̽��ֱ�� of Cambridge - genes

Study suggests embryos could be susceptible to coronavirus as early as second week of pregnancy

cjb250 — Tue, 04 Aug 2020 23:22:16 +0000

̽��ֱ��researchers say this could mean embryos are susceptible to COVID-19 if the mother gets sick, potentially affecting the chances of a successful pregnancy.

While initially recognised as causing respiratory disease, the SARS-CoV-2 virus, which causes COVID-19 disease, also affects many other organs. Advanced age and obesity are risk factors for complications but questions concerning the potential effects on fetal health and successful pregnancy for those infected with SARS-CoV-2 remain largely unanswered.

To examine the risks, a team of researchers used technology developed by Professor Magdalena Zernicka-Goetz at the ̽��ֱ�� of Cambridge to culture human embryos through the stage they normally implant in the body of the mother to look at the activity – or ‘expression’ – of key genes in the embryo. Their findings are published today in the Royal Society’s journal Open Biology.

On the surface of the SARS-CoV-2 virus are large ‘spike’ proteins. Spike proteins bind to ACE2, a protein receptor found on the surface of cells in our body. Both the spike protein and ACE2 are then cleaved, allowing genetic material from the virus to enter the host cell. ̽��ֱ��virus manipulates the host cell’s machinery to allow the virus to replicate and spread.

̽��ֱ��researchers found patterns of expression of the genes ACE2, which provide the genetic code for the SARS-CoV-2 receptor, and TMPRSS2, which provides the code for a molecule that cleaves both the viral spike protein and the ACE2 receptor, allowing infection to occur. These genes were expressed during key stages of the embryo’s development, and in parts of the embryo that go on to develop into tissues that interact with the maternal blood supply for nutrient exchange. Gene expression requires that the DNA code is first copied into an RNA message, which then directs the synthesis of the encoded protein. ̽��ֱ��study reports the finding of the RNA messengers.

Professor Magdalena Zernicka-Goetz, who holds positions at both the ̽��ֱ�� of Cambridge and Caltech, said: “Our work suggests that the human embryo could be susceptible to COVID-19 as early as the second week of pregnancy if the mother gets sick.

“To know whether this really could happen, it now becomes very important to know whether the ACE2 and TMPRSS2 proteins are made and become correctly positioned at cell surfaces. If these next steps are also taking place, it is possible that the virus could be transmitted from the mother and infect the embryo’s cells.”

Professor David Glover, also from Cambridge and Caltech, added: “Genes encoding proteins that make cells susceptible to infection by this novel coronavirus become expressed very early on in the embryo’s development. This is an important stage when the embryo attaches to the mother’s womb and undertakes a major remodelling of all of its tissues and for the first time starts to grow. COVID-19 could affect the ability of the embryo to properly implant into the womb or could have implications for future fetal health.”

̽��ֱ��team say that further research is required using stem cell models and in non-human primates to better understand the risk. However, they say their findings emphasise the importance for women planning for a family to try to reduce their risk of infection.

“We don’t want women to be unduly worried by these findings, but they do reinforce the importance of doing everything they can to minimise their risk of infection,” said Bailey Weatherbee, a PhD student at the ̽��ֱ�� of Cambridge.

Reference
Weatherbee, BAT, et al. Expression of SARS-CoV-2 receptor ACE2 and the protease TMPRSS2 suggests susceptibility of the human embryo in the first trimester. Open Biology; 5 Aug 2020; DOI: 10.1098/rsob.200162

Image
Image of a human embryo cultured in vitro through the implantation stages and stained to reveal OCT4 transcription factor, magenta; GATA6 transcription factor, white; F-actin, green; and DNA, blue. Analysis of patterns of gene expression in such embryos reveals that ACE2, the receptor for the SARS-CoV-2 virus, and the TMPRSS2 protease that facilitates viral infection are expressed in these embryos, which represent the very early stages of pregnancy. (Credit: Zernicka-Goetz Lab)

Genes that are thought to play a role in how the SARS-CoV-2 virus infects our cells have been found to be active in embryos as early as during the second week of pregnancy, say scientists at the ̽��ֱ�� of Cambridge and the California Institute of Technology (Caltech).

