No abstract

Apical-basal polarity is a hallmark of epithelia and needs to be remodeled when epithelial cells undergo morphogenetic cell movements. Here, we analyze border cells in the ovary to address how apical-basal polarity is remodeled and turned into front-back and inside-outside as well as apical-basal polarities, during collective migration. We find that the Crumbs (Crb) complex is required for the generation of the three distinct but interconnected cell polarities of border cells. Specifically, the Crb complex, together with the Par complex and the endocytic recycling machinery, ensures the strict distribution of two distinct populations of aPKC at the inside apical junction and near the outside lateral membrane. Interestingly, aPKC distributed near the outside lateral membrane interacts with Sif and promotes Rac-induced protrusions, whereas alteration of the aPKC distribution pattern changes the pattern of protrusion formation, leading to disruption of all three polarities. Therefore, we demonstrate that aPKC, spatially controlled by the Crb complex, is a key polarity molecule coordinating the generation of three distinct but interconnected cell polarities during collective migration.

No abstract

The ability to repeatedly regenerate limbs during the entire lifespan of an animal is restricted to certain salamander species among vertebrates. This ability involves dedifferentiation of post-mitotic cells into progenitors that in turn form new structures. A long-term enigma has been how injury leads to dedifferentiation. Here we show that skeletal muscle dedifferentiation during newt limb regeneration depends on a programmed cell death response by myofibres. We find that programmed cell death-induced muscle fragmentation produces a population of ‘undead’ intermediate cells, which have the capacity to resume proliferation and contribute to muscle regeneration. We demonstrate the derivation of proliferating progeny from differentiated, multinucleated muscle cells by first inducing and subsequently intercepting a programmed cell death response. We conclude that cell survival may be manifested by the production of a dedifferentiated cell with broader potential and that the diversion of a programmed cell death response is an instrument to achieve dedifferentiation.