Open AccessCytokine exocytosis and JAK/STAT activation in the Drosophila ovary requires the vesicle trafficking regulator α-Snap
Author(s) -
Afsoon Saadin,
Michelle StarzGaiano
Publication year - 2018
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.217638
Subject(s) - biology , microbiology and biotechnology , exocytosis , stat protein , exocyst , regulator , janus kinase , paracrine signalling , jak stat signaling pathway , secretory vesicle , signal transduction , stat , vesicular transport protein , vesicle , secretion , stat3 , tyrosine kinase , genetics , receptor , biochemistry , membrane , gene
How vesicle trafficking components actively contribute to regulation of paracrine signaling is unclear. We genetically uncovered a requirement for α-Soluble NSF Attachment Protein (α-Snap) in the activation of the Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway during Drosophila egg development. α-Snap, a well-conserved vesicle trafficking regulator, mediates association of N-ethylmaleimide-Sensitive Factor (NSF) and SNAREs to promote vesicle fusion. Depletion of α-Snap or the SNARE family member Syntaxin1A in epithelia blocks polar cells maintenance and prevents specification of motile border cells. Blocking apoptosis rescues polar cell maintenance in α-Snap-depleted egg chambers, indicating that the lack of border cells in mutants is due to impaired signaling. Genetic experiments implicate α-Snap and NSF in secretion of a STAT-activating cytokine. Live imaging suggests that changes in intracellular calcium may be linked to this event. Our data suggest a cell-type specific requirement for particular vesicle trafficking components in regulated exocytosis during development. Given the central role for STAT signaling in immunity, this work may shed light on regulation of cytokine release in humans.