RRC ID 70751
Author Huang YC, Chen KH, Chen YY, Tsao LH, Yeh TH, Chen YC, Wu PY, Wang TW, Yu JY.
Title βPS-Integrin acts downstream of Innexin 2 in modulating stretched cell morphogenesis in the Drosophila ovary.
Journal G3 (Bethesda)
Abstract 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 βPS-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 βPS-Integrin is sufficient to induce early StCs flattening. Taken together, our data suggest that βPS-Integrin acts downstream of Innexin 2 in modulating StCs morphogenesis.
Volume 11(9)
Published 2021-9-6
DOI 10.1093/g3journal/jkab215
PII 6310741
PMID 34544125
PMC PMC8496311
MeSH Animals Connexins / genetics Drosophila* / genetics Drosophila Proteins* / genetics Female Integrins Morphogenesis / genetics Ovary
IF 2.781