Fig 11. Intestinal morphogenesis defects in
efn-4,
mab-20, and
sax-3 mutant embryos. (A-B) Intestine primordium in
sax-3 mutant embryos; theseembryos express only the general membrane reporter (red). Panel A shows dorsal and ventral sides of the E20 primordium; note that the second ringconsists of three cells (2R, 3R, and 2L). The
int3 and
int4 rings rotated, but 2R stalled at the RaL contact between 3R and 1LD. Panel B shows a transverse view of an improperly oriented
int1 ring. Both R and L cells in the
int1 ring contact
bz1 in most wild-type embryos (78%, n = 32) and in most
sax-3 mutant embryos (63%, n = 33). The wild-type R or L cells can cover most or all of
bz1 in the remaining embryos, but never extend beyond
bz1 (0/32). By contrast, R cells extended past
bz1 in 14% of the
sax-3 mutant embryos. (C) Transverse projections through successive int rings in an
efn-4 mutant embryo; note that the second int ring contains three cells. (D) Left lateral view of a
mab-20 embryo showing four cells in the second int ring (3R, 3L, 2L, and 2R). (E) Dorsal view of the primordium in an
efn-4 mutant embryo. 2R intercalation stalled when 1R divided, as in wild-type embryos. However, 2R failed to resume intercalation and instead retracted. (F)
efn-4 mutant embryo expressing an
end-1::GFP transgene from a non-integrated array. The mosaic expression in 2R shows a persistent lateral protrusion (arrow) between 1RD and 3R, but a failure in
int2 intercalation/closure. (G) Early stages of the intestine primordium in a
mab-20 mutant embryo showing the normal pre-rotation shift of 2L (30/31 embryos) and normal RaL asymmetry (23/25 embryos). (H) EFN-4-GFP expression. The panel at left shows expression in the
int2,
int5,and
int8 cells before
int5 intercalation, and the panel at right shows the lack of intestinal expression at later stages. The asterisk indicates EFN-4-GFP accumulation outside the embryo, but within the eggshell. Panels = A,F [JJ2517], B,D [JJ2486], C,G [JJ2583], H[JJ2502]. Bars = 5 microns.