The Small GTPase CsRAC1 Is Important for Fungal Development and Pepper Anthracnose in

The pepper anthracnose fungus, Colletotrichum scovillei, causes severe losses of pepper fruit production in the tropical and temperate zones. RAC1 is a highly conserved small GTP-binding protein in the Rho GT-Pase family. This protein has been demonstrated to play a role in fungal development, and p...

Full description

Saved in:
Bibliographic Details
Published inThe plant pathology journal Vol. 37; no. 6; pp. 607 - 618
Main Authors Noh-Hyun Lee, Teng Fu, Jong-Hwan Shin, Yong-Won Song, Dong-Cheol Jang, Kyoung Su Kim
Format Journal Article
LanguageEnglish
Published Hanrimwon Publishing Company 01.12.2021
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The pepper anthracnose fungus, Colletotrichum scovillei, causes severe losses of pepper fruit production in the tropical and temperate zones. RAC1 is a highly conserved small GTP-binding protein in the Rho GT-Pase family. This protein has been demonstrated to play a role in fungal development, and pathogenicity in several plant pathogenic fungi. However, the functional roles of RAC1 are not characterized in C. scovillei causing anthracnose on pepper fruits. Here, we generated a deletion mutant (ΔCsrac1) via homologous recombination to investigate the functional roles of CsRAC1. The ΔCsrac1 showed pleiotropic defects in fungal growth and developments, including vegetative growth, conidiogenesis, conidial germination and appressorium formation, compared to wild-type. Although ΔCsrac1 was able to develop appressoria, it failed to differentiate appressorium pegs. However, ΔCsrac1 still caused anthracnose disease with significantly reduced rate on wounded pepper fruits. Further analyses revealed that ΔCsrac1 was defective in tolerance to oxidative stress and suppression of host-defense genes. Taken together, our results suggest that CsRAC1 plays essential roles in fungal development and pathogenicity in C. scovillei-pepper fruit pathosystem.
ISSN:1598-2254
2093-9280
DOI:10.5423/PPJ.OA.09.2021.0140