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Fig. 7. Epidermal cell apoptosis in spitz group mutants causes denticle
belt fusions. (A-D) Apoptosis of ventral epidermal cells was greatly elevated
in spitz null embryos compared to wild-type or balanced embryos
carrying one null copy of spitz. The ventral surface is shown for
each embryo, with anterior being up in all images. Homozygous spitz
null embryos were marked by the absence of Engrailed/ß-galactosidase
staining (in red), and apoptotic cells were detected by TUNEL labelling (in
green). Although epidermal apoptosis was elevated as early as stage 10/11 (A),
apoptosis in stage 13/14 spitz null embryos was much stronger,
particularly in medial regions (B). Note that these spitz null
embryos display the strongest fusion phenotype of any spitz group
mutants (Fig. 4A,B). (C)
Removing the three main apoptosis activators (grim, reaper, hid)
using the H99 deletion (White et
al., 1994) suppressed the fusion phenotype of rhomboid-3
rhomboid-1 double mutant embryos, but did not eliminate it completely. It
should be noted that some apoptosis has been observed in the absence of these
genes (Foley and Cooley,
1998). (D) No additional phenotypes were detected in
smooth-cuticle cells of rhomboid-3 rhomboid-1 double mutant embryos
partially blocked for apoptosis by virtue of the H99 deletion.
Unexpectedly, the entire A4 denticle belt was frequently missing in these
embryos.
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