Abstract
The necrotrophic fungal pathogen Alternaria alternata attacks many citrus species, causing brown spot disease. Its pathogenic capability depends primarily on the production of host-selective ACT toxin. In the current study a Ste12 transcription factor was characterized to be required for conidial formation and the production of cell-wall-degrading enzymes (CWDEs) in the tangerine pathotype of A. alternata. The Ste12 deficiency strain (ΔSte12) retained wild-type growth, ACT toxin production, and sensitivity to oxidative and osmotic stress. However, pathogenicity tests assayed on detached Dancy leaves revealed a marked reduction in virulence of ΔSte12. Transcriptome and quantitative RT-PCR analyses revealed that many genes associated with Carbohydrate-Active Enzymes (CAZymes) were downregulated in ΔSte12. Two cutinase-coding genes (AaCut3 and AaCut7) regulated by Ste12 were individually and simultaneously inactivated. The AaCut3 or AaCut7 deficiency strain unchanged in cutinase activities and incited wild-type lesions on Dancy leaves. However, the strain carrying an AaCut3 AaCut7 double mutation produced and secreted significantly fewer cutinases and incited smaller necrotic lesions than wild type. Not only is the host-selective toxin (HST) produced by A. alternata required for fungal penetration and lesion formation, but so too are CWDEs required for full virulence. Overall, this study expands our understanding of how A. alternata overcomes citrus physical barriers to carry out successful penetration and colonization.
Highlights
Plant pathogenic fungi utilize a wide range of arsenals to penetrate and colonize their hosts
alternata Ste12 gene (AaSte12) sequence was retrieved from completely sequenced genome of A. alternata
Transformation of a functional copy of AaSte12 translationally fused with GFP under control of its endogenous promoter (AaSte12:GFP:neo) into protoplasts prepared from Ste12-B identified a te12 strain that restored conidial formation at levels similar to that of wild type
Summary
Plant pathogenic fungi utilize a wide range of arsenals to penetrate and colonize their hosts. Toxins and cell-wall-degrading enzymes (CWDEs) are the two most common weapons utilized by fungal necrotrophs to attack host plants. In addition to ACT toxin, previous studies have demonstrated that the ability to detoxify toxic reactive oxygen species (ROS) is critical to colonize host tissue. Several factors or pathways required for ROS detoxification have been identified in A. alternata. Those include the glutaredoxin/thioredoxin systems, the Yap transcription factor, the Skn response regulator, the NADPH oxidase-mediated H2O2 production, the siderophore-mediated iron homeostasis, methionine biosynthesis regulator, and the Hog mitogen-activated protein kinase (MAPK)-mediated pathway (Yang and Chung, 2013; Chung, 2014; Yang et al, 2016; Ma et al, 2018; Gai et al, 2019)
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