Apoptosis
signaling in response to
DNA damage
The Drosophila melanogaster
anterior-posterior axis becomes polarized early during oogenesis by the
posterior localization of the oocyte within the egg chamber. The invariant
position of the oocyte is thought to be driven by an upregulation of the
adhesion molecule DE-cadherin in the oocyte and the posterior somatic follicle
cells, providing the first in vivo example of cell sorting that is specified by
quantitative differences in cell-cell adhesion. However, it has remained
unclear how DE-cadherin levels are regulated. Here, we show that talin, known
for its role in linking integrins to the actin cytoskeleton, has the unexpected
function of specifically inhibiting DE-cadherin transcription. Follicle cells
that are mutant for talin show a strikingly high level of DE-cadherin, due to
elevated transcription of DE-cadherin. We demonstrate that this deregulation of
DE-cadherin is sufficient to attract the oocyte to lateral and anterior
positions. Surprisingly, this function of talin is independent of integrins.
These results uncover a new role for talin in regulating cadherin-mediated cell
adhesion.
