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Benjamin A. Horwitz - One of the best experts on this subject based on the ideXlab platform.

  • The AP-1-like transcription factor ChAP1 balances tolerance and cell death in the response of the maize pathogen Cochliobolus heterostrophus to a plant phenolic
    Current Genetics, 2020
    Co-Authors: Hiba Simaan, Samer Shalaby, Maor Hatoel, Olga Karinski, Orit Goldshmidt-tran, Benjamin A. Horwitz
    Abstract:

    Fungal pathogens need to contend with stresses including oxidants and antimicrobial chemicals resulting from host defenses. ChAP1 of Cochliobolus heterostrophus , agent of Southern corn leaf blight, encodes an ortholog of yeast YAP1 . ChAP1 is retained in the nucleus in response to plant-derived phenolic acids, in addition to its well-studied activation by oxidants. Here, we used transcriptome profiling to ask which genes are regulated in response to ChAP1 activation by ferulic acid (FA), a phenolic abundant in the maize host. Nuclearization of ChAP1 in response to phenolics is not followed by strong expression of genes needed for oxidative stress tolerance. We, therefore, compared the transcriptomes of the wild-type pathogen and a ChAP1 deletion mutant, to study the function of ChAP1 in response to FA. We hypothesized that if ChAP1 is retained in the nucleus under plant-related stress conditions yet in the absence of obvious oxidant stress, it should have additional regulatory functions. The transcriptional signature in response to FA in the wild type compared to the mutant sheds light on the signaling mechanisms and response pathways by which ChAP1 can mediate tolerance to ferulic acid, distinct from its previously known role in the antioxidant response. The ChAP1-dependent FA regulon consists mainly of two large clusters. The enrichment of transport and metabolism-related genes in cluster 1 indicates that C. heterostrophus degrades FA and removes it from the cell. When this fails at increasing stress levels, FA provides a signal for cell death, indicated by the enrichment of cell death-related genes in cluster 2. By quantitation of survival and by TUNEL assays, we show that ChAP1 promotes survival and mitigates cell death. Growth rate data show a time window in which the mutant colony expands faster than the wild type. The results delineate a transcriptional regulatory pattern in which ChAP1 helps balance a survival response for tolerance to FA, against a pathway promoting cell death in the pathogen. A general model for the transition from a phase where the return to homeostasis dominates to a phase leading to the onset of cell death provides a context for understanding these findings.

  • genetic interaction of the stress response factors chap1 and skn7 in the maize pathogen Cochliobolus heterostrophus
    Fems Microbiology Letters, 2014
    Co-Authors: Samer Shalaby, Olga Larkov, Netta Li Lamdan, Benjamin A. Horwitz
    Abstract:

    The transcription factors ChAP1 and Skn7 of the maize pathogen Cochliobolus heterostrophus are orthologs of Yap1 and Skn7 in yeast, where they are predicted to work together in a complex. Previous work showed that in C. heterostrophus, as in yeast, ChAP1 accumulates in the nucleus in response to reactive oxygen species (ROS). The expression of genes whose products counteract oxidative stress depends on ChAP1, as shown by impaired ability of a Δchap1 mutant to induce these ‘antioxidant’ genes. In this study, we found that under oxidative stress, antioxidant gene expression is also partially impaired in the Δskn7 mutant but to a milder extent than in the Δchap1 mutant, whereas in the double mutant – Δchap1-Δskn7 – none of the tested genes was induced, with the exception of one catalase gene, CAT2. Both single mutants are capable of infecting the plant, showing similar virulence to the WT. The double mutant, however, showed clearly decreased virulence, pointing to additive contributions of ChAP1 and Skn7. Possible mechanisms are discussed, including additive regulation of gene expression by oxidative stress.

  • iron oxidative stress and virulence roles of iron sensitive transcription factor sre1 and the redox sensor chap1 in the maize pathogen Cochliobolus heterostrophus
    Molecular Plant-microbe Interactions, 2013
    Co-Authors: Ning Zhang, Benjamin A. Horwitz, Bradford Condon, Nur A I Mohdzainudin, Keren Scher, Gillian B Turgeon
    Abstract:

