Regulation of cell contacts and cell shape during mouth formation in Caenorhabditis elegans

秀丽隐杆线虫的口腔形成代表了细胞行为、形状和细胞接触的一系列协调一致的变化，这些变化的机制尚未得到很好的理解。我们发现口腔的形成是由大约50个神经外胚层细胞的形状改变和内陷引起的。这些过程导致形成一个短暂的孔，逐渐连接到前肠腔。我们观察到，最初的细胞接触特征是指间突起和缺乏根尖连接，而神经外胚层细胞内陷。因此，内陷细胞似乎在顶端收缩的同时形成了顶端连接。这表明细胞接触的动态调节在口腔形成中起着核心作用。我们将进行细胞分割以及皮质，连接和细胞粘附动力学的跟踪和定量分析，以剖析顶端收缩和连接形成的功能关系。此外，顶端收缩是在8个由4到6个细胞组成的小集群中开始的，这些细胞会聚成一个连续的孔。但趋同的机制尚不清楚。我们发现神经外胚层需要保守的Ets转录因子AST-1/Etv1/ER81来维持根尖收缩。我们将讨论AST-1在口形成过程中调节簇形成和收敛的作用。

Mouth formation in C. elegans represents a concerted series of changes in cell behaviour, shape and cell contacts that are not well understood mechanistically. We found that mouth formation is initiated by cell shape changes and invagination of approximately 50 cells from the neuroectoderm. These processes lead to the formation of a transient pore which gradually connects to the foregut lumen. We observe that the initial cell contacts characterised by interdigitated protrusions and absence of apical junctions are transformed into apical junctions, while neuroectodermal cells invaginate. Thus, invaginating cells seem to apically constrict while apical junctions form simultaneously. This suggests that the dynamic regulation of cell contacts plays a central role in mouth formation. We will perform cell segmentation as well as tracking and quantitative analysis of cortical, junctional, and cell adhesion dynamics to dissect the functional relationship of apical constriction and junction formation. Moreover, apical constriction is initiated in eight small clusters of four to six cells that converge into a continuous pore. But the mechanism of convergence is unknown. We found that neuroectoderm requires the conserved Ets transcription factor AST-1/Etv1/ER81 for maintenance of apical constriction. We will address the role of AST-1 in regulating cluster formation and convergence during mouth formation.