All transcripts were created with artificial intelligence software and modified with manual review by a third party. Although we make every effort to ensure accuracy with the manual review, some may contain computer-generated mistranslations resulting in inaccurate or nonsensical word combinations, or unintentional language. FASEB and the presenting speakers did not review the transcripts and are not responsible and will not be held liable for damages, financial or otherwise, that occur as a result of transcript inaccuracies.
Mechanisms of ER Neutral Lipid Flux and Lipid Storage
James A. Olzmann1-3
1 Department of Molecular and Cell Biology 2 Department of Nutritional Sciences & Toxicology 3 Chan Zuckerberg Biohub
Lipid droplets (LDs) are endoplasmic reticulum (ER)-derived organelles that function as dynamic lipid storage depots,
sequestering toxic lipids and providing a source of lipids that can be rapidly mobilized for membranes, signaling, and
energy. Structurally, LDs consist of a neutral lipid core (mostly triacylglycerol and cholesterol esters) encircled by a
phospholipid monolayer that is decorated with integral and peripheral proteins. These LD proteins, such as the perilipins
(PLINs), play key roles in regulating LD biogenesis and breakdown, trafficking, and inter-organelle interactions. In this
presentation I will discuss a series of CRIPSR-Cas9 loss-of-function screens that advance our understanding of the
metabolic state-dependent regulation of LD biogenesis and proteome dynamics. These CRISPR screens provide the
foundation for CRISPRlipid (http://crisprlipid.org), an extensible, online data commons for lipid-related functional
genomics data. Moreover, the data from our screens provide a phenotype-rich resource for the exploration of LD
biology and reveal new mechanisms that control neutral lipid flux in the ER and LD protein stability.