COVID-19 could affect the ability of the embryo to properly implant into the womb or could have implications for future fetal health

David Glover

Zernicka-Goetz Lab

human embryo cultured in vitro

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Genetic variants for autism linked to higher rates of self-harm and childhood maltreatment

cjb250 — Tue, 29 Oct 2019 01:03:43 +0000

Previous studies by the Cambridge team established that autistic individuals experience higher levels of self-harm, including suicidal thoughts and feelings, and higher rates of childhood maltreatment. This new study shows that the findings hold true even for those with a higher genetic likelihood of autism rather than a formal diagnosis.

̽��ֱ��team calculated the genetic likelihood for autism in 100,000 individuals from the UK Biobank Study who had their DNA analysed and who had also provided self-reported information about childhood maltreatment, suicidal ideation, and self-harm. They found that individuals with higher number of genetic variants associated with autism are more likely to report childhood maltreatment, self-harm and suicidal ideation. Those with the highest genetic predisposition to autism on average have a 28% increase in childhood maltreatment, and a 33% increase in self-harm and suicidal ideation, compared to those with the lowest genetic predisposition to autism.

Dr Varun Warrier, who led the study, said: “While we have found an association between a genetic likelihood for autism and adverse life events, we cannot conclude the former causes the latter. We suspect this association reflects that genes partly influence how many autistic traits you have, and some autistic traits such as difficulties in social understanding may lead to a person to be vulnerable to maltreatment. This research highlights the risks of such adverse outcomes for those with a high number of autistic traits, if adequate safe-guarding and support aren’t provided.”

Professor Simon Baron-Cohen, Director of the Autism Research Centre at Cambridge, said: “This new study extends our earlier work by showing that individuals who carry more of the genes associated with autism have higher risks for maltreatment and self-harm. Our work highlighting unacceptably high rates of suicide in autistic people was published 5 years ago, yet almost no new support has been provided. Governments need to provide far greater support for autistic individuals and for those with a high number of autistic traits.”

He added: “Autistic individuals may need a variety of interventions – there’s no ‘one size fits all’ – and these may include an individual support worker, a mentor, opportunities to build social and communication skills and self confidence through activities that the person enjoys, peer support groups, and supported employment schemes. Schools may also need to increase safe-guarding given the risks of victimisation.”

This study was supported by the Autism Research Trust, the Medical Research Council, Wellcome, and the Templeton World Charity Foundation., Inc. It was conducted in association with the NIHR CLAHRC for Cambridgeshire and Peterborough NHS Foundation Trust, and the NIHR Cambridge Biomedical Research Centre.

Reference
Warrier, V and Baron-Cohen, S. Childhood trauma, life-time self-harm, and suicidal behaviour and ideation are associated with polygenic scores for autism. Molecular Psychiatry; 29 Oct 2019; DOI: 10.1038/s41380-019-0550-x

People with a higher genetic likelihood of autism are more likely to report higher childhood maltreatment, self-harm and suicidal thoughts according to a new study by researchers at the ̽��ֱ�� of Cambridge. A better understanding of these issues is critical to improving wellbeing in autistic people. ̽��ֱ��results are published today in Molecular Psychiatry.

Our work highlighting unacceptably high rates of suicide in autistic people was published 5 years ago, yet almost no new support has been provided. Governments need to provide far greater support for autistic individuals and for those with a high number of autistic traits

Simon Baron Cohen

Sasha Freemind

Man standing in front of window

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Family history and location of genetic fault affect risk for carriers of key breast and ovarian cancer genes

cjb250 — Tue, 20 Jun 2017 15:00:31 +0000

Cancer is caused by a combination of inherited genetic faults and environmental factors. While many hundreds of genetic mutations each increase an individual’s risk by a small amount, faults in two particular genes – BRCA1 and BRCA2 – are known to greatly elevate the risk of breast and ovarian cancers.

̽��ֱ��clinical management of women with faults in the BRCA1 and BRCA2 genes requires accurate estimates of their risk of developing breast cancer and how this changes with age. These can be used to estimate how prevention strategies such as medication, surgery and changing lifestyle factors reduce a woman’s risk, and can assist with decisions about the age to commence cancer screening, hence enabling better-informed decision-making.

