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Journal Article

Thioredoxins are involved in the activation of the PMK1 MAP kinase pathway during appressorium penetration and invasive growth in Magnaporthe oryzae

Shijie Zhang; Cong Jiang; Qiang Zhang; Linlu Qi; Chaohui Li; Jin‐Rong Xu
Environmental Microbiology · Vol. 18, Issue 11 · pp. 3768-3784 · 2016

Abstract

Summary In Magnaporthe oryzae , the Mst11‐Mst7‐Pmk1 MAP kinase pathway is essential for appressorium formation and invasive growth. To determine their roles in Pmk1 activation and plant infection, we characterized the two thioredoxin genes, TRX1 and TRX2 , in M. oryzae . Whereas the Δ trx1 mutants had no detectable phenotypes, deletion of TRX2 caused pleiotropic defects in growth, conidiation, light sensing, responses to stresses and plant infection progresses. The Δ trx1 Δ trx2 double mutant had more severe defects than the Δ trx2 mutant and was non‐pathogenic in infection assays. The Δ trx2 and Δ trx1 Δ trx2 mutant rarely formed appressoria on hyphal tips and were defective in invasive growth after penetration. Pmk1 phosphorylation was barely detectable in the Δ trx2 and Δ trx1 Δ trx2 mutants. Deletion of TRX2 affected proper folding or intra‐/inter‐molecular interaction of Mst7 and expression of the dominant active MST7 allele partially rescued the defects of the Δ trx1 Δ trx2 mutant. Furthermore, Cys305 is important for Mst7 function and Trx2 directly interacts with Mst7 in co‐IP assays. Our data indicated that thioredoxins play important roles in intra‐cellular ROS signalling and pathogenesis in M. oryzae . As the predominant thioredoxin gene, TRX2 may regulate the activation of Pmk1 MAPK via its effects on Mst7.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2016-11-01
Publication Year2016
Volume18
Issue11
Pages3768-3784
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.13315
SubjectMicrobial Ecology

Access Information

NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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