A Signaling-Regulated, Short-Chain Dehydrogenase of Stagonospora nodorum Regulates Asexual Development

Abstract

The fungus Stagonospora nodorum is a causal agent of leaf and glume blotch disease of wheat. It has been previously shown that inactivation of heterotrimeric G protein signaling in Stagonospora nodorum caused development defects and reduced pathogenicity [P. S. Solomon et al., Mol. Plant-Microbe Interact. 17: [456][457][458][459][460][461][462][463][464][465][466] 2004]. In this study, we sought to identify targets of the signaling pathway that may have contributed to phenotypic defects of the signaling mutants. A comparative analysis of Stagonospora nodorum wild-type and G␣-defective mutant (gna1) intracellular proteomes was performed via two-dimensional polyacrylamide gel electrophoresis. Several proteins showed significantly altered abundances when comparing the two strains. One such protein, the short-chain dehydrogenase Sch1, was 18-fold less abundant in the gna1 strain, implying that it is positively regulated by G␣ signaling. Gene expression and transcriptional enhanced green fluorescent protein fusion analyses of Sch1 indicates strong expression during asexual development. Mutant strains of Stagonospora nodorum lacking Sch1 demonstrated poor growth on minimal media and exhibited a significant reduction in asexual sporulation on all growth media examined. Detailed histological experiments on sch1 pycnidia revealed that the gene is required for the differentiation of the subparietal layers of asexual pycnidia resulting in a significant reduction in both pycnidiospore size and numbers.

The Transcription Factor StuA Regulates Central Carbon Metabolism, Mycotoxin Production, and Effector Gene Expression in the Wheat Pathogen Stagonospora nodorum

“…Various signaling genes have also been shown to be required for sporulation (24,26,30). The short-chain dehydrogenase Sch1 was recently demonstrated to have a role in the structural formation of the pycnidia (31). Strains of S. nodorum lacking sch1 surprisingly produced vast quantities of the mycotoxin alternariol, although this appeared to be not related to the mutant's inability to sporulate (32).…”

Metabolite profiling identifies the mycotoxin alternariol in the pathogen Stagonospora nodorum

“…Surprisingly, the synthesis of alternariol in vivo is poorly understood with none of the genes involved yet to be identified. Sch1 is a short chain dehydrogenase of unknown function but has a demonstrated role in maturation of asexual sporulation structures known as pycnidia (Tan et al, 2008). At this point, it is difficult to comment on putative roles of Sch1 apart from speculating on its role as a potential negative regulator of alternariol production.…”

“…nodorum wild-type SN15 was obtained from Department of Agriculture, Western Australia. The sch1 mutants used during this study were developed and described previously (Tan et al, 2008). All fungal cultures were maintained on artificial agar media as described elsewhere (Solomon et al, 2004c).…”

“…The downstream genes and proteins regulated by these signalling pathways are poorly defined. Recent studies in S. nodorum have used comparative proteomics to identify Sch1, a gene encoding a hypothetical short-chain dehydrogenase that is positively regulated by the G subunit, Gna1 (Tan et al, 2008).…”

Characterization and disruption of the cipC gene in the ochratoxigenic fungus Aspergillus carbonarius

“…Reviewing published information about cipC we found that this gene is up-regulated in pathogenicity processes in V. alboatrum (Mandelc, Radisek, Jamnik, & Javornik, 2009), V. dahliae, S. nodorum and S. sclerotiorum (Sexton et al, 2006;Tan et al, 2008), during the ectomycorrhizal symbiosis in Paxillus (Le Queré et al, 2004), during meningitis infection in the human pathogen C.…”