Almost all previous reports on cancer risks for BRCA1 and BRCA2 mutation carriers have been based on ‘retrospective’ studies – looking at women who had already developed cancer – and estimates are therefore susceptible to biases associated with such study designs, for example inaccuracies in family history reporting and assessment in women born many decades previously (when breast cancer incidence was much lower) that are not relevant to today’s women.

Prospective cohort studies, in which scientists recruit and follow over time carriers of the mutations who have not yet developed breast cancer, overcome these issues. But the prospective studies of women with the BRCA1 and BRCA2 genes published to date have been very small, with the largest based on just 64 incident breast cancers.

Now, in a study published in JAMA: ̽��ֱ��Journal of the American Medical Association, an international team of researchers led by the ̽��ֱ�� of Cambridge, UK, has recruited almost 10,000 mutation carriers for a prospective cohort study. This enabled the team to estimate more precisely the breast and ovarian cancer risks for women with faults in BRCA1 and BRCA2.

“We have been able to provide the most precise estimates of age-specific risks to date,” says the study’s lead author, Dr Antonis Antoniou from the Department of Public Health and Primary Care at the ̽��ֱ�� of Cambridge. “These should provide more confidence in the counselling and clinical management of women with faults in the BRCA1 and BRCA2 genes.”

̽��ֱ��researchers found that 72% of women carrying a faulty BRCA1 gene will develop breast cancer risk and 44% will develop ovarian cancer by age 80. Similarly, they found that 69% of women carrying a faulty BRCA2 gene will develop breast cancer and 17% will develop ovarian cancer by age 80. However, for both cancers, a woman’s family history affected the risk – in other words, if a woman’s relative had had a breast cancer diagnosis, then her own risk would be higher than that of a carrier with no family history.

̽��ֱ��researchers also found that the position of the specific fault within the gene affected the cancer risk. Mutations in genes occur when the ‘letters’ of DNA – A, C, G and T – get ‘mistyped’ and replaced with a different letter.

“ ̽��ֱ��results show clearly and for the first time in a prospective study, that the cancer risks for women with faults in BRCA1 and BRCA2 depend both on the precise mutation and the woman’s family cancer history,” says Professor Douglas Easton, also from Cambridge and principal investigator of the UK-based EMBRACE study, the largest national cohort of women with mutations that contributed to the study.

Advances in sequencing technologies have opened up the potential of screening all women for BRCA1 and BRCA2 mutations, rather than just those with a significant family history of cancer, as is currently the case in the UK and most other countries. Such population-based screening, however, depends on having reliable estimates of risk to provide to women with and without a family history.

“Now that we understand more clearly the risks faced by women who carry these genetic faults, we should be in a better position to counsel them about the outcomes from screening and prevention programmes,” says Professor Gareth Evans, Consultant in Medical Genetics and co-author from ̽��ֱ�� of Manchester.

“This will also have practical implications on clinical management decisions, for example on the timing of surgery in order to reduce cancer risk. Such decisions tend to be taken around childbearing age, but some women with lower risks may opt to delay surgery until they complete their families.”

̽��ֱ��cancer risk estimates obtained by the present study were made possible because of over two decades of investment from Cancer Research UK, the European Union and other funders in establishing and following the cohorts.

Professor Arnie Purushotham, Cancer Research UK’s senior clinical adviser, said: “Women who carry faulty BRCA genes are much more likely to develop breast or ovarian cancers, and this large study could help women and their doctors better understand their risk of developing these cancers.

“This information – combining family medical history and the specific position of the faults in the BRCA genes – could help women decide the steps that they may want to take to reduce their risk of breast cancer, such as preventative surgery, medication or lifestyle changes.”

Reference
Kuchenbaecker, KB et al. Risks of Breast, Ovarian, and Contralateral Breast Cancer for BRCA1 and BRCA2 Mutation Carriers. JAMA; 20 June 2017; DOI: 10.1001/jama.2017.7112

A large scale study of women carrying faults in important cancer genes should enable doctors to provide better advice and counselling for treatments and lifestyle changes aimed at reducing this risk.

