̽��ֱ�� of Cambridge - Eric Miska

10 Cambridge spinouts changing the story of cancer

skbf2 — Thu, 17 Oct 2024 12:57:43 +0000

10 Cambridge spinouts on putting their research into practice to improve outcomes for cancer patients - and why Cambridge is a great place to do this.

Cambridge researchers elected to Academy of Medical Sciences Fellowship 2023

lw355 — Thu, 18 May 2023 08:00:52 +0000

̽��ֱ��new Fellows have been elected to the Academy in recognition of their exceptional contributions to the advancement of biomedical and health science, cutting-edge research discoveries and translating developments into benefits for patients and wider society.

They join a prestigious Fellowship of 1,400 esteemed researchers who are central to the Academy’s work. This includes providing career support to the next generation of researchers and contributing to the Academy’s influential policy work to improve health in the UK and globally.

Professor Dame Anne Johnson PMedSci, President of the Academy of Medical Sciences, said: “These new Fellows are pioneering biomedical research and driving life-saving improvements in healthcare. It’s a pleasure to recognise and celebrate their exceptional talent by welcoming them to the Fellowship.

“This year, we are celebrating our 25th anniversary. ̽��ֱ��Fellowship is our greatest asset, and their broad expertise and dynamic ability has shaped the Academy to become the influential, expert voice of health. As we look to the future, the collective wisdom our new Fellows bring will be pivotal in achieving our mission to create an open and progressive research sector to improve the health of people everywhere.”

̽��ֱ��new Cambridge Fellows are:

Professor Charlotte Coles FMedSci

Professor of Breast Cancer Clinical Oncology, Department of Oncology, NIHR Research Professor and Director of Cancer Research UK RadNet Cambridge

Professor Coles leads practice-changing breast radiotherapy trials, has influenced international hypofractionation policy and is addressing global health, gender and equity challenges within the Lancet Breast Cancer Commission.

“It’s an honour to be elected as a new Fellow of the Academy of Medical Sciences. This is a result of research collaborations in Cambridge, the UK and internationally and I’d like to thank these wonderful colleagues, especially patient advocates,” said Coles.

“I hope to contribute to the Academy’s work to increase equity, diversity and inclusion within leadership roles, including lower- and middle-income countries, to enrich research and improve the culture in Medical Sciences.”

Professor Emanuele Di Angelantonio FMedSci

Professor of Clinical Epidemiology and Donor Health, Department of Public Health and Primary Care, and Head of Health Data Science Centre, Human Technopole (Milan)

Professor Di Angelantonio’s research has focused on addressing major clinical and public health priorities in cardiovascular disease (CVD) and transfusion medicine. His election recognises his many contributions both in helping resolve important controversies in CVD prevention strategies and in improving the safety and efficiency of blood donation.

“I am delighted and honoured to be elected to the Fellowship of the Academy of Medical Sciences, which I recognise is an outcome of the collaborations with many colleagues in UK and worldwide,” said Di Angelantonio.

“Research excellence across medical sciences and translation to health improvements has been at the centre of the Academy’s mission and I am very pleased to now be able to contribute to fulfilling this aim as a Fellow.”

Dr Rita Horvath FMedSci

Director of Research in Genetics of Rare Neurological Disorders in the Department of Clinical Neurosciences and Honorary Consultant in Neurology

Dr Horvath is an academic neurologist using genomics and biochemistry to diagnose rare, inherited neurological disorders, with a focus on mitochondrial diseases. Throughout her career she has combined fundamental experimental work with clinical studies. She pioneered the development and implementation of next generation sequencing in the diagnosis of rare neurogenetic diseases in the UK, leading to precision genetic approaches. She has established extensive international collaborations, having impact in Europe, but also for underserved groups in countries where such expertise is lacking.

“I am delighted and honoured to be elected to this Fellowship, which recognises the impact of my work. I would not have achieved it without the support of my excellent colleagues and research team, for which I give my sincere thanks,” said Horvath.

“As a Hungarian woman working in different countries before I arrived in the UK in 2007, I feel particularly proud of this award, which I recognise is an outcome of the open and fair research environment in Cambridge. This Fellowship enables me to further expand my research to develop effective treatments for patients with rare inherited neurological diseases.”

