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.