OSM-11 Facilitates LIN-12 Notch Signaling during Caenorhabditis elegans Vulval Development (original) (raw)
Figure 3
OSM-11 Loss Results in Cell Fate Specification Defects
(A) A simplified diagram of cell fate GFP marker expression in P5.p, P6.p, and P7.p. GFP expression is schematically shown in green. Note that equivalence group members P3.p, P4.p, and P8.p are not shown. In wild-type animals, primary (1°) cell fate markers are expressed in P6.p (top left), whereas secondary (2°) cell fate markers are normally expressed in P5.p and P7.p (top right). The first Pn.p division (by P5.p, P6.p, and P7.p) in mid-L3 larvae gives rise to Pn.px cells; the next divisions give rise to Pn.pxx cells in late-L3 larvae. Loss of Notch signaling does not stop 1° cell fate assumption by P6.p, but results in inappropriate adoption of 1° cell fates by P5.p, P7.p, and their descendents. Loss of EGF/Ras signaling results in adoption of the tertiary fate by P5.p and P7.p, and in some cases, P6.p, depending on the severity of the defect [96].
(B) Quantification of data from (C–E). p < 0.05 based on χ2 for each marker.
(C) Ten percent of L3 osm-11(lf) animals (right) ectopically express the 1° cell fate marker egl-17p::gfp in P5.p or P7.p, which normally adapt the 2° fate (left).
(D) Sixty-seven percent of L3 osm-11(lf) animals lack expression of the 2° cell fate marker lin-11p::gfp in descendants of P5.p and/or P7.p.
(E) Thirty-five percent of L3 osm-11(lf) animals do not up-regulate expression of the 2° fate marker lip-1p::gfp in P5.p and/or P7.p. p < 0.05 based on χ2 for each marker. These data suggest osm-11(lf) animals have a loss of 2° cell fate specification consistent with loss of LIN-12 Notch signaling.
In (C–E), arrowheads indicate the positions of P5.p, P6.p, and P7.p.