Echanism by which EndoMT in EC produces EVs that may well propagate angiostatic effects throughout 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.Various exosome subtypes have distinct ESCRT-associated BTNL9 Proteins web biology and control 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, Adrian Harrisa, Clive Wilsona and Deborah C I. Goberdhana University of Oxford, Oxford, UK; Melbourne, Australiaa bFunding: This function was funded by Cancer Research 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 role 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: Figuring out the function of specific extracellular vesicle (EV) and exosome subtypes has proved challenging, in component due to the difficulty in untangling the mechanisms leading to their generation. Methods: We investigated the cell biology behind exosome formation employing the large endosomal compartments supplied by an in vivo fly model, and evaluation in human HCT116 as well as 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 utilizing Tandem Mass Tag labelling to identify modifications in protein cargo of EVs in response to microenvironmental pressure. Outcomes: Utilizing these complementary approaches, we show that microenvironmental stress, such as glutamine depletion, results in a switch in membrane trafficking in the classic late endosomal multivesicular endosomes to Rab11a-positive recycling endosomes plus the production of Rab11a-positive exosomes, which market cell development below strain conditions. This activity is suppressed by blocking Rab11a-dependent trafficking and ESCRT function. Our proteomics and fly information suggest that some ESCRTs are differentially involved in these two exosome-generating processes. Furthermore, mouse xenografts highlight roles for stress-induced EVs in increasing the turnover of tumour cells, top to an increase in hypoxic strain, connected with Integrin Associated Protein/CD47 Proteins Storage & Stability choice for aggressive cells which can market tumour progression. These stress-induced vesicles also have a potent effect on blood vessel growth in vivo. Summary/Conclusion: We conclude that stressinduced EVs and exosomes created in Rab11a-positive recycling endosomes are involved in tumour adaptation.Division 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 Health-related Study, Melbourne, Australia; d Centre for Dynamic Imaging, Walter and Eliza Hall Institute of Medical Analysis, Melbourne, Australia; eLa Trobe University, Bundoora, AustraliaIntroduction: Dying cells normally break into smaller sized membrane-bound fragments, referred to as apoptotic.