Barry James Thompson
Barry James Thompson is an Australian and British developmental biologist and cancer biologist. Thompson is known for identifying genes, proteins and mechanisms involved in epithelial polarity, morphogenesis and cell signaling via the Wnt and Hippo signaling pathways, which have key roles in human cancer.
Early life and education
Barry Thompson was born in 1978 into a British-Australian family. He was raised on the Atherton Tableland and in Brisbane in the state of Queensland. He attended Atherton State Primary School and Brisbane State High School and graduated as school Dux in 1995.Scientific career
Thompson became interested in developmental biology and the control of tissue growth in 2000 when studying BSc at the University of Queensland's Institute for Molecular Biology with Professor Michael Waters.He earned his PhD degree at the MRC Laboratory of Molecular Biology and University of Cambridge, where he studied the Wnt signaling pathway in Drosophila melanogaster with Dr Mariann Bienz.
He then moved to Germany to work at the European Molecular Biology Laboratory with Prof Stephen M Cohen. There he studied the role of the Hippo signaling pathway during Drosophila development.
In 2007, Thompson was a visiting scientist at the Research Institute of Molecular Pathology in Vienna, where he worked in the laboratory of Dr Barry Dickson to perform a genome-wide in vivo RNAi screen in Drosophila. In 2008, Thompson established his own laboratory at the Cancer Research UK London Research Institute, which became part of the Francis Crick Institute in 2015. In 2019, Thompson was appointed Professor at the John Curtin School of Medical Research at the Australian National University. His service was terminated in October 2023 due to his actions of sexual harassment.
Research areas
Epithelial cell polarity
His laboratory works on the molecular mechanisms of epithelial polarity, including both apical-basal polarity and planar cell polarity, using Drosophila melanogaster epithelial tissues as an experimental model system. His laboratory discovered that apical-basal polarisation of the transmembrane protein Crumbs - a key apical determinant - depends upon both a Cdc42-driven positive feedback loop as well as mutual antagonism between apical and basolateral determinants. The Cdc42-driven positive feedback loop involves recruitment of Cdc42 complexes by Crumbs, followed by Cdc42-mediated polarisation of the cytoskeleton, including both actin filaments and microtubules, that allow transport of Crumbs-containing vesicles by the microtubule motor protein Dynein and the actin motor protein Myosin-V. How Cdc42 polarises the cytoskeleton remains an important unsolved problem, but Cdc42 appears to act primarily via activating the kinases aPKC and Pak1 in Drosophila follicle cells.His laboratory also discovered that planar cell polarisation of the atypical myosin Dachs by the Fat and Dachsous cadherins is responsible for polarising tension at adherens junctions and thus influencing the orientation of cell shapes and cell divisions within the plane of the epithelium. His lab subsequently found that this involved recruitment of the ubiquitin ligase FbxL7 to Fat, in order to degrade Dachs on one side of the cell, such that Dachs binds to Dachsous on the opposite side of the cell.