̽��ֱ��results show clearly... that the cancer risks for women with faults in BRCA1 and BRCA2 depend both on the precise mutation and the woman’s family cancer history

Doug Easton

MIKI Yoshihito

DNA

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Genes influence ability to read a person’s mind from their eyes

cjb250 — Wed, 07 Jun 2017 10:59:54 +0000

Twenty years ago, a team of scientists at the ̽��ֱ�� of Cambridge developed a test of ‘cognitive empathy’ called the ‘Reading the Mind in the Eyes’ Test (or the Eyes Test, for short). This revealed that people can rapidly interpret what another person is thinking or feeling from looking at their eyes alone. It also showed that some of us are better at this than others, and that women on average score better on this test than men.

Now, the same team, working with the genetics company 23andMe along with scientists from France, Australia and the Netherlands, report results from a new study of performance on this test in 89,000 people across the world. ̽��ֱ��majority of these were 23andMe customers who consented to participate in research. ̽��ֱ��results confirmed that women on average do indeed score better on this test.

More importantly, the team confirmed that our genes influence performance on the Eyes Test, and went further to identify genetic variants on chromosome 3 in women that are associated with their ability to “read the mind in the eyes”.

̽��ֱ��study was led by Varun Warrier, a Cambridge PhD student, and Professors Simon Baron-Cohen, Director of the Autism Research Centre at the ̽��ֱ�� of Cambridge, and Thomas Bourgeron, of the ̽��ֱ�� Paris Diderot and the Institut Pasteur.

Interestingly, performance on the Eyes Test in males was not associated with genes in this particular region of chromosome 3. ̽��ֱ��team also found the same pattern of results in an independent cohort of almost 1,500 people who were part of the Brisbane Longitudinal Twin Study, suggesting the genetic association in females is a reliable finding.

̽��ֱ��closest genes in this tiny stretch of chromosome 3 include LRRN1 (Leucine Rich Neuronal 1) which is highly active in a part of the human brain called the striatum, and which has been shown using brain scanning to play a role in cognitive empathy. Consistent with this, genetic variants that contribute to higher scores on the Eyes Test also increase the volume of the striatum in humans, a finding that needs to be investigated further.

Previous studies have found that people with autism and anorexia tend to score lower on the Eyes Test. ̽��ֱ��team found that genetic variants that contribute to higher scores on the Eyes Test also increase the risk for anorexia, but not autism. They speculate that this may be because autism involves both social and non-social traits, and this test only measures a social trait.

Varun Warrier says: “This is the largest ever study of this test of cognitive empathy in the world. This is also the first study to attempt to correlate performance on this test with variation in the human genome. This is an important step forward for the field of social neuroscience and adds one more piece to the puzzle of what may cause variation in cognitive empathy.”

Professor Bourgeron adds: “This new study demonstrates that empathy is partly genetic, but we should not lose sight of other important social factors such as early upbringing and postnatal experience.”

Professor Baron-Cohen says: “We are excited by this new discovery, and are now testing if the results replicate, and exploring precisely what these genetic variants do in the brain, to give rise to individual differences in cognitive empathy. This new study takes us one step closer in understanding such variation in the population.”

Reference
Warrier, V et al. Genome-wide meta-analysis of cognitive empathy: heritability, and correlates with sex, neuropsychiatric conditions and cognition. Molecular Psychiatry; 6 June 2017; DOI: 10.1038/MP.2017.122

Our DNA influences our ability to read a person’s thoughts and emotions from looking at their eyes, suggests a new study published in the journal Molecular Psychiatry.

This is the first study to attempt to correlate performance on the Eye Test with variation in the human genome

Varun Warrier

Dboybaker

Eyes

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Study identifies hundreds of genes that influence timing of puberty and alter risk of several cancers

cjb250 — Mon, 24 Apr 2017 15:15:26 +0000

̽��ֱ��study, published today in Nature Genetics and led by researchers from the Medical Research Council (MRC) Epidemiology Unit at the ̽��ֱ�� of Cambridge and other scientists in the international ReproGen consortium, also found new genetic evidence linking earlier timing of puberty to higher risk of several cancers known to be sensitive to sex-hormones in later life, including breast, ovary and endometrial cancers in women, and prostate cancer in men. These influences remained after controlling for body weight, which is important as body weight itself influences both the timing of puberty and the risk of some cancers.

