High impact information on bif

• Here we show that Homer and Bifocal act redundantly to promote posterior anchoring of the osk gene products [1].
• Our data suggest that two processes, one requiring Bifocal and an intact F-actin cytoskeleton and a second requiring Homer but independent of intact F-actin, may act redundantly to mediate posterior anchoring of the osk gene products [1].
• Here, we show that Bifocal (Bif), a putative cytoskeletal regulator, is a component of the Msn pathway for regulating R cell growth cone targeting. bif displays strong genetic interaction with msn [2].
• The gene bifocal (bif), required for photoreceptor morphogenesis in the Drosophila compound eye, encodes a protein that is shown to interact with protein phosphatase 1 (PP1) using the yeast two-hybrid system [3].
• In contrast, expression of transgenes encoding the Bif F995A mutant, which disrupts binding to PP1, was unable to rescue any aspect of the bif phenotype [3].

Biological context of bif

• Expression of wild-type bif transgenes resulted in significant rescue of these abnormalities [3].
• The data show that the functions of bif and PP1-87B in either stabilizing R-cell morphology (for Bif) or regulating the cell cycle (for PP1-87B) can be uncoupled from their function in visual axon targeting [4].

Anatomical context of bif

• Null bif mutants exhibit a rough eye phenotype, disorganized rhabdomeres (light-gathering rhodopsin-rich microvillar membrane structures in the photoreceptor cells) and alterations in the actin cytoskeleton [3].
• Roles of Bifocal, Homer, and F-actin in anchoring Oskar to the posterior cortex of Drosophila oocytes [1].

References