Phosphatidylserine and GTPase activation control Cdc42 nanoclustering to counter dissipative diffusion
MBoC. 2018-06-01; 29(11): 1299-1310
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1. Mol Biol Cell. 2018 Jun 1;29(11):1299-1310. doi: 10.1091/mbc.E18-01-0051. Epub
2018 Apr 18.
Phosphatidylserine and GTPase activation control Cdc42 nanoclustering to counter
Sartorel E(1), Ünlü C(1), Jose M(1), Massoni-Laporte A(1), Meca J(1), Sibarita
JB(2)(3), McCusker D(1).
(1)Université Bordeaux, CNRS, UMR 5095, European Institute of Chemistry and
Biology, Pessac 33607, France.
(2)Université Bordeaux, Institut Interdisciplinaire de Neurosciences, Bordeaux
(3)CNRS UMR 5297, Institut Interdisciplinaire de Neurosciences, Bordeaux 33077,
The anisotropic organization of plasma membrane constituents is indicative of
mechanisms that drive the membrane away from equilibrium. However, defining these
mechanisms is challenging due to the short spatiotemporal scales at which
diffusion operates. Here, we use high-density single protein tracking combined
with photoactivation localization microscopy (sptPALM) to monitor Cdc42 in
budding yeast, a system in which Cdc42 exhibits anisotropic organization. Cdc42
exhibited reduced mobility at the cell pole, where it was organized in
nanoclusters. The Cdc42 nanoclusters were larger at the cell pole than those
observed elsewhere in the cell. These features were exacerbated in cells
expressing Cdc42-GTP, and were dependent on the scaffold Bem1, which contributed
to the range of mobility and nanocluster size exhibited by Cdc42. The lipid
environment, in particular phosphatidylserine levels, also played a role in
regulating Cdc42 nanoclustering. These studies reveal how the mobility of a Rho
GTPase is controlled to counter the depletive effects of diffusion, thus
stabilizing Cdc42 on the plasma membrane and sustaining cell polarity.
PMID: 29668348 [Indexed for MEDLINE]