During development, forces transmitted between cells are critical for sculpting epithelial tissues. Actomyosin contractility in the middle of the cell apex (medioapical) can change cell shape (e.g., apical constriction) but can also result in force transmission between cells via attachments to adherens junctions. How actomyosin networks maintain attachments to adherens junctions under tension is poorly understood. Here, we discovered that microtubules promote actomyosin intercellular attachments in epithelia during Drosophila melanogaster mesoderm invagination. First, we used live imaging to show a novel arrangement of the microtubule cytoskeleton during apical constriction: medioapical Patronin (CAMSAP) foci formed by actomyosin contraction organized an apical noncentrosomal microtubule network. Microtubules were required for mesoderm invagination but were not necessary for initiating apical contractility or adherens junction assembly. Instead, microtubules promoted connections between medioapical actomyosin and adherens junctions. These results delineate a role for coordination between actin and microtubule cytoskeletal systems in intercellular force transmission during tissue morphogenesis.
1During development, coordinated cell shape changes and cell divisions sculpt 2 tissues. While these individual cell behaviors have been extensively studied, how cell 3 shape changes and cell divisions that occur concurrently in epithelia influence tissue 4 shape is less understood. We addressed this question in two contexts of the early 5Drosophila embryo: premature cell division during mesoderm invagination, and native 6 ectodermal cell divisions with ectopic activation of apical contractility. Using quantitative 7 live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by 8 interfering with medioapical RhoA signaling. While premature mitotic entry inhibits 9 mesoderm invagination, which relies on apical constriction, mitotic entry in an artificially 10 contractile ectoderm induced ectopic tissue invaginations. Ectopic invaginations 11 resulted from medioapical myosin loss in neighboring mitotic cells. This myosin loss 12 enabled non-mitotic cells to apically constrict through mitotic cell stretching. Thus, the 13 spatial pattern of mitotic entry can differentially regulate tissue shape through signal 14 interference between apical contractility and mitosis. 15To determine whether loss of medioapical myosin was a general feature of 131 dividing, contractile epithelial cells, we took advantage of the stereotyped cell divisions 132 in the early mitotic domains that occur on the dorsal side of the head (Foe, 1989), 133 particularly focusing on mitotic domains 1 and 5 ( Figure 2C). We artificially increased 134 ectoderm apical contractility by ectopically expressing folded gastrulation (fog), a ligand 135 for a G-protein-coupled receptor (GPCR) that is expressed in the mesoderm and 136 functions upstream of apical myosin activation (Costa et al., 1994; Dawes-Hoang et al., 137 ,-.
Cell divisions can either promote or inhibit tissue morphogenesis. In contractile epithelia, mitotic entry disrupts medioapical myosin activation and reverses apical constriction. We found that different spatiotemporal patterns of mitotic entry and the resultant changes in force generation at the tissue level dictate distinct tissue shape outcomes.
Proper cell-type identity relies on highly coordinated regulation of gene expression. Regulatory elements such as enhancers can produce cell type-specific expression patterns, but the mechanisms underlying specificity are not well understood. We previously identified an enhancer region capable of driving specific expression in giant cells, which are large, highly endoreduplicated cells in the Arabidopsis thaliana sepal epidermis. In this study, we use the giant cell enhancer as a model to understand the regulatory logic that promotes cell type-specific expression. Our dissection of the enhancer revealed that giant cell specificity is mediated primarily through the combination of two activators and one repressor. HD-ZIP and TCP transcription factors are involved in the activation of expression throughout the epidermis. High expression of HD-ZIP transcription factor genes in giant cells promoted higher expression driven by the enhancer in giant cells. Dof transcription factors repressed the activity of the enhancer such that only giant cells have higher expression levels driven by the enhancer. Thus, our data are consistent with a conceptual model whereby cell type-specific expression emerges from the combined activities of three transcription factor families activating and repressing expression in epidermal cells.
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