Professor Eric Miska FMedSci

Herchel Smith Chair of Molecular Genetics and Head of Department of Biochemistry, Affiliated Senior Group Leader at the Gurdon Institute, Associate Faculty at the Wellcome Sanger Institute and Fellow of St John’s College

Professor Miska is a molecular geneticist who has carried out pioneering work on RNA biology. His work led to fundamentally new insights into how small RNA molecules control our genes and protect organisms from selfish genes and viruses, and how RNA can carry heritable information across generations. Miska is Founder and Director of STORM Therapeutics Ltd, which creates novel therapies that inhibit RNA modifying enzymes for use in oncology and other diseases.

“Wonderful recognition of the work of an amazing team of researchers I have the pleasure to work with,” said Miska. “Most of our research has been done using the roundworm C. elegans. As Friedrich Nietzsche wrote in Thus Spoke Zarathustra: ‘You have evolved from worm to man, but much within you is still worm’.”

Professor Serena Nik-Zainal FMedSci

NIHR Research Professor, Professor of Genomic Medicine and Bioinformatics, Department of Medical Genetics and Early Cancer Institute, and Honorary Fellow of Murray Edwards College

Professor Nik-Zainal’s research is focused on investigating the vast number of mutations that occur in human DNA from birth, causing patterns called ‘mutational signatures’, and the associated physiological changes to cellular function, in progressive diseases such as cancer and neurodegeneration. She uses a combination of experimental and computational methods to understand biology and to develop clinical tests for early detection and precision diagnostics. Her team also builds computational tools to enable genomic advances become more accessible across the NHS.

“What an honour it is to be elected to the Fellowship. This is a wonderful recognition of the work from my team,” said Nik-Zainal. “We are thrilled and hugely indebted to all our inspiring collaborators, supporters and patients, who have shared in our passion and joined us on our path, exploring biomedical science and translating insights into patient benefit.”

Professor Julian Rayner FMedSci

Director of the Cambridge Institute for Medical Research, School of Clinical Medicine, Honorary Faculty at the Wellcome Sanger Institute, and Director of Wellcome Connecting Science

Professor Rayner’s research has made significant contributions to our understanding of how malaria parasites recognise and invade human red blood cells to cause disease. His work has helped to identify new vaccine targets, such as a protein essential for red blood cell invasion that is now in early stage human vaccine testing, and inform antimalarial drug development, through co-leading the first ever genome-scale functional screens in malaria parasites. He collaborates closely with researchers in malaria-endemic countries and is strongly committed to engaging public audiences with the process and outcomes of science.

“Malaria is a devastating and too often forgotten disease that still kills more than half a million children every year. Tackling it requires deep collaboration and working across disciplines. I’m enormously honoured by this announcement, which reflects not my work but the work of all the talented people I’ve been lucky enough to host in my lab, and collaborations with friends and colleagues across the world,” said Rayner.

“I’m excited to become a Fellow of the Academy of Medical Sciences because I strongly share their conviction that science is not just for scientists. I believe that dialogue, learning and public engagement are all fundamental and essential parts of the research process, and I look forward to contributing to their leading role in these areas.”

Professor James Rowe FMedSci

Professor of Cognitive Neurology, Department of Clinical Neurosciences, and MRC Cognition and Brain Sciences Unit

Professor Rowe leads a highly interdisciplinary research team at the Cambridge Centre for Frontotemporal Dementia and at Dementias Platform UK to improve the diagnosis and treatment of people affected by dementia. His work integrates cognitive neuroscience, brain imaging, fluidic biomarkers, computational models and neuropathology for experimental medicine studies and clinical trials. He is motivated by his busy clinical practice and the need for better diversity and inclusivity throughout medical research.

“I am delighted and honoured to be elected to the Fellowship of the Academy of Medical Sciences. It is a testament to the many wonderful colleagues and students I have been fortunate to work with, and to inspirational mentors,” said Rowe.

“Research excellence, and translation of research for direct human benefit, comes from innovation and collaboration in diverse cross-disciplinary teams. I believe in the vision and values of the Academy as the route to better health for all.”

In addition, two researchers from the wider community have also been elected:

Dr Trevor Lawley FMedSci, Senior Group Leader, Wellcome Sanger Institute and Chief Scientific Officer, Microbiotica

Professor Ben Lehner FRS FMedSci, Senior Group Leader, Human Genetics Programme, Wellcome Sanger Institute

Seven Cambridge ̽��ֱ�� researchers are among the 59 biomedical and health researchers elected to the Academy of Medical Sciences Fellowship.

