A novel protein Moat prevents ectopic epithelial folding by limiting Bazooka/Par3-dependent adherens junctions.

IF 3.1 3区 生物学 Q3 CELL BIOLOGY
Molecular Biology of the Cell Pub Date : 2024-08-01 Epub Date: 2024-06-26 DOI:10.1091/mbc.E24-04-0177
Lingkun Gu, Rolin Sauceda, Jasneet Brar, Ferdos Fessahaye, Minsang Joo, Joan Lee, Jacqueline Nguyen, Marissa Teng, Mo Weng
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Abstract

Contractile myosin and cell adhesion work together to induce tissue shape changes, but how they are patterned to achieve diverse morphogenetic outcomes remains unclear. Epithelial folding occurs via apical constriction, mediated by apical contractile myosin engaged with adherens junctions, as in Drosophila ventral furrow formation. While it has been shown that a multicellular gradient of myosin contractility determines folding shape, the impact of multicellular patterning of adherens junction levels on tissue folding is unknown. We identified a novel Drosophila gene moat essential for differential apical constriction and folding behaviors across the ventral epithelium which contains both folding ventral furrow and nonfolding ectodermal anterior midgut (ectoAMG). We show that Moat functions to downregulate polarity-dependent adherens junctions through inhibiting cortical clustering of Bazooka/Par3 proteins. Such downregulation of polarity-dependent junctions is critical for establishing a myosin-dependent pattern of adherens junctions, which in turn mediates differential apical constriction in the ventral epithelium. In moat mutants, abnormally high levels of polarity-dependent junctions promote ectopic apical constriction in cells with low-level contractile myosin, resulting in expansion of infolding from ventral furrow to ectoAMG, and flattening of ventral furrow constriction gradient. Our results demonstrate that tissue-scale distribution of adhesion levels patterns apical constriction and establishes morphogenetic boundaries.

一种新型蛋白质 Moat 可通过限制 Bazooka/Par3 依赖性粘连接头来防止上皮异位折叠。
收缩肌球蛋白和细胞粘附力共同诱导组织形状的改变,但它们是如何形成模式以实现不同的形态发生结果的仍不清楚。上皮折叠是通过顶端收缩发生的,由顶端收缩肌球蛋白与粘连连接介导,如果蝇腹侧沟的形成。虽然已经证明肌球蛋白收缩性的多细胞梯度决定了折叠形状,但粘连接头水平的多细胞模式化对组织折叠的影响尚不清楚。我们发现了一个新的果蝇基因 Moat,该基因对腹侧上皮的不同顶端收缩和折叠行为至关重要,腹侧上皮包含折叠腹沟和非折叠外胚层前中肠(ectoAMG)。我们发现,Moat 的功能是通过抑制 Bazooka/Par3 蛋白的皮层集群来下调极性依赖性粘连接头。这种对极性依赖性连接的下调对于建立肌球蛋白依赖性粘连连接模式至关重要,而这种模式反过来又介导了腹侧上皮细胞不同的顶端收缩。在堑突变体中,异常高水平的极性依赖性连接促进了低水平收缩肌球蛋白细胞的异位顶端收缩,导致从腹侧沟到外侧AMG的折叠扩大,腹侧沟收缩梯度变平。我们的研究结果表明,粘附水平的组织尺度分布会形成顶端收缩,并建立形态发生边界。[媒体:见正文] [媒体:见正文] [媒体:见正文] [媒体:见正文] [媒体:见正文
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Molecular Biology of the Cell
Molecular Biology of the Cell 生物-细胞生物学
CiteScore
6.00
自引率
6.10%
发文量
402
审稿时长
2 months
期刊介绍: MBoC publishes research articles that present conceptual advances of broad interest and significance within all areas of cell, molecular, and developmental biology. We welcome manuscripts that describe advances with applications across topics including but not limited to: cell growth and division; nuclear and cytoskeletal processes; membrane trafficking and autophagy; organelle biology; quantitative cell biology; physical cell biology and mechanobiology; cell signaling; stem cell biology and development; cancer biology; cellular immunology and microbial pathogenesis; cellular neurobiology; prokaryotic cell biology; and cell biology of disease.
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