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The Edwardsiella T3SS effector EseQ promotes invasion by altering the cell’s cytoskeleton and disrupting the epithelial barrier
The Edwardsiella T3SS effector EseQ promotes invasion by altering the cell’s cytoskeleton and disrupting the epithelial barrier
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The Edwardsiella T3SS effector EseQ promotes invasion by altering the cell’s cytoskeleton and disrupting the epithelial barrier
The Edwardsiella T3SS effector EseQ promotes invasion by altering the cell’s cytoskeleton and disrupting the epithelial barrier

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The Edwardsiella T3SS effector EseQ promotes invasion by altering the cell’s cytoskeleton and disrupting the epithelial barrier
The Edwardsiella T3SS effector EseQ promotes invasion by altering the cell’s cytoskeleton and disrupting the epithelial barrier
Journal Article

The Edwardsiella T3SS effector EseQ promotes invasion by altering the cell’s cytoskeleton and disrupting the epithelial barrier

2025
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Overview
Edwardsiella piscicida causes severe hemorrhagic septicemia in marine and freshwater fish worldwide, resulting in significant economic losses for the aquaculture industry (K. Y. Leung, Q. Wang, Z. Yang, and B. A. Siame, Virulence 10:555–567, 2019, https://doi.org/10.1080/21505594.2019.1621648 ). Our previous research identified a novel type III secretion system effector, EseQ, in E. piscicida whose function remains to be elucidated. In this work, we showed that EseQ binds to tubulin and GEF-H1 and destabilizes microtubules. GEF-H1 released from microtubules activates the RhoA-ROCK-MLCII signaling pathway, leading to stress fiber formation in epithelial cells. EseQ deforms the epithelial barrier and promotes E. piscicida ’s invasion in a stress fiber-dependent manner. This work contributes to the understanding of the mechanism by which E. piscicida invades host cells.