Asymmetric cell division is an important mechanism to produce cellular diversity during development. In C. elegans, asymmetric divisions of many cells are regulated by Wnt signaling. In particular, the polarity of the T cell division is controlled by
lin-17/frizzled and
lin-44/wnt. In wild type, the anterior daughter (T.a) of the T cell produces hypodermal cells and the posterior one (T.p) makes neural cells including phasmid socket cells. In
lin-17 mutants, both daughters produce hypodermal cells. To identify genes involved in asymmetric cell divisions, we screened for mutants that lack phasmid socket cells (the phenotype is called Psa for phasmid socket cell absent). We have identified 110 mutants of 55 different genes. To characterize these mutants, we are examining expression and localization of two genes that are regulated by Wnt signaling. In wild type, Expression of
tlp-1::GFP is stronger in the posterior T cell daughter (T.p) than the anterior one (T.a) after the asymmetric division (Zhao et al. 2002). We analyzed
tlp-1::GFP expression in psa mutants of 22 different genes so far that have not cloned or characterized in other studies. 15 mutants showed abnormal expression pattern. One mutants showed reversed expression (higher in T.a than in T.p), 7 showed symmetric expression, while 7 showed weak or not expression. These mutants are probably defective in either polarity of the T cell or transcriptional regulation of the
tlp-1 gene. To identify mutants defective in polarity of the T cell, we are analyzing localization of WRM-1::GFP in mutants that showed abnormal expression of
tlp-1::GFP. In wild type, WRM-1::GFP is localized to the anterior cortex before and during division and to the posterior (T.p) nucleus after the division (Takeshita and Sawa 2005). So far, we observed abnormal localization of WRM-1 in three mutants, suggesting that these mutants are defective in the polarity of the T cell. We will continue the analyses to identify more genes involved in the T cell polarity.