RacGAP50C Is Sufficient to Signal Cleavage Furrow Formation During Cytokinesis

JCS 119::4402
David Glover @ University of Cambridge, UK

In this paper, authors forced RacGAP50C localized on the cortex during cytokinesis by fusing with CD8, a membrane protein. Authors found this CD8::RacGAP50C fusion protein is sufficient for triggering ectopic furrowing even in the absence of its motor partner MKLP1, in Drosophila S2 cells.

The first part of this paper was nothing special. It showed cleavage furrowing is centralspindlin dependent but the astral microtubules contacted the equatorial cortex is not. In the second part, authors mislocalized the GAP-signaling component around the entire cortex using a membrane-tethering motif and caused ectopic furrowing. Ed Salmon’s taxol stabilized microtubules experiment showed that the entire cortex has the ability to generate furrows. This paper further demonstrated that only RacGAP50C is sufficient for ectopic furrowing in cytokinesis. Unfortunately pictures in the paper were very bad. Cannot clearly see the cortical localization of various proteins in those pictures. It was also a hugh shame that aurhors could not demonstrate cortical localizations of other Rho pathway proteins such as Rho and Ect2, although authors did it on anillin and septin.

Centralspindlin’s cortical localization is astral/midzone microtubule dependent. Results from this paper also suggested that those proteins might not involve in the global inhibitory (if it exists). It appeared that anillin was recruited and concentrated to the furrow region. If that is true, RacGAP50C might also involve in the local amplification processes.