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Development, Vol 127, Issue 4 881-892, Copyright © 2000 by Company of Biologists
JOURNAL ARTICLES |
J Andrews, D Garcia-Estefania, I Delon, J Lu, M Mevel-Ninio, A Spierer, F Payre, D Pauli and B Oliver
Laboratory of Cellular and Developmental Biology, NIDDK, National Institutes of Health, Bethesda MD, USA.
OVO controls germline and epidermis differentiation in flies and mice. In the Drosophila germline, alternative OVO-B and OVO-A isoforms have a common DNA-binding domain, but different N-termini. We show that these isoforms are transcription factors with opposite regulatory activities. Using yeast one-hybrid assays, we identified a strong activation domain within a common region and a counteracting repression domain within the OVO-A-specific region. In flies, OVO-B positively regulated the ovarian tumor promoter, while OVO-A was a negative regulator of the ovarian tumor and ovo promoters. OVO-B isoforms supplied ovo(+) function in the female germline and epidermis, while OVO-A isoforms had dominant-negative activity in both tissues. Moreover, elevated expression of OVO-A resulted in maternal-effect lethality while the absence of OVO-A resulted in maternal-effect sterility. Our data indicate that tight regulation of antagonistic OVO-B and OVO-A isoforms is critical for germline formation and differentiation.
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