CBIS welcomes Prof Ashok Venkitaraman, Director, MRC Cancer Unit, University of Cambridge

Ashok VenkitaramanProfessor Ashok Venkitaraman

CBIS is pleased to welcome Prof Ashok Venkitaraman, Director, MRC Cancer Unit, The Ursula Zoellner Professor of Cancer Research, University of Cambridge

He will be arriving in Singapore on 13 September 2016 and will be with us until 22 October 2016.

He will be spending half of his time at MBI and half at CBIS. His CBIS office is room #02-15. His email is pa-venkitaraman@mrc-cu.cam.ac.uk.

Biography

Ashok is the Ursula Zoellner Professor of Cancer Research at the University of Cambridge, and the Director of the Medical Research Council (MRC) Cancer Unit. He trained in medicine at the Christian Medical College, Vellore, India, before completing his PhD at University College London. Ashok was a faculty member at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge, before appointment to the Zoellner Professorship in 1998.

Ashok is widely recognized for his contributions to understanding the genetics and biology of cancer, particularly in elucidating the impact of genome instability on carcinogenesis and cancer therapy. His research has not only illuminated the fundamental mechanisms governing genome repair, replication and segregation during cell division, but has also provided insight into their connections with cancer pathogenesis and treatment.

Translation of these insights to clinical practice is a major focus in Ashok’s current work. He has been instrumental in establishing initiatives that link chemists, physicists, structural biologists, cancer biologists and clinicians in Cambridge and elsewhere, with the aim to pioneer innovative new approaches for the discovery and early clinical development of next-generation medicines.

Ashok was elected a Fellow of the Academy of Medical Sciences, London, in 2001 and a Member of the EMBO European academy, Heidelberg, in 2004.

Learn more about Prof Venkitaraman.

Visualization of Assembly Intermediates and Budding Vacuoles of Singapore Grouper Iridovirus in Grouper Embryonic Cells

by Yang Liu, Bich Ngoc Tran, Fan Wang, Puey Ounjai, Jinlu Wu & Choy L. Hew

Scientific Reports 6, Article number: 18696 (2016)
doi:10.1038/srep18696

Iridovirid infection is associated with the catastrophic loss in aquaculture industry and the population decline of wild amphibians and reptiles, but none of the iridovirid life cycles have been well explored. Here, we report the detailed visualization of the life cycle of Singapore grouper iridovirus (SGIV) in grouper cells by cryo-electron microscopy (cryoEM) and tomography (ET). EM imaging revealed that SGIV viral particles have an outer capsid layer, and the interaction of this layer with cellular plasma membrane initiates viral entry. Subsequent viral replication leads to formation of a viral assembly site (VAS), where membranous structures emerge as precursors to recruit capsid proteins to form an intermediate, double-shell, crescent-shaped structure, which curves to form icosahedral capsids. Knockdown of the major capsid protein eliminates the formation of viral capsids. As capsid formation progresses, electron-dense materials known to be involved in DNA encapsidation accumulate within the capsid until it is fully occupied. Besides the well-known budding mechanism through the cell periphery, we demonstrate a novel budding process in which viral particles bud into a tubular-like structure within vacuoles. This budding process may denote a new strategy used by SGIV to disseminate viral particles into neighbor cells while evading host immune response.

Read online: Scientific Reports.

Frequency and amplitude control of cortical oscillations by phosphoinositide waves

by Ding Xiong, Shengping Xiao, Su Guo, Qinsong Lin, Fubito Nakatsu & Min Wu

Nature Chemical Biology (2016) doi:10.1038/nchembio.2000
Published online 11 January 2016

Rhythmicity is prevalent in the cortical dynamics of diverse single and multicellular systems. Current models of cortical oscillations focus primarily on cytoskeleton-based feedbacks, but information on signals upstream of the actin cytoskeleton is limited. In addition, inhibitory mechanisms—especially local inhibitory mechanisms, which ensure proper spatial and kinetic controls of activation—are not well understood. Here, we identified two phosphoinositide phosphatases, synaptojanin 2 and SHIP1, that function in periodic traveling waves of rat basophilic leukemia (RBL) mast cells. The local, phase-shifted activation of lipid phosphatases generates sequential waves of phosphoinositides. By acutely perturbing phosphoinositide composition using optogenetic methods, we showed that pulses of PtdIns(4,5)P2 regulate the amplitude of cyclic membrane waves while PtdIns(3,4)P2 sets the frequency. Collectively, these data suggest that the spatiotemporal dynamics of lipid metabolism have a key role in governing cortical oscillations and reveal how phosphatidylinositol 3-kinases (PI3K) activity could be frequency-encoded by a phosphatase-dependent inhibitory reaction.

Read online: Nature Chemical Biology.

Learn more about Wu Min‘s research.