Biology

Dr. Sachin Kotak
Department of Microbiology and Cell Biology (MCB) Indian Institute of Science (IISc), Bangalore

Abstract:

The proper establishment of the cell polarity is essential for development and morphogenesis. C. elegans one-cell stage embryo has proven to be an important model for characterizing the molecular determinants of polarity establishment. In this system, a centrosome-localized signal provides spatial information that is responsible for generating a single polarity axis. It is hypothesized that such a signal causes local inhibition of cortical actomyosin network in the vicinity of the centrosome. This pivotal event initiates symmetry breaking to direct partitioning of the partition defective proteins (PARs) in the one-cell embryo. However, the molecular nature of the centrosome regulated signal that impinges on the posterior cortex to bring upon cortical anisotropy in the actomyosin network and to promote polarity establishment remains elusive. Here, we discover that depletion of Aurora A kinase (AIR-1 in C. elegans; and referred to as Aurora A) causes pronounced cortical contractions on the entire embryo surface during polarity establishment phase, and this creates more than one PAR-2 polarity axis. Notably, we reveal this function of Aurora A is independent of its role in centrosomes maturation. Notably, we show that in the absence of Aurora A, centrosome positioning becomes dispensable in dictating the PAR-2 polarity axis. Interestingly, we identify that Rho Guanine Exchange Factor (GEF) ECT-2 acts downstream to Aurora A to control excess contractility and notably Aurora A loss affects ECT-2 cortical localization and thereby polarity establishment. Overall, our study unravels a novel insight whereby an evolutionarily conserved Aurora A kinase inhibits promiscuous PAR-2 domain formation to ensure only single polarity axis establishes during embryogenesis.