IISER MOHALI

DBS Research Spotlight Seminar Series

Speaker:  

Prof. Vivek Malhotra, ICREA Research Professor and Group Leader, CRG (Centre for Genomic Regulation), Barcelona, Spain

About the speaker:  

Prof. Vivek Malhotra is a world leader on protein secretion and cellular compartmentalization.  His laboratory focuses on elucidating the mechanisms by which cells are compartmentalized and ensure the secretion of essential proteins such as collagens, mucins, insulin, hormones, and cytokines of appropriate quality in response to physiological demands. He leads work on investigating how cells synthesize compartments like the Golgi complex and establish exit sites for cargo export at the endoplasmic reticulum. 

You can know more about his research here: 

https://www.crg.eu/en/programmes-groups/malhotra-lab

Abstract:

Numerous proteins that cannot enter the endoplasmic reticulum (ER)-Golgi pathway of secretion are released to the extracellular space. We have focussed on the secretion of Acyl CoA binding protein (Acb1/Diazepam binding inhibitor) and its export has the following essential requirements. 1, Secretion is triggered upon carbon and nitrogen starvation, and culturing cells in potassium acetate; 2, intracellular production of reactive oxygen species (ROS); 3, the need of a peripherally Golgi/ER exit site localized protein called Grh1 (GORASPs in mammals); and 4, a membrane bound compartment called CUPS. CUPS form by COPI independent extraction of membranes from the early Golgi cisterna, lacks Golgi specific glycosyltransferases, require PI4P for biogenesis and PI3P for its stability.  Our new data reveal that CUPS contact a modified TGN, which is devoid of Glycosylating enzymes. The modified TGN contains specific proteins and SNAREs that are essential for Acb1 secretion.  Incidentally, while CUPS are stable, the modified TGN is vesiculated at late stages of starvation. We have also reconstituted this process in mammalian cells and based on our data, I will discuss the pathway of Acb1 secretion and antigen presentation by dendritic cells, which involves some of the components of the autophagy, CUPS and modified TGN.