    The gene SRE1, encoding the GATA transcription factor siderophore biosynthesis repressor (Sre1), was identified in the genome of the maize pathogen Cochliobolus heterostrophus and deleted. Mutants were altered in sensitivity to iron, oxidative stress, and virulence to the host. To gain insight into mechanisms of this combined regulation, genetic interactions among SRE1 (the nonribosomal peptide synthetase encoding gene NPS6, which is responsible for extracellular siderophore biosynthesis) and ChAP1 (encoding a transcription factor regulating redox homeostasis) were studied. To identify members of the Sre1 regulon, expression of candidate iron and oxidative stress-related genes was assessed in wild-type (WT) and sre1 mutants using quantitative reverse-transcription polymerase chain reaction. In sre1 mutants, NPS6 and NPS2 genes, responsible for siderophore biosynthesis, were derepressed under iron replete conditions, whereas the high-affinity reductive iron uptake pathway associated gene, FTR1, was not, in contrast to outcomes with other well-studied fungal models. C. heterostrophus L-ornithine-N(5)- monooxygenase (SIDA2), ATP-binding cassette (ABC6), catalase (CAT1), and superoxide dismutase (SOD1) genes were also derepressed under iron-replete conditions in sre1 mutants. Chap1nps6 double mutants were more sensitive to oxidative stress than either Chap1 or nps6 single mutants, while Chap1sre1 double mutants showed a modest increase in resistance compared with single Chap1 mutants but were much more sensitive than sre1 mutants. These findings suggest that the NPS6 siderophore indirectly contributes to redox homeostasis via iron sequestration, while Sre1 misregulation may render cells more sensitive to oxidative stress. The double-mutant phenotypes are consistent with a model in which iron sequestration by NPS6 defends the pathogen against oxidative stress. C. heterostrophus sre1, nps6, Chap1, Chap1nps6, and Chap1sre1 mutants are all reduced in virulence toward the host, compared with the WT.

  • role of the transcription factor chap1 in cytoplasmic redox homeostasis imaging with a genetically encoded sensor in the maize pathogen Cochliobolus heterostrophus
    Molecular Plant Pathology, 2013
    Co-Authors: Mordechai Ronen, Samer Shalaby, Benjamin A. Horwitz
    Abstract:

    Summary The redox-sensitive transcription factor ChAP1 [Cochliobolus heterostrophus YAP1 (Yeast Activator Protein 1) orthologue] of C. heterostrophus is required for oxidative stress tolerance. It is not known, however, to what extent the intracellular redox state changes on exposure of the fungus to oxidants, and whether ChAP1 is involved in the return of the cell to redox homeostasis. In order to answer these questions, we expressed a ratiometric redox-sensitive fluorescent protein sensor, pHyper, in C. heterostrophus. The fluorescence ratio was sensitive to extracellular hydrogen peroxide (H2O2) concentrations that had been shown previously to inhibit the germination of conidia and growth of the pathogen in culture. chap1 mutants showed a slower return to redox homeostasis than the wild-type on exposure to H2O2. Plant extracts that mimic oxidants in their ability to promote nuclear retention of ChAP1 reduced, rather than oxidized, the fungal cells. This result is consistent with other data suggesting that ChAP1 responds to plant-derived signals other than oxidants. pHyper should be a useful reporter of the intracellular redox state in filamentous fungi.

  • Cochliobolus heterostrophus: A Dothideomycete Pathogen of Maize
    Genomics of Soil- and Plant-Associated Fungi, 2013
    Co-Authors: Benjamin A. Horwitz, Bradford J. Condon, B. Gillian Turgeon
    Abstract:

    Cochliobolus heterostrophus is a foliar pathogen of maize, causing Southern Corn Leaf Blight. It is a necrotrophic pathogen that causes lesions on leaves and other aboveground organs of the plant. If the host is sensitive to the polyketide T-toxin produced by the pathogen, symptoms are severe, as manifested in major crop loss in the early 1970s. The genomes of several members of the genus have been sequenced and those of additional members of the class Dothideomycetes too. In this chapter, we review how C. heterostrophus has been studied as a model necrotroph, and what has been learned and can be learned in the future from the genome sequences. Among the subjects of detailed molecular genetic studies are signal transduction pathways, stress responses, and secondary metabolite production. Finally, we discuss this primarily aboveground pathogen in relation to soil biology.

Gillian B Turgeon - One of the best experts on this subject based on the ideXlab platform.