Dr John Perry, Senior Investigator Scientist from the MRC Epidemiology Unit and senior author on the paper, says: "Previous studies suggested that the timing of puberty in childhood was associated with risks of disease decades later, but until now it was unclear if those were circumstantial observations, for example secondary to other factors such as body weight.

“Our current study identifies direct causal links between earlier puberty timing itself and increased cancer risk. This link could possibly be explained by higher levels of sex hormones throughout life, but we need to do more work to understand the exact mechanisms involved. We aim to understand these disease links and thereby contribute to the prevention of diseases in later life."

̽��ֱ��timing of puberty varies widely between individuals but tends to run closely within families. Earlier puberty timing may have advantages for some adolescents, for example for boys who engage actively in sports, but it appears to have largely negative effects on later health, such as higher risks of heart disease and some cancers.

By performing detailed assessments of genetic variants across the whole genome in 329,345 women, comprising data from 40 studies in the ReproGen consortium, UK Biobank, and consented 23andMe customers, this study identified 389 independent genetic signals for age at puberty in women. This observation was then confirmed in a further 39,543 women from the deCODE study, Iceland. Many of these genetic associations were also found to influence age at voice breaking, a comparable measure of puberty timing in men.

These findings shed light on the mechanisms that regulate puberty timing. Dr Perry adds: "These newly identified genetic factors explain one quarter of the estimated heritability of puberty timing. Our findings highlight the remarkable biological complexity of puberty timing, with likely thousands of genetic factors, in combination with numerous environmental triggers, acting together to control the timing of this key transition from childhood to adult life.”

Dr Ken Ong, also from the MRC Epidemiology Unit and joint senior author on the paper, says: "One of the more remarkable findings concerns the role of certain types of genes called imprinted genes, which are only active in your body when inherited specifically from one parent but not the other. We identified rare variants in two genes, which both lower the age of puberty when inherited from your father, but have no effect when inherited from your mother. This is intriguing as it suggests that mothers and fathers might benefit differently from puberty occurring at earlier or later ages in their children."

Reference
Felix R. Day, Deborah J. Thompson, Hannes Helgason et al. Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk. Nature Genetics; 24 April 2017; DOI: 10.1038/ng.3841

̽��ֱ��largest genomic analysis of puberty timing in men and women conducted to date has identified 389 genetic signals associated with puberty timing, four times the number that were previously known.

Our findings highlight the remarkable biological complexity of puberty timing, with likely thousands of genetic factors, in combination with numerous environmental triggers, acting together to control the timing of this key transition from childhood to adult life

John Perry

Jon Bunting

girl in the poppies

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‘Red gene’ in birds and turtles suggests dinosaurs had bird-like colour vision

fpjl2 — Wed, 03 Aug 2016 08:35:11 +0000

Earlier this year, scientists used zebra finches to pinpoint the gene that enables birds to produce and display the colour red.

Now, a new study shows the same ‘red gene’ is also found in turtles, which share an ancient common ancestor with birds. Both share a common ancestor with dinosaurs.

̽��ֱ��gene, called CYP2J19, allows birds and turtles to convert the yellow pigments in their diets into red, which they then use to heighten colour vision in the red spectrum through droplets of red oil in their retinas.

Birds and turtles are the only existing tetrapods, or land vertebrates, to have these red retinal oil droplets. In some birds and a few turtle species, red pigment produced by the gene is also used for external display: red beaks and feathers, or the red neck patches and rims of shells seen in species such as the painted turtle.

̽��ֱ��scientists mined the genetic data of various bird and reptile species to reconstruct an evolutionary history of the CYP2J19 gene, and found that it dated back hundreds of millions of years in the ancient archelosaur genetic line - the ancestral lineage of turtles, birds and dinosaurs.

̽��ֱ��findings, published today in the journal Proceedings of the Royal Society B, provide evidence that the ‘red gene’ originated around 250 million years ago, predating the split of the turtle lineage from the archosaur line, and runs right the way through turtle and bird evolution.

Scientists say that, as dinosaurs split from this lineage after turtles, and were closely related to birds, this strongly suggests that they would have carried the CYP2J19 gene, and had the enhanced ‘red vision’ from the red retinal oil.