As we look to the future, the collective wisdom our new Fellows bring will be pivotal in achieving our mission to create an open and progressive research sector to improve the health of people everywhere

Professor Dame Anne Johnson, President of the Academy of Medical Sciences

Clockwise from top left: E. Di Angelantonio, J. Rayner, J. Rowe, R. Horvath, S. Nik-Zainal, E. Miska, C. Coles

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Discovery of shape of the SARS-CoV-2 genome after infection could inform new COVID-19 treatments

jg533 — Thu, 05 Nov 2020 16:58:26 +0000

SARS-CoV-2 is one of many coronaviruses. All share the characteristic of having the largest single-stranded RNA genome in nature. This genome contains all the genetic code the virus needs to produce proteins, evade the immune system and replicate inside the human body. Much of that information is contained in the 3D structure adopted by this RNA genome when it infects cells.

̽��ֱ��researchers say most current work to find drugs and vaccines for COVID-19 is focused on targeting the proteins of the virus. Because the shape of the RNA molecule is critical to its function, targeting the RNA directly with drugs to disrupt its structure would block the lifecycle and stop the virus replicating.

In a study published today in the journal Molecular Cell, the team uncovered the entire structure of the SARS-CoV-2 genome inside the host cell, revealing a network of RNA-RNA interactions spanning very long sections of the genome. Different functional parts along the genome need to work together despite the great distance between them, and the new structural data shows how this is accomplished to enable the coronavirus life cycle and cause disease.

“ ̽��ֱ��RNA genome of coronaviruses is about three times bigger than an average viral RNA genome – it’s huge,” said lead author Dr Omer Ziv at the ̽��ֱ�� of Cambridge’s Wellcome Trust/Cancer Research UK Gurdon Institute.

He added: “Researchers previously proposed that long-distance interactions along coronavirus genomes are critical for their replication and for producing the viral proteins, but until recently we didn’t have the right tools to map these interactions in full. Now that we understand this network of connectivity, we can start designing ways to target it effectively with therapeutics.”

In all cells the genome holds the code for the production of specific proteins, which are made when a molecular machine called a ribosome runs along the RNA reading the code until a ‘stop sign’ tells it to terminate. In coronaviruses, there is a special spot where the ribosome only stops 50% of the times in front of the stop sign. In the other 50% of cases, a unique RNA shape makes the ribosome jump over the stop sign and produce additional viral proteins. By mapping this RNA structure and the long-range interactions involved, the new research uncovers the strategies by which coronaviruses produce their proteins to manipulate our cells.

“We show that interactions occur between sections of the SARS-CoV-2 RNA that are very long distances apart, and we can monitor these interactions as they occur during early SARS-CoV-2 replication,” said Dr Lyudmila Shalamova, a co-lead investigator at Justus-Liebig ̽��ֱ��, Germany.

Dr Jon Price, a postdoctoral associate at the Gurdon Institute and co-lead of this study, has developed a free, open-access interactive website hosting the entire RNA structure of SARS-CoV-2. This will enable researchers world-wide to use the new data in the development of drugs to target specific regions of the virus’s RNA genome.

̽��ֱ��genome of most human viruses is made of RNA rather than DNA. Ziv developed methods to investigate such long-range interactions across viral RNA genomes inside the host cells, in work to understand the Zika virus genome. This has proved a valuable methodological basis for understanding SARS-CoV-2.

This research is a collaborative study between the group of Professor Eric Miska at the ̽��ֱ�� of Cambridge’s Gurdon Institute and Department of Genetics, and the group of Professor Friedemann Weber from the Institute for Virology, Justus-Liebig ̽��ֱ��, Gießen, Germany. ̽��ֱ��authors are grateful for the support of the Biochemistry Department at the ̽��ֱ�� of Cambridge, who provided specialist laboratory facilities for performing part of this research.

̽��ֱ��work was funded by Cancer Research UK, Wellcome, and Deutsche Forschungsgemeinschaft (DFG).

