OSM-11 Facilitates LIN-12 Notch Signaling during Caenorhabditis elegans Vulval Development (original) (raw)
Figure 7
OSM-11 Acts Synergistically with DSL Ligands and Other DOS Proteins
In (A and B), phenotypes were scored as in Figure 1. (A) Genetic interactions between osm-11 and DOS-motif genes osm-7 and dos-1 (ZK507.4). dos-1(lf) and osm-7(lf) are both presumptive null alleles, and animals harboring these alleles had normal vulvas. dos-1(lf);osm-11(lf) and osm-7(lf);osm-11(lf) animals had significantly more severe defects than osm-11(lf) animals (p < 0.005, χ2 test). Mutant alleles of dos-2 (K10G6.2) and dos-3 (K02F3.7) are not currently available.
(B) Genetic interactions between osm-11 and DSL-domain genes lag-2 and dsl-1. lag-2(dn) is the dominant negative allele sa37; dsl-1(lf) is ok810 and is a presumptive null allele. lag-2(dn) and dsl-1(lf) animals had few or no vulval defects. lag-2(dn);osm-11(lf) and dsl-1(lf);osm-11(lf) animals had significantly more-severe defects that osm-11(lf) animals (p < 0.005, χ2 test).
(C) Vulval precursor cell (VPC) fate analysis for osm-11 and dsl-1. Arrowheads indicate the positions of P5.p, P6.p, and P7.p. Secondary (2°) cell fates were scored as in Figure 3 using lip-1p::GFP as illustrated (right). dsl-1;osm-11 double-mutant animals had significantly more severe 2° fate specification defects compared to either single mutant alone (p < 0.005 by χ2). n ≥ 48 for each genotype in all panels.