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Fig. 4. Epidermal defects in sax-3(ky123), vab-1(dx31), and
vab-1(dx31); slt-1(eh15) mutants. Columns from left to right show
ventral, lateral and dorsal views, with the exception of K and L, which are
dorsolateral views. In all panels anterior is to the left. All animals carry
the ajm-1::GFP (jcIs1) epidermal cell marker. (A-C) Wild-type embryo
development. (A) The contralateral epidermal cells meet at the ventral midline
and enclose the embryo (arrows point to the leading cell). (B) The seam cells
are organized in a lateral row of 10 cells (H0, H1, H2, V1-V6, T). (C) The
dorsal epidermal cells fuse to form the hyp 7 syncytium. (D-F) Defects in
sax-3 mutants. (D) One of the left leading cells maintained
inappropriate contact (double arrow) with both leading cells on the opposite
side. The unclosed gastrulation cleft (gc) prevented the pocket cells from
connecting at the ventral midline. (E) The positions of V1 and V3 seam cells
are ventrally shifted (arrows), leading to abnormal seam cell contacts. (F)
One of the dorsal epidermal cells did not fuse with its neighbours and exists
as a single cell within the hyp 7 syncytium (arrowhead). (G-I) Defects in
vab-1 mutants. (G) The unclosed gastrulation cleft (gc) prevented the
leading and pocket cells from enclosing the embryo. (H) V5 is shifted
ventrally, allowing a direct contact of V4 with V6. (I) No defects are
observed for the dorsal epidermis; however, one of the seam cells (V1) is
shifted dorsally (arrow), allowing H2 to contact V2. (J-L) Defects in
vab-1; slt-1 double mutants. (J) The ventral epidermis structure is
drastically disrupted because of the presence of the enlarged gastrulation
cleft (gc). (K) V3 is shifted ventrally (arrow) and the V2 cell makes direct
contact to V4. (L) The shape and position of anterior epidermal cells and seam
cells are drastically changed. Arrows indicate unidentified (?) seam cells
because some appear to fuse to dorsal hyp 7.
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