βPS-Integrin acts downstream of Innexin 2 in modulating stretched cell morphogenesis in the Drosophila ovary

Yi Chia Huang, Kuan Han Chen, Yu Yang Chen, Liang Hsuan Tsao, Tsung Han Yeh, Yu Chia Chen, Ping Yen Wu, Tsu Wei Wang, Jenn Yah Yu

研究成果: Article同行評審

2 引文 斯高帕斯(Scopus)

摘要

During oogenesis, a group of specialized follicle cells, known as stretched cells (StCs), flatten drastically from cuboidal to squamous shape. While morphogenesis of epithelia is critical for organogenesis, genes and signaling pathways involved in this process remain to be revealed. In addition to formation of gap junctions for intercellular exchange of small molecules, gap junction proteins form channels or act as adaptor proteins to regulate various cellular behaviors. In invertebrates, gap junction proteins are Innexins. Knockdown of Innexin 2 but not other Innexins expressed in follicle cells attenuates StC morphogenesis. Interestingly, blocking of gap junctions with an inhibitor carbenoxolone does not affect StC morphogenesis, suggesting that Innexin 2 might control StCs flattening in a gap-junction-independent manner. An excessive level of bPS-Integrin encoded by myospheroid is detected in Innexin 2 mutant cells specifically during StC morphogenesis. Simultaneous knockdown of Innexin 2 and myospheroid partially rescues the morphogenetic defect resulted from Innexin 2 knockdown. Furthermore, reduction of bPS-Integrin is sufficient to induce early StCs flattening. Taken together, our data suggest that bPS-Integrin acts downstream of Innexin 2 in modulating StCs morphogenesis.

原文English
文章編號jkab215
期刊G3: Genes, Genomes, Genetics
11
發行號9
DOIs
出版狀態Published - 9月 2021

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