This may have even resulted in some dinosaurs producing bright red pigment for display purposes as well as colour vision, as seen in some birds and turtles today, although researchers say this is more speculative.

“These findings are evidence that the red gene originated in the archelosaur lineage to produce red for colour vision, and was much later independently deployed in both birds and turtles to be displayed in the red feathers and shells of some species, going from seeing red to being red,” says senior author Dr Nick Mundy, from the ̽��ֱ�� of Cambridge’s Department of Zoology.

“This external redness was often sexually selected as an ‘honest signal’ of genuine high quality in a mate,” he says.

̽��ֱ��previous research in zebra finches showed a possible link between red beaks and the ability to break down toxins in the body, suggesting external redness signals physiological quality, and there is some evidence that colouration in red-eared terrapins is also linked to honest signalling.

“ ̽��ֱ��excellent red spectrum vision provided by the CYP2J19 gene would help female birds and turtles pick the brightest red males,” says Hanlu Twyman, the PhD student who is lead author on the work.

̽��ֱ��structure of retinas in the eye includes cone-shaped photoreceptor cells. Unlike mammals, avian and turtle retinal cones contain a range of brightly-coloured oil droplets, including green, yellow and red.

These oil droplets function in a similar way to filters on a camera lens. “By filtering the incoming light, the oil droplets lead to greater separation of the range of wavelengths that each cone responds to, creating much better colour sensitivity,” explains Mundy.

“Humans can distinguish between some shades of red such as scarlet and crimson. However, birds and turtles can see a host of intermediate reds between these two shades, for example. Our work suggests that dinosaurs would have also had this ability to see a wide spectrum of redness,” he says.

Over hundreds of millennia of evolution, the CYP2J19 gene was independently deployed to generate the red pigments in the external displays of some bird species and a few turtle species. ̽��ֱ��scientists say their data indicate that co-option of CYP2J19 for red colouration in dinosaurs would also have been possible.

̽��ֱ��ancestral lineage that led to scaly lizards and snakes split from the archosaur line before turtles, and, as the findings suggest, before the origin of the red gene. These reptiles either lack retinal oil droplets, or have yellow and green but not red.

However, the crocodilian lineage split from the archelosaur line after turtles, yet crocodiles appear to have lost the CYP2J19 gene, and have no oil droplets of any colour in their retinal cones.

Mundy says there is some evidence that oil droplets were lost from the retinas of species that were nocturnal for long periods of their genetic past, and that this hypothesis fits for mammals and snakes, and may also be the case with crocodiles.

A gene for red colour vision that originated in the reptile lineage around 250m years ago has resulted in the bright red bird feathers and ‘painted’ turtles we see today, and may be evidence that dinosaurs could see as many shades of red as birds - and perhaps even displayed more red than we might think.

̽��ֱ��excellent red spectrum vision provided by the CYP2J19 gene would help female birds and turtles pick the brightest red males

Hanlu Twyman

Nicole Valenzuela

A Painted Turtle

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Opinion: Can genes really predict how well you’ll do academically?

Anonymous — Tue, 26 Jul 2016 10:26:13 +0000

Researchers at King’s College London say they are able to predict educational achievement from DNA alone. Using a new type of analysis called a “genome-wide polygenic score”, or GPS, they analysed DNA samples from 3,497 people in the ongoing Twins Early Development Study. They found that people whose DNA had the highest GPS score performed substantially better at school. In fact, by age 16, there was a whole school-grade difference between those with the highest GPS scores and the lowest. ̽��ֱ��researchers herald their findings as a “tipping point” in the ability to use DNA – and DNA alone – in predicting educational achievement.

These findings will certainly generate debate, particularly about nature versus nurture. It’s a debate that forces us – often uncomfortably – to think about what makes us who we are. Are our careers, hobbies, food preferences, income levels, emotional dispositions, or even general success in life rooted in our genes (nature)? Or are we shaped more by our environment (nurture)? If it’s all down to our genes, what happens to the idea of determining our own destiny?

When it comes to the subject of intelligence, which today includes behavioural genetics research into “g (a measure of intelligence commonly used as a variable in research in this area) and cognitive ability, the nature-nurture debate becomes that much more heated.

