Cambridge scientists recognised by major European research organisation

cjb250 — Tue, 18 Jun 2019 11:42:19 +0000

Cambridge ̽��ֱ�� has the highest number of new members of any institution within Europe. Five ̽��ֱ�� of Cambridge researchers are among the 48 scientists from 17 countries elected:

Professor Sadaf Farooqi – Wellcome-Medical Research Council (MRC) Institute of Metabolic Science
Dr Fanni Gergely – Cancer Research UK Cambridge Institute
Professor Paul Lehner – Department of Medicine and the Cambridge Institute for Medical Research
Professor Lalita Ramakrishnan – Department of Medicine and the MRC Laboratory of Molecular Biology
Professor Nicole Soranzo – Department of Haematology and Wellcome Sanger Institute

In addition, Dr Garib Murshudov from the MRC Laboratory of Molecular Biology has also been elected.

EMBO is an organisation of more than 1800 leading researchers in Europe and around the world, whose mission is to promote excellence in the life sciences in Europe and beyond. ̽��ֱ��major goals of the organisation are to support talented researchers at all stages of their careers, stimulate the exchange of scientific information and help build a research environment where scientists can achieve their best work.

“EMBO Members are excellent scientists who conduct research at the forefront of all life science disciplines, ranging from computational models or analyses of single molecules and cellular mechanics to the study of higher-order systems in development, cognitive neuroscience and evolution,” says EMBO Director Maria Leptin.

“We’re very honoured to have been elected as members of EMBO,” says Professor Farooqi. “This is great recognition for the excellent science taking place across our city, particularly on the Cambridge Biomedical Campus. We are proud of the role we play in European science and look forward to continuing to work in partnership with colleagues across the continent.”

Researchers from the Cambridge Biomedical Campus have featured prominently in this year’s election to the prestigious European Molecular Biology Organisation (EMBO).

We are proud of the role we play in European science and look forward to continuing to work in partnership with colleagues across the continent

Sadaf Farooqi

CDC/ Melissa Brower

This illustration depicts a three-dimensional (3D) computer-generated image of a cluster of rod-shaped drug-resistant Mycobacterium tuberculosis bacteria, the pathogen responsible for causing the disease tuberculosis (TB).

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New insights into how the Zika virus causes brain birth defect

cjb250 — Thu, 01 Jun 2017 18:00:56 +0000

A study published today in Science shows that the Zika virus hijacks a human protein called Musashi-1 (MSI1) to allow it to replicate in, and kill, neural stem cells. Almost all MSI1 protein in the developing embryo is produced in the neural stem cells that will eventually develop into the baby’s brain, which could explain why these cells are so vulnerable to Zika.

Since 2016 thousands of children across South America have been born with microcephaly, which causes abnormally small heads, after their mothers became infected with the Zika virus during pregnancy. ̽��ֱ��overlap between Zika cases in pregnant women and an increase in babies born with microcephaly strongly suggested that the virus targets stem cells in the developing human brain, but why and how has remained a mystery. Today’s study is the first to associate MSI1 with microcephaly and the Zika virus.

Dr Fanni Gergely from the Cancer Research UK (CRUK) Cambridge Institute at the ̽��ֱ�� of Cambridge said: “ ̽��ֱ��development of a healthy human brain is an incredibly complex process that relies on stem cells and the coordinated actions of many genes. We’ve shown for the first time this interaction between Zika and MSI1 - with MSI1 getting exploited by the virus for its own destructive life cycle, turning MSI1 into the enemy within. We hope that in the future this discovery could lead to ways of generating potential Zika virus vaccines.”

Dr Mike Turner, Head of Infection and Immunobiology at Wellcome said: “This is the first study to show a clear link between a specific protein, the Zika virus and microcephaly. This new finding really helps to explain why neural stem cells are so vulnerable to Zika infection and I hope this can be a first step in determining how we could stop this interaction and disease. It will also be interesting to investigate whether this protein is involved in other viruses, such as Rubella, that also access and impair the developing human brain.”

Researchers from the CRUK Cambridge Institute, together with colleagues at the ̽��ֱ��’s Department of Pathology and the Cambridge Institute for Medical Research, studied a variety of cell lines, including human neural stem cells, to investigate how Zika virus infection can lead to microcephaly. They suspected that MSI1 – and RNA binding protein - might be important in this process because it is involved in regulating the pool of neural stem cells that are required for normal brain development.

̽��ֱ��researchers show that when the Zika virus enters these stem cells, it hijacks MSI1 for its own replication and damages the cells in at least two ways. Firstly, MSI1 binds to the Zika virus genome allowing it to replicate and making the cells more vulnerable virus-induced cell death. When the researchers infected cells that had been rendered unable to produce MSI1, virus replication was significantly reduced, as was cell death, indicating that the presence of MSI1 is required for efficient Zika replication.

Secondly, they showed that MSI1 also disrupts the normal development programme of neural stem cells. In cells infected with Zika virus MSI1 binds to the virus genome in favour of its normal targets in the cell. ̽��ֱ��virus essentially acts like a ‘sponge’, preventing MSI1 from working correctly and altering the expression of many genes involved in neuronal development.

In both of these scenarios, neural stem cells, which are crucial for normal neural development, are lost, leading to reduced brain size.

To confirm that MSI1 is important to grow a normal size brain, the scientists demonstrated that MSI1 is mutated in individuals with a rare type of inherited microcephaly (autosomal recessive primary microcephaly) unrelated to Zika infection.

These results collectively suggest that neural stem cells need MSI1 to generate enough neurons for normal brain size, but the presence of MSI1 also increases the vulnerability of these cells to Zika infection, leading to the death of the population which ultimately results in microcephaly.

This study was funded by Wellcome and Cancer Research UK.

Reference
Chavali, PL et al. Neurodevelopmental protein Musashi 1 interacts with the Zika genome and promotes viral replication. Science; 1 June 2017; DOI: 10.1126/science.aam9243

Adapted from a press release from Wellcome

Scientists have uncovered why Zika virus may specifically target neural stem cells in the developing brain, potentially leading to microcephaly – a potentially serious birth defect where the brain fails to develop properly, leading to a smaller head.

We hope that in the future this discovery could lead to ways of generating potential Zika virus vaccines

Fanni Gergely

Sumaia Villela/Agência Brasil

Baby with microcephaly

̽��ֱ��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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̽��ֱ�� of Cambridge - Fanni Gergely

Cambridge scientists recognised by major European research organisation

New insights into how the Zika virus causes brain birth defect