An asymmetric pattern of PAR proteins

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Current work in our lab focuses on the conserved PAR polarity network using the nematode worm Caenorhabditis elegans as a model system. Although the PAR network plays essential roles in all animals, including humans, embryos of C. elegans are a particularly good system for investigation. Embryonic development, including the establishment of polarity, is reproducible and rapid. Early developmental stages are accessible to both physical and chemical manipulation as well as live imaging. Moreover, there is a robust set of genetic and RNAi-based tools that allow us to probe PAR protein function in live developing animals.

C. elegans embryo polarization
C. elegans embryo polarization.

Time-lapse images of an embryo undergoing polarisation. Embryos are initially unpolarised with aPARs localised throughout the membrane (e.g. PAR-6, red). Polarisation is induced through a dramatic rearrangement of non-muscle myosin 2 (NMY-2, white), which coincides with the appearance of a posterior domain (PAR-2, cyan). Cortical myosin is then down-regulated, leaving two PAR membrane domains.

The first cell division of C. elegans embryos is highly asymmetric, giving rise to a large anterior somatic cell and a small, posterior, stem-cell like germ cell. The PAR network is essential for both the size and fate asymmetry of this division. For asymmetric cell division to occur, PAR proteins must first segregate within the cell membrane to generate anterior and posterior domains (Figure 1). These domains then signal to the cell interior to trigger both the asymmetric placement of the division site and the partitioning of germ cell determinants into the posterior half of the embryo so that they are unequally inherited at cytokinesis to generate daughter cells with different fates. The goal of our current research is to reveal the physical mechanisms that drive this segregation of PAR proteins within cells