RT Journal Article
SR Electronic
T1 FYCO1 regulates accumulation of post-mitotic midbodies by mediating LC3-dependent midbody degradation
JF Journal of Cell Science
JO J. Cell Sci.
FD The Company of Biologists Ltd
SP 4051
OP 4062
DO 10.1242/jcs.208983
VO 130
IS 23
A1 Dionne, Lai Kuan
A1 Peterman, Eric
A1 Schiel, John
A1 Gibieža, Paulius
A1 Skeberdis, Vytenis Arvydas
A1 Jimeno, Antonio
A1 Wang, Xiao-Jing
A1 Prekeris, Rytis
YR 2017
UL http://jcs.biologists.org/content/130/23/4051.abstract
AB The post-mitotic midbody (MB) is a remnant of cytokinesis that can be asymmetrically inherited by one of the daughter cells following cytokinesis. Until recently, the MB was thought to be degraded immediately following cytokinesis. However, recent evidence suggests that the MB is a protein-rich organelle that accumulates in stem cell and cancer cell populations, indicating that it may have post-mitotic functions. Here, we investigate the role of FYCO1, an LC3-binding protein (herein, LC3 refers to MAP1LC3B), and its function in regulating the degradation of post-mitotic MBs. We show that FYCO1 is responsible for formation of LC3-containing membrane around the post-mitotic MB and that FYCO1 knockdown increases MB accumulation. Although MBs accumulate in the stem-cell-like population of squamous cell carcinomas, FYCO1 depletion does not affect the clonogenicity of these cells. Instead, MB accumulation leads to an increase in anchorage-independent growth and invadopodia formation in HeLa cells and squamous carcinoma cells. Collectively, our data suggest that FYCO1 regulates MB degradation, and we present the first evidence that cancer invasiveness is a feature that can be modulated by the accumulation of MBs in cancer stem cells.This article has an associated First Person interview with the first author of the paper.