There is a growing body of research that suggests intelligence is a highly heritable and polygenic trait, meaning that there are many genes that predict intelligence, each with a small effect size. While the connection between genetics research on educational achievement and findings on intelligence might not seem direct, studies like the one out of King’s establishes a biological connection between “g” and educational achievement. ̽��ֱ��findings mark the strongest genetic prediction for educational achievement so far, estimating up to 9% of variance in educational achievement at age 16.

But despite claims that this research moves “us closer to the possibility of early intervention and personalised learning”, there are important ethical concerns to take into account. For example, who would early intervention and personalised learning reach first? Is it possible parents with money, means, awareness and access would be first to place their children in “genetically sensitive schools” in the hope of getting an extra advantage?

Dark past

It is not a secret that the history of intelligence research, and by extension genetics research on cognitive ability or educational achievement, is rooted in eugenics and racism, and has been used to validate the existence of racial and class differences. So how does this shameful past impact the field of behavioural genetics research today?

Many behavioural geneticists, like Robert Plomin, the senior author on the King’s study, believe the field has moved past this dark history and that the science is objective, neutral (as neutral as any research can be) and clear. ̽��ֱ��controversies that surround this research, at least in the eyes of Plomin and others, are fuelled by media sensationalism.

But many bioethicists and social scientists disagree with him. They argue that society values intelligence too much for this research to remain in neutral territory. Previously, the field was largely used to marginalise certain groups, particularly low-income or ethnic minority groups.

For some, attributing intelligence to genetics justifies the adverse circumstances many low-income and ethnic minority groups find themselves in; it wasn’t nurture that led to the under-performance of low-income or ethnic minority students in the classroom, it was nature, and nature cannot be changed. For bioethicists today, the question hanging over this branch of behavioural genetics is: who’s to say new research in this area won’t perpetuate the same social inequalities that similar work has done before?

Genetic research in an area once used to oppress people should openly acknowledge this past and explicitly state what its findings can and cannot prove (what many bioethicists call “trustworthy research”).

Stark class and race divides still persist in the UK and US, two countries where this branch of research is rapidly growing. While the study mentions the impact of a person’s place in society with educational achievement, it links this status back to genetics, highlighting the genetic overlap between educational achievement, g and family socioeconomic status.

̽��ֱ��possibility that this kind of research may influence attitudes towards certain ethnic minorities and the less well off is real, as is the risk that this work might be used to justify social inequality. These concerns should be admitted and addressed by behavioural geneticists. ̽��ֱ��alternative could be a new form of eugenics.

Daphne Martschenko, PhD Candidate, ̽��ֱ�� of Cambridge

This article was originally published on ̽��ֱ��Conversation. Read the original article.

̽��ֱ��opinions expressed in this article are those of the individual author(s) and do not represent the views of the ̽��ֱ�� of Cambridge.

Daphne Martschenko (Faculty of Education) discusses whether DNA can predict our educational achievement.

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Genetic switch that turned moths black also colours butterflies

tdk25 — Thu, 02 Jun 2016 04:00:22 +0000

̽��ֱ��same gene that enables tropical butterflies to mimic each other’s bright and colourful patterning also caused British moths to turn black amid the grime of the industrial revolution, researchers have found.

Writing in the journal Nature, a team of researchers led by academics at the Universities of Cambridge and Sheffield, report that a fast-evolving gene known as “cortex” appears to play a critical role in dictating the colours and patterns on butterfly wings.

A parallel paper in the same journal by researchers from the ̽��ֱ�� of Liverpool shows that this same gene also caused the peppered moth to turn black during the mid-19th century, when it evolved to find new ways to camouflage itself; a side-effect of industrial pollution at the time.

̽��ֱ��finding offers clues about how genetics plays a role in making evolution a predictable process. For reasons the researchers have yet to understand in full, the cortex gene, which helps to regulate cell division in butterflies and moths, has become a major target for natural selection acting on colour and pattern on the wings.

