Echanism by which EndoMT in EC produces EVs that may possibly propagate angiostatic effects all through the AT vasculature in obesity. Funding: NIHR15NHLBI, American Heart AssociationAIREA.ISEV2019 ABSTRACT BOOKSymposium Session 9: EV Biogenesis II Chairs: Bong Hwan Sung; Graca Raposo Location: Level B1, Hall B 17:008:OT09.Diverse exosome subtypes have distinct ESCRT-associated biology and manage tumour cell adaptation in vivo Shih-Jung Fana, Benjamin Kroegerb, Pauline Mariea, Esther Bridgesa, Kristie McCormicka, John Masona, Helen Sheldona, Claudia Mendesa, Mark Wainwrighta, John Morrisa, ADAM10 Inhibitor Storage & Stability Adrian Harrisa, Clive Wilsona and Deborah C I. Goberdhana University of Oxford, Oxford, UK; Melbourne, Australiaa bFunding: This operate was funded by Cancer Investigation UK [C19591/A19076], the CRUK Oxford Centre Development Fund [C38302/A12278], BBSRC [BB/ K017462/1, BB/N016300/1, BB/R004862/1], John Fell Fund, Oxford, Wellcome Trust [MICRON; #091911, #107457], Royal College of Surgeons.Peter MacCallum Cancer Centre,OT09.Emerging part of L-type calcium channel-mediated calcium influx in regulating apoptotic bodies formation Thanh Kha Phana, Bo Shib, Niall Geogheganc, Kelly Rogersd and Ivan PooneaIntroduction: Determining the function of distinct extracellular vesicle (EV) and exosome subtypes has proved challenging, in part as a result of difficulty in untangling the mechanisms major to their generation. Techniques: We investigated the cell biology behind exosome formation applying the significant endosomal compartments PKCθ custom synthesis offered by an in vivo fly model, and analysis in human HCT116 and also other cancer cell lines. EV preparations were also tested in vivo following injection in to human xenografts in mice. We analysed diverse EV preparations by mass spectrometry employing Tandem Mass Tag labelling to identify changes in protein cargo of EVs in response to microenvironmental anxiety. Results: Making use of these complementary approaches, we show that microenvironmental strain, including glutamine depletion, results in a switch in membrane trafficking from the classic late endosomal multivesicular endosomes to Rab11a-positive recycling endosomes plus the production of Rab11a-positive exosomes, which promote cell development under strain circumstances. This activity is suppressed by blocking Rab11a-dependent trafficking and ESCRT function. Our proteomics and fly data suggest that some ESCRTs are differentially involved in these two exosome-generating processes. Moreover, mouse xenografts highlight roles for stress-induced EVs in growing the turnover of tumour cells, top to a rise in hypoxic stress, related with selection for aggressive cells that will market tumour progression. These stress-induced vesicles also possess a potent effect on blood vessel growth in vivo. Summary/Conclusion: We conclude that stressinduced EVs and exosomes made in Rab11a-positive recycling endosomes are involved in tumour adaptation.Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Australia; bDepartment of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Australia; cCentre for Dynamic Imaging, Walter and Eliza Hall Institute of Healthcare Analysis, Melbourne, Australia; d Centre for Dynamic Imaging, Walter and Eliza Hall Institute of Healthcare Research, Melbourne, Australia; eLa Trobe University, Bundoora, AustraliaIntroduction: Dying cells often break into smaller membrane-bound fragments, called apoptotic.