Journal
SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-37056-x
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Funding
- Rosetrees Trust [M155]
- MRC Doctoral Training Grant [1132770]
- UCL Bogue Fellowship
- National Institutes of Health, USA [HL119843, T32DK007257]
- Medical Research Council [MR/K015826/1]
- Biotechnology and Biological Sciences Research Council [BB/M022374/1]
- BBSRC [BB/M022374/1] Funding Source: UKRI
- MRC [MR/K015826/1] Funding Source: UKRI
- Rosetrees Trust [M155] Funding Source: researchfish
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TMEM16F is a Ca2+ -gated ion channel that is required for Ca2+ -activated phosphatidylserine exposure on the surface of many eukaryotic cells. TMEM16F is widely expressed and has roles in platelet activation during blood clotting, bone formation and T cell activation. By combining microscopy and patch clamp recording we demonstrate that activation of TMEM16F by Ca2+ ionophores in Jurkat T cells triggers large-scale surface membrane expansion in parallel with phospholipid scrambling. With continued ionophore application, TMEM16F-expressing cells then undergo extensive shedding of ectosomes. The T cell co-receptor PD-1 is selectively incorporated into ectosomes. This selectivity depends on its transmembrane sequence. Surprisingly, cells lacking TMEM16F not only fail to expand surface membrane in response to elevated cytoplasmic Ca2+, but instead undergo rapid massive endocytosis with PD-1 internalisation. These results establish a new role for TMEM16F as a regulator of Ca2+ activated membrane trafficking.
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