  • septins are required for reproductive propagule development and virulence of the maize pathogen Cochliobolus heterostrophus
    Fungal Genetics and Biology, 2020
    Co-Authors: Jonathan B Gonzalez, Xianghui Zhang, Gillian B Turgeon
    Abstract:

    Septins are highly conserved GTP-binding proteins that function in cell cytokinesis, polarity and morphogenesis. To evaluate the roles of these proteins in inoculum health and disease, mutants deleted for each of five septin proteins (Cdc3, Cdc10, Cdc11, Cdc12, and Cdc100) were characterized in the ascomycete Cochliobolus heterostrophus for ability to develop asexual and sexual spores and for virulence to the host maize. Strains deleted for CDC3, CDC10, CDC11, and CDC12 genes showed significant changes in hyphal growth, and in development of conidia and ascospores compared to the wild-type strain. Conidia had dramatically reduced numbers of septa and rates of germination, while ascospore development was blocked in the meiotic process. Although asci were produced, wild-type ascospores were not. When equal numbers of conidia from wild type and mutants were used to inoculate maize, cdc10 mutants showed reduced virulence compared to the wild-type strain and other mutants. This reduced virulence was demonstrated to be correlated with lower germination rate of cdc10 mutant conidia. When adjusted for germination rate, virulence was equivalent to the wild-type strain. Double mutants (cdc3cdc10, cdc3cdc11) showed augmented reduced growth phenotypes. cdc100 mutants were wild type in all assays. Taken together, these findings indicate that all four conserved septin proteins play a major role in reproductive propagule formation and that mutants with deletions of CDC10 are reduced in virulence to the host maize.

  • ChLae1 and ChVel1 regulate T-toxin production, virulence, oxidative stress response, and development of the maize pathogen Cochliobolus heterostrophus. PLoS Pathog
    2016
    Co-Authors: Shinichi Oide, May Yee Choi, Ning Zhang, Gillian B Turgeon
    Abstract:

    LaeA and VeA coordinate secondary metabolism and differentiation in response to light signals in Aspergillus spp. Their orthologs, ChLae1 and ChVel1, were identified in the maize pathogen Cochliobolus heterostrophus, known to produce a wealth of secondary metabolites, including the host selective toxin, T-toxin. Produced by race T, T-toxin promotes high virulence to maize carrying Texas male sterile cytoplasm (T-cms). T-toxin production is significantly increased in the dark in wild type (WT), whereas Chvel1 and Chlae1 mutant toxin levels are much reduced in the dark compared to WT. Correspondingly, expression of T-toxin biosynthetic genes (Tox1) is up-regulated in the dark in WT, while dark-induced expression is much reduced/minimal in Chvel1 and Chlae1 mutants. Toxin production and Tox1 gene expression are increased in ChVEL1 overexpression (OE) strains grown in the dark and in ChLAE1 strains grown in either light or dark, compared to WT. These observations establish ChLae1 and ChVel1 as the first factors known to regulate host selective toxin production. Virulence of Chlae1 and Chvel1 mutants and OE strains is altered on both T-cms and normal cytoplasm maize, indicating that both T-toxin mediated super virulence and basic pathogenic ability are affected. Deletion of ChLAE1 or ChVEL1 reduces tolerance to H2O2. Expression of CAT3, one of the three catalase genes, is reduced in the Chvel1 mutant. Chlae1 and Chvel1 mutants also show decreased aerial hyphal growth, increased asexual sporulation and female sterility. ChLAE1 OE strains are female sterile, while ChVEL1 OE strains are more fertile than WT. ChLae1 and ChVel1 repres

  • iron oxidative stress and virulence roles of iron sensitive transcription factor sre1 and the redox sensor chap1 in the maize pathogen Cochliobolus heterostrophus
    Molecular Plant-microbe Interactions, 2013
    Co-Authors: Ning Zhang, Benjamin A. Horwitz, Bradford Condon, Nur A I Mohdzainudin, Keren Scher, Gillian B Turgeon
    Abstract:

    The gene SRE1, encoding the GATA transcription factor siderophore biosynthesis repressor (Sre1), was identified in the genome of the maize pathogen Cochliobolus heterostrophus and deleted. Mutants were altered in sensitivity to iron, oxidative stress, and virulence to the host. To gain insight into mechanisms of this combined regulation, genetic interactions among SRE1 (the nonribosomal peptide synthetase encoding gene NPS6, which is responsible for extracellular siderophore biosynthesis) and ChAP1 (encoding a transcription factor regulating redox homeostasis) were studied. To identify members of the Sre1 regulon, expression of candidate iron and oxidative stress-related genes was assessed in wild-type (WT) and sre1 mutants using quantitative reverse-transcription polymerase chain reaction. In sre1 mutants, NPS6 and NPS2 genes, responsible for siderophore biosynthesis, were derepressed under iron replete conditions, whereas the high-affinity reductive iron uptake pathway associated gene, FTR1, was not, in contrast to outcomes with other well-studied fungal models. C. heterostrophus L-ornithine-N(5)- monooxygenase (SIDA2), ATP-binding cassette (ABC6), catalase (CAT1), and superoxide dismutase (SOD1) genes were also derepressed under iron-replete conditions in sre1 mutants. Chap1nps6 double mutants were more sensitive to oxidative stress than either Chap1 or nps6 single mutants, while Chap1sre1 double mutants showed a modest increase in resistance compared with single Chap1 mutants but were much more sensitive than sre1 mutants. These findings suggest that the NPS6 siderophore indirectly contributes to redox homeostasis via iron sequestration, while Sre1 misregulation may render cells more sensitive to oxidative stress. The double-mutant phenotypes are consistent with a model in which iron sequestration by NPS6 defends the pathogen against oxidative stress. C. heterostrophus sre1, nps6, Chap1, Chap1nps6, and Chap1sre1 mutants are all reduced in virulence toward the host, compared with the WT.

