Notch-mediated lateral inhibition is a conserved patterning process that controls alternative cell fate decisions and produces regular cell fate patterns. Prevailing models posit that lateral inhibition singles-out cells from fields of initially equipotent cells by amplifying stochastic fluctuations of Notch or pre-existing fate biases. Here, we revisited the role of Notch in early Drosophila neurogenesis, studying the dynamics of Neuroblast specification by live imaging the transcription of two proneural genes, scute and lethal of scute. We found that proneural gene expression is biased spatially along the dorsal-ventral axis prior to germ band extension and that early proneural expression predicts Neuroblast fate acquisition. This indicated that Neuroblast specification is pre-patterned by positional cues. Additionally, positional cues appeared to instruct individual cells to delaminate in a correct stereotyped pattern in proneural mutant embryos. Finally, contrary to current models, Notch signaling, measured by E(spl)m8 expression, was not detectable within proneural clusters until after Neuroblasts had initiated delamination. This indicated that Notch functions to stabilize rather than initiate fate decisions. We therefore propose that positional cues, not Notch, single-out Neuroblasts during early Drosophila neurogenesis, challenging long-held assumptions about the role of Notch in Neuroblast selection. ### Competing Interest Statement The authors have declared no competing interest. Agence Nationale de la Recherche, ANR-10-LABX-0073 Fondation pour la Recherche MΓ©dicale, FRM-DEQ20180339219
Gastrulation involves multiple, physically-coupled tissue rearrangements. During Drosophila gastrulation, posterior midgut (PMG) invagination promotes both germband extension and hindgut invagination, but whether the normal epithelial rearrangement of PMG invagination is required for morphogenesis o β¦
Convergent extension of epithelial tissue is a key motif of animal morphogenesis. On a coarse scale, cell motion resembles laminar fluid flow; yet in contrast to a fluid, epithelial cells adhere to each other and maintain the tissue layer under actively generated internal tension. To resolve this apparent paradox, we formulate a model in which tissue flow in the tension-dominated regime occurs through adiabatic remodeling of force balance in the network of adherens junctions. We propose that the slow dynamics within the manifold of force-balanced configurations is driven by positive feedback on myosin-generated cytoskeletal tension. Shifting force balance within a tension network causes active cell rearrangements (T1 transitions) resulting in net tissue deformation oriented by initial tension anisotropy. Strikingly, we find that the total extent of tissue deformation depends on the initial cellular packing order. T1s degrade this order so that tissue flow is self-limiting. We explain these findings by showing that coordination of T1s depends on coherence in local tension configurations, quantified by a geometric order parameter in tension space. Our model reproduces the salient tissue- and cell-scale features of germ band elongation during Drosophila gastrulation, in particular the slowdown of tissue flow after approximately twofold longation concomitant with a loss of order in tension configurations. This suggests local cell geometry contains morphogenetic information and yields experimentally testable predictions. Defining biologically controlled active tension dynamics on the manifold of force-balanced states may provide a general approach to the description of morphogenetic flow.
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