Council.

The Dynamics of Population Declines

By Claire Asher, on 2 July 2013

Widespread declines in wildlife populations are a major concern, but global and regional targets to reduce the rate of biodiversity loss have so far not been met. Conservation practitioners are faced with an increasingly difficult task of balancing limited funding against increasing human pressures on wild populations. Methods for identifying detrimental human activities, identifying and classifying declines and prioritising species for conservation interventions are critical to ensure conservation efforts are invested wisely over the coming decades. Researchers at the Institute of Zoology (IOZ), Imperial College London and GEE have been working towards developing innovative methods for identifying pressures and determining conservation priorities in wild mammal populations.

Theoretical work suggests that different human pressures may result in different types of population decline, leaving a fingerprint of anthropogenic stress on the history of a population. Human activity might cause a constant pressure, or one that changes in proportion to the abundance of a species. Pressures may become more extreme as populations become smaller, for example when the value of a species to hunters increases as it becomes rarer. By contrast, a constant hunting effort would create a declining pressure over time, as individuals become increasingly difficult to find. Previous work by CBER’s Georgina Mace has suggested that the shape of the population decline curve observed may be characteristic of certain types of human pressure. A recent paper in Ecology and Evolution by IOZ’s Martina Di Fonzo, and Ben Collen and Georgina Mace from GEE, uses computer simulations and long-term monitoring data from nearly 60 species of mammal worldwide to test these theoretical predictions.

Different Population Decline Curve Shapes for Different Types of Human Pressure

Different Population Decline
Curve Shapes for Different Types
of Human Pressure

Taking a number of biological traits into account, such as life-history speed (e.g. generation time) and the carrying capacity of the environment, Di Fonzo, Collen and Mace (2013) simulated population size trends under a number of different types of human pressure. They looked at threats that are constant, increase or decrease in intensity as the population declines, and threats that act in proportion to the population size or that remain fixed as population size changes. They then statistically characterised the shape of the resulting curves using three different statistical models (linear, exponential, quadratic) and different curve shapes (concave or convex). This produced mixed results. Some types of pressure consistently produced the same type of decline curve regardless of the biological and environmental characteristics of the population, but others were more strongly influenced by generation length and habitat carrying capacity. This makes sense, since populations with a short generation time are likely to be better able to cope with and recover from human pressure. For most types of pressure, however, some tell-tale signs were usually identifiable. For example, pressures that are proportional to population size and increase over time tended to produce convex declines, whilst proportional pressure that decreases over time is more likely to produce a concave curve.

From Simulation to the Wild
That’s all very well and good, but how well does the simulated data match up to real-world wildlife populations? Using data from the Living Planet Index, the authors attempted to characterise the shape of real population declines and compared the model predictions with data about real human pressures impacting on these populations. Across 124 populations for 57 different species of mammal, they found that populations were most commonly experiencing concave declines, suggesting human pressures that are in proportion to population size, but decrease in intensity over time. There was some association between curve-shape and the actual sources of pressure, with exponential concave declines being associated with habitats suffering from exploitation, habitat loss, invasive species and pollution, and quadratic convex declines being more characteristic of disease-affected populations. However, most populations were subject to multiple human-pressures simultaneously, which may have partly obscured the relationship predicted by theory.

Population decline curves may not enable us to identify specifically which threats are affecting a population, however they can reveal important details of how those pressures are changing over time. The International Union for the Conservation of Nature (IUCN) Red list attempts to categorise species’ conservation status. Currently, the Red List includes population size decline when assessing conservation status, however this does not take into account whether those declines are accelerating or decelerating over time. Incorporating information about the shape of the decline curve can provide important insights for conservation – species experiencing accelerating declines may be prioritised when determining how to use limited funding. Population-level data can highlight the impact of human activities more rapidly than studying species-level information, as populations are likely to show more rapid responses to human change, and may act as an early warning of longer-term species decline.

The dynamics of real populations are complex, and species’ biological traits in combination with multiple human pressures acting on a population simultaneously can mean that reality does not always match perfectly with theory. However, studying the shape of population declines can reveal characteristics of the pressure being exerted on the population, may provide an early-warning system for species-level declines, and can be used to inform conservation priorities. This relatively simple method for assessing the type of decline a population is experiencing can provide valuable information to conservationists about which types of pressures are most influential, and how to act to prevent extinction.

Original Article:

() Ecology and Evolution

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