Cell & Developmental Biology
Open Access

Liang Ge

Biography

Liang Ge pursued his PhD in the lab of Dr Bao-Liang Song at the Institutes of Biochemistry and Cell Biology, Chinese Academy of Sciences, where he studied the molecular mechanisms of cholesterol absorption. In 2011 he moved to California for a postdoc and later a research specialist position with Randy Schekman at the University of California, Berkeley. There, he discovered key roles for LC3 lipidation and the ER–Golgi intermediate compartment in autophagosome biogenesis. Liang established his group in the School of Life Sciences at Tsinghua University at the end of 2017.

Research Interest

Autophagy is a catabolic process for bulk degradation of cytosolic components. It plays a fundamental role in intracellular quality control and material recycling as well as adaptation to multiple stresses. Misregulation of autophagy has been indicated in many human disorders including cancer, neurodegeneration and aging. A key feature of autophagy is the de novo formation of double-membrane vesicles, termed autophagosomes, by a substantial membrane investment from various endomembrane sources. Since its discovery more than 50 years ago, the mechanism accounting for the membrane mobilization to generate the autophagosome has been a mystery. Dr. Ge’s research interest is to functionally dissect the process of membrane mobilization from existing cellular pools for autophagosome biogenesis. He developed a functional assay which recapitulates multiple landmarks of autophagosome biogenesis regulation based on LC3 lipidation, a key early step in autophagy. He has used this reaction and a complete organelle fractionation scheme to identify a novel source of membrane template for lipidation the endoplasmic reticulum-Golgi intermediate compartment (ERGIC), a sorting station for cargo transport between the endoplasmic reticulum and the Golgi appratus. Dr. Ge is currently focusing on the molecular machineries involved in mobilizing membrane from the ERGIC for delivery to a nascent autophagosomal precursor.

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