Open AccessSclerotinia sclerotiorum Thioredoxin1 (SsTrx1) is required for pathogenicity and oxidative stress tolerance
Author(s) -
Rana Kusum,
Ding Yijuan,
Banga Surinder S.,
Liao Hongmei,
Zhao Siqi,
Yu Yang,
Qian Wei
Publication year - 2021
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.13127
Subject(s) - sclerotinia sclerotiorum , biology , gene silencing , nicotiana benthamiana , oxidative stress , reactive oxygen species , microbiology and biotechnology , arabidopsis thaliana , rna interference , gene , genetics , botany , mutant , rna , biochemistry
Sclerotinia sclerotiorum infects host plant tissues by inducing necrosis to source nutrients needed for its establishment. Tissue necrosis results from an enhanced generation of reactive oxygen species (ROS) at the site of infection and apoptosis. Pathogens have evolved ROS scavenging mechanisms to withstand host‐induced oxidative damage. However, the genes associated with ROS scavenging pathways are yet to be fully investigated in S. sclerotiorum . We selected the S. sclerotiorum Thioredoxin1 gene ( SsTrx1 ) for our investigations as its expression is significantly induced during S. sclerotiorum infection. RNA interference‐induced silencing of SsTrx1 in S. sclerotiorum affected the hyphal growth rate, mycelial morphology, and sclerotial development under in vitro conditions. These outcomes confirmed the involvement of SsTrx1 in promoting pathogenicity and oxidative stress tolerance of S. sclerotiorum . We next constructed an SsTrx1 ‐based host‐induced gene silencing (HIGS) vector and mobilized it into Arabidopsis thaliana (HIGS‐ A ) and Nicotiana benthamiana (HIGS‐ N ). The disease resistance analysis revealed significantly reduced pathogenicity and disease progression in the transformed genotypes as compared to the nontransformed and empty vector controls. The relative gene expression of SsTrx1 increased under oxidative stress. Taken together, our results show that normal expression of SsTrx1 is crucial for pathogenicity and oxidative stress tolerance of S. sclerotiorum .