Ziv explains the research finding in this short video:

Reference
Ziv, O. et al: ‘ ̽��ֱ��short- and long-range RNA-RNA Interactome of SARS-CoV-2.’ Mol Cell, November 2020. DOI: 10.1016/j.molcel.2020.11.004

How you can support Cambridge’s COVID-19 research

Scientists at the ̽��ֱ�� of Cambridge, in collaboration with Justus-Liebig ̽��ֱ��, Germany, have uncovered how the genome of SARS-CoV-2 - the coronavirus that causes COVID-19 - uses genome origami to infect and replicate successfully inside host cells. This could inform the development of effective drugs that target specific parts of the virus genome, in the fight against COVID-19.

Now that we understand this network of connectivity, we can start designing ways to target it effectively with therapeutics

Dr Omer Ziv

Pete Linforth on Pixabay

Coronavirus

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Discovery of RNA transfer through royal jelly could aid development of honey bee vaccines

ta385 — Thu, 02 May 2019 14:40:21 +0000

̽��ֱ��findings suggest new ways to protect bees against viruses and the deadly Varroa mite that have been responsible for the recent dramatic decline in honey bee populations. Since around one third of the human diet globally is dependent on honey bee pollination, we need solutions urgently to help maintain flourishing bee colonies, for our food security and sustainability.

Dr Eyal Maori from the Wellcome Trust/Cancer Research UK Gurdon Institute, ̽��ֱ�� of Cambridge, and his collaborators in Israel and the USA had been trialling a new type of antiviral therapy for bees when they got a hint that the bees were able to transmit biologically-active RNA molecules between colony members. ̽��ֱ��scientists today publish the evidence for such a bee-to-bee RNA transfer phenomenon in the journal Cell Reports.

These transmissible RNA molecules are produced by the honey bee’s genes and by disease agents such as viruses. Unlike other RNA in the body, these RNA molecules do not code for protein. Instead, they play a direct role in immunity, gene regulation and other biological mechanisms.

In previous studies, Maori and colleagues fed bees with RNA fragments that included a segment of an RNA virus. They found that similar to how vaccines work, the dietary RNA activated an immune response that prevented disease and death when hives were later exposed to the live virus. Intriguingly, the colony maintained a healthy performance for several months after treatment had finished, suggesting that it was still immune to infection – even though the original treated bees would have died off and been replaced by new generations. This suggested that the immunising RNA fragments were being passed among colony members as well as across generations.

In the study released today, the researchers demonstrated that dietary RNA is taken up from the ingestion system into the bee’s circulatory fluid and spread to the jelly-secreting glands. ̽��ֱ��dietary RNA is then secreted with the jelly and taken-up by larvae fed on the jelly.

While scientists have previously shown in plants and animals that movement of RNA between cells within an organism is possible, these findings identify a molecular mechanism for transmission of RNA molecules between organisms.

“We found that RNA spreads beyond individual honey bees, being transferred not just between parents and their progeny, but also among individuals in the hive,” says Maori.

Further experiments showed that transmissible RNA was able to activate a mechanism called 'RNA interference' to block the activity of some genes and reduce the production of certain honey bee proteins. Importantly, RNA interference is known to provide defence against viral infection in honey bees and other organisms. In other words, these RNA molecules are likely acting to immunise the bees against infections.

̽��ֱ��researchers next analysed the worker and royal jellies and revealed diverse types of naturally occurring RNA, some derived from bee genes and some from pathogens such as fungi and infectious viruses, suggesting that over time the bees had developed – and shared – immunity to these pathogens.

"Our findings demonstrate that bees share ‘transmissible RNA’ among members of the colony, likely as a way of sharing immunity among members and generations in the hive and to enable other bees to adapt to different environmental conditions," says Maori.

In a second study, published last month in the journal Molecular Cell, Maori, working with Professor Eric Miska's lab at the Gurdon Institute, investigated how RNA, which is an unstable molecule, is transferred through the jelly diet. They found that an abundant jelly ingredient, Major Royal Jelly Protein-3 (MRJP-3), binds the RNA to form granules that concentrate and protect it from environmental damage. This is the first identification of RNA granules with functions outside cells and organisms.

Maori added: "Honey bees have evolved a type of ‘glue’ that binds RNA into granules, making it more stable and so able to be shared with other bees. If we can harness this technology, we might be able to use it to develop new ‘vaccines’ that could be used in agricultural settings, in particular to help immunise bees against the devastating losses being suffered by their colonies.

“It is possible that this honey bee protein may even have applications, too, for new vaccines and medicines for humans.”

