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Fig. 1. Ectopic Bcd induces hb transcription in pole cells.
Co-immunostaining of embryos with anti-ß-galactosidase (red) and
anti-Vasa (green) antibodies. The anti-Vasa antibody is used to mark pole
cells. (A,C,E) Anti-ß-galactosidase staining alone. (B,D,F) Merged images
of anti-ß-galactosidase and anti-Vasa staining. (A,B) Embryos produced by
wild-type females mated to males carrying the hb:lacZ reporter
transgene. ß-galactosidase can be detected in somatic cells of wild-type
blastoderm embryos in an anterior cap (not shown) and a posterior stripe
(asterisk at posterior boundary); however, there is no evidence of
ß-galactosidase expression in the pole cells. (C,D) Embryos produced by
bcd nos3'UTR females mated with males carrying the
hb:lacZ reporter transgene. Anti-ß-galactosidase staining
reveals expression of the hb:lacZ reporter in pole cells of
bcd-nos3'UTR embryos (yellow in D). As is evident
here, expression of hb:lacZ is also detected in somatic cells at the
posterior in some bcd-nos3'UTR embryos. In this
respect, the hb:lacZ transgene differs from the endogenous
hb gene as little if any Hb protein is detected in the posterior soma
of bcd-nos3'UTR embryos. It seems likely that we are
able to detect a low level of ß-galactosidase because this protein is
much more stable than Hb. (E,F) Embryos produced by tsl mutant,
bcd-nos3'UTR females mated with males carrying the
hb:lacZ transgene. ß-Galactosidase is no longer detected in pole
cells in the absence of tsl function. Indicative of the tsl
mutation, the posterior boundary of the posterior hb stripe
(asterisk) shifts anteriorly.
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