Follicle cell contact maintains main body axis polarity in the Drosophila melanogaster oocyte
In Drosophila melanogaster the anterior-posterior body axis is maternally established and governed by differential localization of partitioning defective (Par) proteins within the oocyte. At mid-oogenesis, Par-1 accumulates at the posterior end of the oocyte while Par-3/Bazooka is excluded there but maintains its localization along the remaining oocyte cortex. This mutual exclusion leads to a polarized microtubule network and accumulation of posterior determinant oskar later in oogenesis. Reciprocal biochemical interactions between Par proteins can explain their cortical exclusion and domain formation - for example, Par-1 excludes Par-3 by phosphorylation. However, past studies have proposed the need for somatic cells at the posterior end to initiate oocyte polarization by providing a trigger signal. To date, despite modern screening approaches and genetic manipulation, neither the molecular identity nor the nature of the signal is known. Here, we provide the first evidence that mechanical contact of posterior follicle cells (PFCs) with the oocyte cortex causes the posterior exclusion of Bazooka and maintains oocyte polarity. We show that Bazooka prematurely accumulates exclusively where posterior follicle cells have been mechanically detached or ablated. This occurs before Par-1 is removed suggesting that phosphorylation of Bazooka by Par-1 is not sufficient to maintain Bazooka exclusion in the absence of PFC contact. Furthermore, we provide evidence that PFC contact maintains Par-1 and oskar localization and microtubule cytoskeleton polarity in the oocyte. Our observations suggest that cell-cell contact mechanics modulates Par protein binding sites at the oocyte cortex.