References:
E. Maori et al. 'A transmissible RNA pathway in honey bees.' Cell Reports; 2 May 2019; DOI: 10.1016/j.celrep.2019.04.073.
E. Maori et al. 'A secreted RNA binding protein forms RNA-stabilizing granules in the honeybee royal jelly.' Molecular Cell; 18 April 2019; DOI: 10.1016/j.molcel.2019.03.010.

Researchers have discovered that honey bees are able to share immunity with other bees and to their offspring in a hive by transmitting RNA ‘vaccines’ through royal jelly and worker jelly. ̽��ֱ��jelly is the bee equivalent of mother’s milk: a secretion used to provide nutrition to worker and queen bee larvae.

Bees share ‘transmissible RNA’ among members of the colony, likely as a way of sharing immunity

Eyal Maori

Courtesy of Cam Miller under a CC license.

Honey bee approaching a flower.

Acknowledgements

This work was supported by the Orion Foundation and the Israel Science Foundation, a Marie Curie Intra-European Fellowship for Career Development, a Leo Baeck Scholarship and a Herchel Smith Postdoctoral Fellowship a Cancer Research UK Programme Grant and a Wellcome Investigator Award; and by a core grant to The Gurdon Institute from Cancer Research UK and the Wellcome Trust.

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Studies raise questions over how epigenetic information is inherited

cjb250 — Tue, 30 Oct 2018 00:33:26 +0000

A second study, also from Cambridge, suggests, however, that one way that environmental effects are passed on may in fact be through molecules produced from the DNA known as RNA that are found in a father’s sperm.

̽��ֱ��mechanism by which we inherit innate characteristics from our parents is well understood: we inherit half of our genes from our mother and half from our father. However, the mechanism whereby a ‘memory’ of the parent’s environment and behaviour might be passed down through the generations is not understood.

Epigenetic inheritance has proved a compelling and popular explanation. ̽��ֱ��human genome is made up of DNA – our genetic blueprint. But our genome is complemented by a number of ‘epigenomes’ that vary by cell type and developmental time point. Epigenetic marks are attached to our DNA and dictate in part whether a gene is on or off, influencing the function of the gene. ̽��ֱ��best understood epigenetic modification is DNA methylation, which places a methyl group on one of the bases of DNA (the A, C, G or T that make up our genetic code).

One model in which DNA methylation is associated with epigenetic inheritance is a mouse mutant called Agouti Viable Yellow. ̽��ֱ��coat of this mouse can be completely yellow, completely brown, or a pattern of these two colours – yet, remarkably, despite their different coat colours, the mice are genetically identical.

̽��ֱ��explanation of how this occurs lies with epigenetics. Next to one of the key genes for coat colour lies a section of genetic code known as a ‘transposable element’ – a small mobile DNA ‘cassette’ that is actually repeated many times in the mouse genome but here acts to regulate the coat colour gene.

As many of these transposable elements come from external sources – for example, from a virus’s genome – they could be dangerous to the host’s DNA. But organisms have evolved a way of controlling their movement through methylation, which is most often a silencing epigenetic mark.

In the case of the gene for coat colour, if methylation switches off the transposable element completely, the mouse will be brown; if acquisition of methylation fails completely, the mouse will be yellow. But this does not affect the genetic code itself, just the epigenetic landscape of that DNA segment.

And yet, a yellow-coated female is more likely to have yellow-coated offspring and a brown-coated female is more likely to have brown-coated offspring. In other words, the epigenetically regulated behaviour of the transposable element is somehow being inherited from parent to offspring.

A team led by Professor Anne Ferguson-Smith at Cambridge’s Department of Genetics set out to examine this phenomenon in more detail, asking whether similar variably-methylated transposable elements existed elsewhere that could influence a mouse’s traits, and whether the ‘memory’ of these methylation patterns could be passed from one generation to the next. Their results are published in the journal Cell.

̽��ֱ��researchers found that while these transposable elements were common throughout the genome – transposable elements comprise around 40% of a mouse’s total genome – the vast majority were completely silenced by methylation and hence had no influence on genes.

Only around one in a hundred of these sequences were variably-methylated. Some of these are able to regulate nearby genes, whereas others may have the ability to regulate genes located further away in the genome in a long-range capacity.

