Mutations in PINK1 are the second most frequent cause of autosomal recessive early-onset Parkinson’s disease. PINK1 is activated upon mitochondrial damage to phosphorylate Ubiquitin and Parkin to stimulate Parkin E3 ligase activity, and this is critical for removal of damaged mitochondria by autophagy (mitophagy).

Two researchers from the MRC PPU have been awarded places in the Scottish Universities Life Sciences Alliance (SULSA) Forging Futures Scheme. …more

The Royal Society’s first open access title, Open Biology, has reached its 10th Anniversary. To kick off a year of celebration, Subject Editors have highlighted their favourite articles from the past decade. Of the nine top publications selected, work from the research group of Miratul Muqit is being highlighted.

Three PhD students from the MRC PPU have successfully made It through to the final round of the Biotechnology Young Entrepreneurs Scheme (YES). Ailsa Black (Rousseau lab), Bill Carton (Sapkota lab) and Lee Armstrong (Kulathu lab) took part as team “Affinitas Biosciences Ltd” with their idea to supplement a chewing gum with a nanobody that specifically targets and inhibits tooth decaying bacteria.

In 1998, mutations in the Parkin gene were discovered as a cause of early-onset Parkinson’s disease by a Japanese team who in collaboration with Keiji Tanaka then showed in 2000 that it functioned as a ubiquitin E3 ligase. However, the physiological substrates of Parkin remained elusive for many years. A major breakthrough on Parkin’s function was the discovery, by Richard Youle’s lab, that Parkin is recruited from the cytosol to sites of mitochondrial damage to trigger the removal of mitochondria by autophagy known as mitophagy.

A collaborative study published in Nature from Tom Deegan (formerly a postdoc in Karim Labib’s lab, now a group leader at MRC HGU, Edinburgh) and Joe Yeeles’ lab (MRC LMB, Cambridge), has defined a new protective mechanism that cells use to prevent the premature termination of chromosome replication.

Mutations in the gene encoding the CDKL5 kinase are among the most common genetic causes of childhood epilepsy and can also give rise to the severe neurodevelopmental condition CDD (CDKL5 Deficiency Disorder). Despite its importance for human health, the phospho–targets and cellular roles of CDKL5 are poorly understood. Finding the cellular substrates of CDKL5 is critically important because the pathological mutations in CDKL5 reduce kinase activity to varying degrees,  implying that is a reduction in substrate phosphorylation that causes brain dysfunction and neurological disease. …more

We are delighted to announce that Kirby Swatek will open an independent research laboratory in the MRC PPU at the beginning of 2022.  He will take up a core funded MRC Investigator position to investigate the role played by the ubiquitin-like protein ISG15 in key immune responses that protect cells from invading viruses.

Research from the MRC PPU has shed new light into how immune cells  tolerate the presence of harmless food and symbiotic bacteria in the gut, preventing needless immune responses and inflammation in the gut. The new study is published in eLife.

MRC PPU researchers partnered with the Tropicalist Trust to run an event for school pupils in the upper reaches of the Himalayas, northern India to inspire them to consider a career in science.

The event took place online, with over 40 pupils attending from local high schools in the cold desert area of Kargil in the Himalayas. The remote location presented technology challenges, but after date and venue changes in order to find a reliable internet connection the event successfully took place on 6th September 2021.