High impact information on pUf68

• A new study from the Schüpbach lab implicates a splicing factor, Half-pint, in the regulation of oogenesis in Drosophila [1].
• Half-pint: alternative splicing in the Drosophila ovary [1].
• Consistent with this, the cycle 14 G2-arrest of stg mutant embryos is rescued by the hfp mutant [2].
• Here we show that Half pint (Hfp), the Drosophila orthologue of FIR, inhibits cell proliferation in Drosophila [2].
• In particular, hfp mutants display striking defects in the developmentally regulated splicing of ovarian tumor (otu) [3].

Biological context of pUf68

• Here we describe a factor, Half pint (Hfp), that regulates RNA splicing in Drosophila [3].
• Females harboring hypomorphic mutations in hfp lay short eggs and show defects in germline mitosis, nuclear morphology, and RNA localization during oogenesis [3].
• Furthermore, transgenic expression of the missing otu splice form can rescue the ovarian phenotypes of hfp [3].

References