Abstract

Integrin signaling relies on multiple, distinct pathways to impact a diverse set of cell behaviors. The Rho family of GTPases are well-established downstream signaling partners of integrins that regulate cell shape, polarity, and migration. The nematode C. elegans provides a simple in vivo system for studying both integrins and the Rho family. Our previous work showed that the C. elegans α integrin cytoplasmic tails have tissue-specific functions during development. Here, we use chimeric α integrins to show that the cytoplasmic tails can rescue the loss of the Rho family of GTPases in three cell types in the somatic gonad. Knockdown of rho-1 by RNAi causes defects in sheath cell actin organization, ovulation, and vulva morphology. Chimeric α integrin ina-1 with the pat-2 cytoplasmic tail can rescue both actin organization and ovulation after rho-1 RNAi, yet cannot restore vulva morphology. Knockdown of cdc-42 by RNAi causes defects in sheath cell actin organization, ovulation, vulva morphology, and distal tip cell migration. Chimeric α integrin pat-2 with the ina-1 cytoplasmic tail can rescue vulva morphology defects and distal tip cell migration after cdc-42 RNAi, yet cannot restore sheath cell actin organization or ovulation. Disruption of Rac yields the same phenotype in distal tip cells regardless of α integrin cytoplasmic tail composition. Taken together, the cytoplasmic tails of α integrins can bypass signaling from members of the Rho family of GTPases during development.

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