Fig. 2.

Defects observed in lsy-9/nhr-67 mutant animals. (A) lsy-9/nhr-67 regulates ASEL-, ASER-specific and bilateral cell fate markers. Quantification of these data can be found in Table 1. Strains presented from the second row down contain lsy-9(ot85) in the background. Animals were scored as adults. (B) Allelic series of lsy-9 alleles. (C) Apparent L/R reversal defects are caused by a mixture of class I (`2 ASEL') and class III (`no ASE') mutant phenotypes, as revealed by a correlation analysis in which lim-6 (ASEL fate) and ceh-36 (ASEL+ASER bilateral fate) are simultaneously scored with reporter transgenes (lim-6::gfp-otIs114; ceh-36::rfp-otIs151) in a lsy-9(ot85) mutant background. (D) lsy-9/nhr-67 positively regulates expression of the ciliated sensory marker osm-6, as scored with osm-6::gfp (oyIs59). White arrow indicates presence or absence of osm-6 expression in ASE, which was identified by its location relative to surrounding amphid sensory cells. Nomarski image indicates that the ASE nucleus is still present, immediately posterior to ASH. (E) lsy-9/nhr-67 does not affect expression of the pan-neuronal marker F25B3.3. Colored dots indicate cell types as in D. D, dorsal; V, ventral; A, anterior; P, posterior.