139) shows that Notch signaling remodels adherens junctions while cells change shape during development.
Developmental programs generally require plenty of changes in cell shape. In the developing fly oocyte, a set of cells on the posterior end acquire a columnar shape, whereas anterior cells flatten. Notch has been implicated in several aspects of oogenesis in flies. To better dissect its role, Grammont analyzed developing oocytes with somatic clones mutant for Notch signaling.
The clones revealed that Notch activity is necessary for the anterior cells to take on their new flattened shapes at the proper time. Mutant clones were delayed in changing shape. The delays did not stem from differentiation problems, as cell fates were unaffected. Rather, Grammont noted abnormalities in adherens junction remodeling.
In normal developing oocytes, the flattening cells first disassembled their adherens junctions, starting from the anterior end. Junctions linking three cells were the first to go. Next were two-cell junctions linking a cell to its anterior neighbor. Those that lay parallel to the direction of stretching were maintained.
Junction disassembly was delayed in and just around clones that lacked Notch signaling. These enduring linkages probably prevent cells from taking on their new elongated shape.
Grammont's next big task will be to determine exactly how Notch leads to the remodeling. Its ability to activate transcription was required, but the relevant gene targets are not yet known. Possibilities include myosin II, which accumulated at disassembling junctions and was necessary for flattening. Another putative target is E-cadherin, which is removed from dismantling junctions and added to growing junctions along the anterior–posterior axis.