Chris Jiggins, Professor of Evolutionary Biology and a Fellow of St John’s College, ̽��ֱ�� of Cambridge, said: “What’s exciting is that it turns out to be the same gene in both cases. For the moths, the dark colouration developed because they were trying to hide, but the butterflies use bright colours to advertise their toxicity to predators. It raises the question that given the diversity in butterflies and moths, and the hundreds of genes involved in making a wing, why is it this one every time?”

Dr Nicola Nadeau, a NERC Research Fellow from the ̽��ֱ�� of Sheffield added: “It’s amazing that the same gene controls such a diversity of different colours and patterns in butterflies and a moth. Our study, together with the findings from the ̽��ֱ�� of Liverpool, shows that the cortex gene is important for colour and pattern evolution in this whole group of insects.”

Butterflies and moths comprise the order of insects known as Lepidoptera. Nearly all of the 160,000 types of moth and 17,000 types of butterfly have different wing patterns, which are adapted for purposes like attracting mates, giving off warnings, camouflage (also known as “crypsis”), and thermal regulation.

These wing patterns are actually made up of tiny coloured scales arranged like tiles on a roof. Although they have been studied by biologists for over a century, the molecular mechanisms which control their development are only now starting to be uncovered.

̽��ֱ��peppered moth is one of the most famous examples of evolution by natural selection. Until the 19th Century, peppered moths were predominantly pale-coloured, and used this to camouflage themselves against lichen-covered tree trunks, which made them almost invisible to predators.

During the industrial revolution, however, the lichen on trees in some parts of the country was killed by pollution, and soot turned the trunks black. A corresponding change was seen in the in peppered moths which turned black as well, helping them to remain camouflaged from birds. ̽��ֱ��process is known as industrial melanism – melanism meaning the development of dark coloured pigmentation.

̽��ֱ��Liverpool-led team found that this colour change was produced by a mutation in the cortex gene, which occurred during the mid 1800s, just before the first reported sighting of black peppered moths. Fascinatingly, however, the Cambridge-Sheffield study has now shown that exactly the same gene also influences the extremely bright and colourful patterns of Heliconius – the name given to about 40 different closely-related species of beautiful, tropical butterflies found in South America.

Heliconius colour patterns are used to send a signal to potential predators that the butterflies are toxic if eaten, and different types of Heliconius butterfly mimic one another by using their bright colours as warning signals. Unlike the dark colouring of the peppered moth, it is therefore an evolutionary development that is meant to be seen.

̽��ֱ��researchers carried out fine-scale mapping, looking for parts of the DNA sequence that were specifically different in butterflies with different patterns, in three different Heliconius species, and in each case the cortex gene was found to be responsible for this adaptation in their patterning.

Because Heliconius species are extremely diverse, the study of what causes variations in their patterning can provide more general clues about the genetic switches that control diversification in species.

In most cases, the genes responsible for these processes are known as “transcription factors” – meaning that they are responsible for turning other genes on and off. Intriguingly, what made cortex such an elusive switch to spot was the fact that it does not do this. Instead, it is a cell cycle regulator, which means that it controls when cells divide and thus when different coloured scales develop within a butterfly wing.

“It’s a different gene to the one we might have expected and we still need to do more to understand exactly what it’s doing, and how it’s doing it,” Jiggins said. Dr Nadeau added “Our results are even more surprising because the cortex gene was previously thought to only be involved in producing egg cells in female insects, and is very similar to a gene that controls cell division in everything from yeast to humans.”

Reference

Nadeau N. et al. ̽��ֱ��gene cortex controls mimicry and crypsis in butterflies and moths. Nature, 2 June 2016; DOI: 10.1038/nature17961

Additional image: ̽��ֱ��study reveals that the black colour of the moth (above) and the yellow patches on the butterfly (below) were caused by the same gene, known as “cortex”. Credits: Yikrazuul and Loz, both via Wikimedia Commons.

Heliconius butterflies have evolved bright yellow colours to deter predators, while peppered moths famously turned black to hide from birds. A new study reveals that the same gene causes both, raising fascinating questions about how evolution by natural selection occurs in these species.

It raises the question that given the diversity in butterflies and moths, and the hundreds of genes involved in making a wing, why is it this one every time?

Chris Jiggins

Chris Jiggins, ̽��ֱ�� of Cambridge

Heliconius Melpomene.

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

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