When the team looked at the extent to which the methylation patterns on these regions could be passed down to subsequent generations, only one of the six regions they studied in detail showed evidence of epigenetic inheritance – and even then, the effect size was small. Furthermore, only methylation patterns from the mother, not the father, were passed on.

“One might have assumed that all the variably-methylated elements we identified would show memory of parental epigenetic state, as is observed for coat colour in Agouti Viable Yellow mice,” says Tessa Bertozzi, a PhD candidate and one of the study’s first authors. “There’s been a lot of excitement and hype surrounding the extent to which our epigenetic information is passed on to subsequent generations, but our work suggests that it’s not as pervasive as was previously thought.”

“In fact, what we showed was that methylation marks at these transposable elements are reprogrammed from one generation to the next,” adds Professor Ferguson-Smith. “There’s a mechanism that removes methylation from the vast majority of the genome and puts it back on again, once in the process of generating eggs and sperms and again before the fertilised egg implants into the uterus. How the methylation patterns at the regions we have identified get reconstructed after this genome-wide erasure is still somewhat of a mystery.

“We know there are some genes – imprinted genes for example– that do not get reprogrammed in this way in the early embryo. But these are exceptions, not the rule.”

Professor Ferguson-Smith says that there is evidence that some environmentally-induced information can somehow be passed down generations. For example, her studies in mice show that the offspring of a mother who is undernourished during pregnancy are at increased risk of type 2 diabetes and obesity – and their offspring will in turn go on to be obese and diabetic. Again, she showed that DNA methylation was not the culprit – so how does this occur?

Every sperm is scarred?

̽��ֱ��answer may come from research at the Wellcome/Cancer Research UK Gurdon Institute, also at the ̽��ֱ�� of Cambridge, in collaboration with the lab of Professor Isabelle Mansuy from the ̽��ֱ�� of Zürich and Swiss Federal Institute of Technology. In a study carried out in mice and published in the journal Molecular Psychiatry, they report how the ‘memory’ of early life trauma can be passed down to the next generation via RNA molecules carried by sperm.

Dr Katharina Gapp from Erica Miska's lab at the Gurdon Institute and the Mansuy lab have previously shown that trauma in postnatal life increases the risk of behavioural and metabolic disorders not only in the directly exposed individuals but also in their subsequent offspring.

Now, the team has shown that the trauma can cause alterations in ‘long RNA’ (RNA molecules containing more than 200 nucleotides) in the father’s sperm and that these contribute to the inter-generational effect. This complements earlier research that found alterations in ‘short RNA’ molecules (with fewer than 200 nucleotides) in the sperm. RNA is a molecule that serves a number of functions, including, for some of the long versions called messenger RNA, ‘translating’ DNA code into functional proteins and regulating functions within cells.

Using a set of behavioural tests, the team showed that specific effects on the resulting offspring mediated by long RNA included risk-taking, increased insulin sensitivity and overeating, whereas small RNA conveyed the depressive-like behaviour of despair.

Dr Gapp said: "While other research groups have recently shown that small RNAs contribute to inheritance of the effects of chronic stress or changes in nutrition, our study indicates that long RNA can also contribute to transmitting some of the effects of early life trauma. We have added another piece to the puzzle for potential interventions in transfer of information down the generations."

References
Kazachenka, A, Bertozzi, TM et al. Identification, Characterization, and Heritability of Murine Metastable Epialleles: Implications for Non-genetic Inheritance. Cell; 25 Oct 2018; DOI: 10.1016/j.cell.2018.09.043

Gapp K et al. Alterations in sperm long RNA contribute to the epigenetic inheritance of the effects of postnatal trauma. Molecular Psychiatry; 30 Oct 2018; DOI: 10.1038/s41380-018-0271-6

Evidence has been building in recent years that our diet, our habits or traumatic experiences can have consequences for the health of our children – and even our grandchildren. ̽��ֱ��explanation that has gained most currency for how this occurs is so-called ‘epigenetic inheritance’ – patterns of chemical ‘marks’ on or around our DNA that are hypothesised to be passed down the generations. But new research from the ̽��ֱ�� of Cambridge suggests that this mechanism of non-genetic inheritance is likely to be very rare.

