Abstract
Drosophila sensory organ precursor cells (SOPs) divide asymmetrically along the anterior-posterior (a-p) body axis to generate two different daughter cells. Planar Cell Polarity (PCP) regulates the a-p orientation of the SOP division. The localization of the PCP proteins Van Gogh (Vang) and Frizzled (Fz) define anterior and posterior apical membrane domains prior to SOP division. Here, we investigate the relative contributions of Vang, Fz and Dishevelled (Dsh), a membrane-associated protein acting downstream of Fz, in orienting SOP polarity. Genetic and live imaging analyses suggest that Dsh restricts the localization of a centrosome-attracting activity to the anterior cortex and that Vang is a target of Dsh in this process. Using a clone border assay, we provide evidence that the Vang and fz genes act redundantly in SOPs to orient its polarity axis in response to extrinsic local PCP cues. Additionally, we find that the activity of Vang is dispensable for the non-autonomous polarizing activity of fz. These observations indicate that both Vang and Fz act as cues for downstream effectors orienting the planar polarity axis of dividing SOPs.
Highlights
Asymmetric cell division is a fundamental and evolutionarily conserved process for generating cell diversity throughout metazoan development
In wild-type SOPs, Partner of Numb (Pon) localizes in a crescent at the anterior cortex during prophase and prometaphase and segregates into the anterior cell at anaphase because the cell division plane is perpendicular to the crescent
While these studies have clearly established a role for Planar Cell Polarity (PCP) genes in orienting asymmetric cell divisions in the notum, the relative roles of the anterior and posterior PCP complexes in orienting the polarity axis were not addressed
Summary
Asymmetric cell division is a fundamental and evolutionarily conserved process for generating cell diversity throughout metazoan development. This process often relies on the unequal segregation of molecules that regulate the fate of the daughter cells (reviewed in [1,2]). The pIIa vs pIIb binary fate decision relies on the unequal segregation of two regulators of Delta/Notch signaling that localize at the anterior cortex of dividing SOPs. The polar localization of these regulators is controlled by the atypical Protein Kinase C (aPKC)Par complex that localizes at the opposite posterior pole [1,2,5]
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