In the early C. elegans embryo, polarity is established via myosin-dependent contractions that lead to the asymmetric distribution of partitioning-defective (PAR) proteins; PAR-3 and PAR-6, together with the atypical protein kinase C (PKC-3), localize to the anterior cortex, whereas PAR-2 becomes enriched at the posterior cortex. In Drosophila and mammals, PAR-2 is not expressed, but numerous proteins, including Lethal giant larvae (Lgl), act together with the other PAR proteins to establish polarity. Kenneth Kemphues and colleagues (p. 3995) show that the C. elegans homolog of Lgl, LGL-1, functions redundantly with PAR-2 to maintain polarity in the C. elegans embryo. Like PAR-2, LGL-1 localizes to the posterior cortex of the embryo in a PKC-3-dependent manner, and its overexpression is sufficient to rescue loss of PAR-2 function. Importantly, they show that LGL-1 prevents myosin from accumulating in the posterior cortex of the embryo. This provides new insights into the way in which LGL-1 might influence myosin-dependent contractile flows and PAR protein localization, and hence cell polarity.
- © 2010.