There’s been a lot of excitement and hype surrounding the extent to which our epigenetic information is passed on to subsequent generations, but our work suggests that it’s not as pervasive as was previously thought

Tessa Bertozzi

Randy Jirtle and Dana Dolinoy

Agouti mice

Researcher Profile: Tessa Bertozzi

Epigenetics has become something of a buzzword in recent years. It is the study of chemical modifications to DNA that switch genes on and off without changing the underlying DNA sequence. But what particularly excites interest is the extent to which these modifications, which can be altered by our environment – our diet, our behaviour, for example – can be inherited alongside DNA.

“ ̽��ֱ��unknowns far outweigh the knowns in the young field of epigenetics, which is part of what makes it such an exciting time,” explains Tessa Bertozzi, a PhD student in the lab of Professor Anne Ferguson-Smith at Cambridge.

Tessa grew up in Mexico before moving to Seattle, Washington and then to southern California. “I came across Anne’s research in one of my undergraduate courses and found it fascinating. I contacted her soon after that and four years later I’m a final-year PhD student in her lab at Cambridge!”

Professor Ferguson-Smith’s lab has recently identified regions of the mouse genome that show different methylation levels across genetically identical mice. Tessa focuses on the mechanisms underlying the reconstruction of this epigenetic variation across generations.

“I conduct breeding experiments with mice and use specialised sequencing technologies to look at their DNA methylation patterns. While I am often found at the bench or analysing data on my computer, I also spend time developing ideas at meetings, seminars, and conferences, as well as participating in outreach activities.”

Cambridge has been a hub for epigeneticists for a while now, she says. “It is very motivating to be surrounded by like-minded researchers eager to interact and collaborate. In fact, my PhD has relied heavily on a number of collaborations across Cambridge.

“ ̽��ֱ�� ̽��ֱ�� attracts academics from all over the world, making it a vibrant international community of people with different backgrounds and experiences. I have met and interacted with incredibly interesting people over the years.”

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Postdoctoral Fellowships programme for Israeli scientists to pursue research at Cambridge

th288 — Tue, 20 Jan 2015 15:18:41 +0000

̽��ֱ��Funding will be provided by the Blavatnik Family Foundation.

As a world-leading university, Cambridge seeks to bring together the most brilliant minds to freely interact, learn and discover. Its goal is to encourage and support the best people from around the world to work and study at the ̽��ֱ��. ̽��ֱ��new Blavatnik Fellowships offer an important addition in support of this aim.

̽��ֱ��Fellowship programme, which will run for an initial period of five years, will be administered by the British Council in Israel which actively promotes academic and scientific exchange between Israel and the United Kingdom, and is warmly supportive of the initiative.

Fellows will receive an annual stipend of £30,000, and Fellowships will be tenable for up to two years. It is planned that there will be at least three Fellows appointed each year, although it is anticipated that this number may increase in future years.

̽��ֱ��first three Fellows will research in the areas of Engineering, Genetics and Physics.

Potential Fellows are encouraged to apply to the programme by the British Council. Successful applicants are selected by a committee of senior academics.

Professor Eric Miska, the Herchel Smith Professor of Molecular Genetics and Senior Group Leader at the Gurdon Institute at the ̽��ֱ�� of Cambridge said:

“I am delighted to host a Blavatnik Fellow in my lab within the Gurdon Institute. Fellowships such as these enable the exchange of ideas and expertise that is the lifeblood of cutting-edge research. We’re deeply grateful to Leonard Blavatnik and the Blavatnik Family Foundation for their support and hope to host many more fellows in the future.”

Mr Blavatnik, speaking on behalf of the Blavatnik Family Foundation, said: “I am very pleased to strengthen the Foundation’s existing links to Cambridge with this important initiative, which will serve the mutual interests of the ̽��ֱ��, the Israeli scientific community and those selected to be Blavatnik Fellows.”

Professor Sir Leszek Borysiewicz, Vice-Chancellor of the ̽��ֱ�� of Cambridge, said: “We are committed to enabling the very best people from around the world to come to Cambridge, to drive forward our pioneering research and address new questions. We are delighted that the generosity of Leonard Blavatnik and the Blavatnik Family Foundation adds a further way in which we can support this ambition.”

A benefactor of the ̽��ֱ�� of Cambridge, Leonard Blavatnik, has made a multi-million pound pledge to provide funding for Israeli scientists of outstanding ability to study in Cambridge.

Fellowships such as these enable the exchange of ideas and expertise that is the lifeblood of cutting-edge research.

Professor Eric Miska

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