OVO transcription factors function antagonistically in the Drosophila female germline

Abstract

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.

Genomic signatures of recent convergent transitions to social life in spiders

“…For example, the gene lilipod (lili), which experienced intensified selection in social spiders, promotes self-renewal of germline stem cells during oogenesis in fly 74 . The gene transcriptional regulator ovo (ovo), which also experienced intensification in social spiders, regulates female germline development in mouse and fly [75][76][77] . Moreover, genes under relaxation of selection were significantly enriched for GO terms associated with reproduction and development, which could be tightly associated with the shifts in breeding system and sociality in social spiders.…”

Steroid‐dependent switch of OvoL/Shavenbaby controls self‐renewal versus differentiation of intestinal stem cells

“…OvoB is required for the maintenance of germ cells, while OvoA later acts for their differentiation (Andrews et al , 2000; Hayashi et al , 2017). Precocious expression of OvoA leads to germ line loss (Andrews et al , 2000) and other ovo mutations cause ovarian tumors (Oliver et al , 1993). Although relying on different mechanisms between soma (post‐translational processing) and germline (alternative promoters), the REP‐to‐ACT switch appears as a key feature of Ovo/Svb function in the control of stem/progenitor cells.…”

“…ovo / svb is also critical for maintenance and differentiation of the germline (Mevel‐Ninio et al , 1995). There are two Svb germline‐specific isoforms, called OvoA and OvoB, which are insensitive to Pri peptides (Kondo et al , 2010) and act as constitutive repressor and activator (Andrews et al , 2000), respectively. Throughout development, the production of Svb ACT in somatic tissues is triggered by periodic peaks of ecdysone, the main steroid hormone in insects.…”

Hippo pathway and Bonus control developmental cell fate decisions in the Drosophila eye

“…We tested if Svb/Ovo was involved in the regulation of Bon- and Yki-induced trichomes in adult eyes. Overexpression of the constitutive activator OvoB enhanced Bon and Yki-S168A induced trichomes, while overexpression of the constitutive repressor OvoA, or knockdown of somatic svb , strongly suppressed Bon- and Yki-S168A-induced trichomes (Figures 5F, 5K-L, and S5B-C) (Andrews et al, 2000). These results suggest that Svb/Ovo is required for ectopic trichome generation in the eye induced by Bon or Yki.…”