AI Article Synopsis
- The cell wall is crucial for fungal survival and disease-causing potential, and the interaction between Sec3 and Rho1 GTPase is important for maintaining cell wall integrity.
- Disruption of the Sec3-Rho1 interaction does not affect cell growth and secretion directly, indicating an unclear physiological role for Sec3.
- Research shows that mutations affecting Sec3's N-terminus lead to defects in cell wall integrity and exocyst localization, suggesting that Sec3 plays a key role in maintaining cell wall stability in yeast, which may also apply to pathogenic fungi.
Article Abstract
The cell wall is essential for cell viability and pathogenesis of fungi. It was previously shown that the exocytosis landmark Sec3 is an effector of the cell wall integrity (CWI) master regulator Rho1 GTPase. However, disruption of the interaction between Sec3 and Rho1 did not inhibit exocytic secretion and cell growth. The physiological role of Sec3 in fungi is unclear. We have examined the growth, cell wall sensitivity, exocyst localization, and exocytic secretion of Sec3-binding deficient rho1 mutants and Rho1-binding deficient sec3 mutants. We found that the Sec3 N-terminal deletion mutant was defective in cell wall integrity. The cells harboring binding mutation between Rho1 and Sec3 N-terminus were sensitive to cell wall antagonists. We also found that the polarized localization of exocyst subunits was disrupted in these mutants. Our study demonstrates that the N-terminus of Sec3 mediates cell wall integrity in yeast. Pathogenic fungi may use similar regulatory mechanisms because components of the exocytic signaling pathways are conserved.
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| http://dx.doi.org/10.1016/j.biochi.2020.07.023 | DOI Listing |
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