The post-abscission midbody is an intracellular signaling organelle that regulates cell proliferation

Eric Peterman, Paulius Gibieža, Johnathon Schafer, Vytenis Arvydas Skeberdis, Algirdas Kaupinis, Mindaugas Valius, Xavier Heiligenstein, Ilse Hurbain, Graca Raposo and Rytis Prekeris ()
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Eric Peterman: University of Colorado Anschutz Medical Campus
Paulius Gibieža: Lithuanian University of Health Sciences
Johnathon Schafer: University of Colorado Anschutz Medical Campus
Vytenis Arvydas Skeberdis: Lithuanian University of Health Sciences
Algirdas Kaupinis: Vilnius University Life Sciences Center, Vilnius University
Mindaugas Valius: Vilnius University Life Sciences Center, Vilnius University
Xavier Heiligenstein: Structure and Membrane Compartments
Ilse Hurbain: Structure and Membrane Compartments
Graca Raposo: Structure and Membrane Compartments
Rytis Prekeris: University of Colorado Anschutz Medical Campus

Nature Communications, 2019, vol. 10, issue 1, 1-16

Abstract: Abstract Once thought to be a remnant of cell division, the midbody (MB) has recently been shown to have roles beyond its primary function of orchestrating abscission. Despite the emerging roles of post-abscission MBs, how MBs accumulate in the cytoplasm and signal to regulate cellular functions remains unknown. Here, we show that extracellular post-abscission MBs can be internalized by interphase cells, where they reside in the cytoplasm as a membrane-bound signaling structure that we have named the MBsome. We demonstrate that MBsomes stimulate cell proliferation and that MBsome formation is a phagocytosis-like process that depends on a phosphatidylserine/integrin complex, driven by actin-rich membrane protrusions. Finally, we show that MBsomes rely on dynamic actin coats to slow lysosomal degradation and propagate their signaling function. In summary, MBsomes may sometimes serve as intracellular organelles that signal via integrin and EGFR-dependent pathways to promote cell proliferation and anchorage-independent growth and survival.

Date: 2019
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DOI: 10.1038/s41467-019-10871-0

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