  • Cochliobolus heterostrophus llm1 a lae1 like methyltransferase regulates t toxin production virulence and development
    Fungal Genetics and Biology, 2013
    Co-Authors: Xudong Zhu, Gillian B Turgeon
    Abstract:

    A Lae1-like methyltransferase, Llm1, was identified in maize pathogen Cochliobolus heterostrophus which is renowned for production of the secondary metabolite host-selective toxin, T-toxin, and is a model for mechanisms of reproduction of heterothallic Dothideomycetes. Previously, we determined that C. heterostrophus mutants lacking Lae1 and Vel1 proteins were decreased in ability to produce T-toxin when the fungus was grown in the dark, demonstrating that these proteins are positive regulators of toxin production. We showed also that Lae1 and Vel1 regulate resistance to oxidative stress and both sexual and asexual reproduction. Here, it is demonstrated that Llm1, one of nine Lae1-like methyltransferases in the C. heterostrophus genome, acts as a negative regulator of T-toxin production and thus impacts virulence to the host. In vitro, in the dark, and in planta, llm1 mutants make more T-toxin than do wild-type (WT) strains, while overexpressing strains make less than WT. Virulence (amount of chlorosis) to maize, due to T-toxin, follows accordingly. Expression of nine genes involved in T-toxin production is elevated in llm1 mutants and reduced in overexpressing strains. llm1 mutations cannot rescue deficiencies in T-toxin production of lae1 or vel1 mutants indicating that Llm1 represses T-toxin biosynthesis, and that vel1 and lae1 mutations are epistatic to llm1 mutations. Thus, increased T-toxin production, and presumably gene expression, in the llm1 mutant is dependent on the presence of Vel1 and Lae1 proteins. There is no evidence that Llm1 has an effect on oxidative stress tolerance. llm1 mutants are fully fertile in crosses to WT mating testers, while LLM1 overexpressing strains and llm1lae1 and llm1vel1 double mutants are unable to act as females. Overexpression of LLM1 leads to de-repression of asexual sporulation during sexual development, and of asexual sporulation in the light and the dark during vegetative growth, as is the case for vel1, llm1vel1, and llm1lae1-deletion strains. llm1vel1 and llm1lae1 double mutants are similar to lae1 single mutants and accumulate more hyphal melanin in liquid medium than do llm1 or vel1 single mutants, implying Llm1 plays a redundant role in regulating pigmentation with Vel1, while Lae1 plays a major role.

  • chlae1 and chvel1 regulate t toxin production virulence oxidative stress response and development of the maize pathogen Cochliobolus heterostrophus
    PLOS Pathogens, 2012
    Co-Authors: Shinichi Oide, May Yee Choi, Ning Zhang, Gillian B Turgeon
    Abstract:

    LaeA and VeA coordinate secondary metabolism and differentiation in response to light signals in Aspergillus spp. Their orthologs, ChLae1 and ChVel1, were identified in the maize pathogen Cochliobolus heterostrophus, known to produce a wealth of secondary metabolites, including the host selective toxin, T-toxin. Produced by race T, T-toxin promotes high virulence to maize carrying Texas male sterile cytoplasm (T-cms). T-toxin production is significantly increased in the dark in wild type (WT), whereas Chvel1 and Chlae1 mutant toxin levels are much reduced in the dark compared to WT. Correspondingly, expression of T-toxin biosynthetic genes (Tox1) is up-regulated in the dark in WT, while dark-induced expression is much reduced/minimal in Chvel1 and Chlae1 mutants. Toxin production and Tox1 gene expression are increased in ChVEL1 overexpression (OE) strains grown in the dark and in ChLAE1 strains grown in either light or dark, compared to WT. These observations establish ChLae1 and ChVel1 as the first factors known to regulate host selective toxin production. Virulence of Chlae1 and Chvel1 mutants and OE strains is altered on both T-cms and normal cytoplasm maize, indicating that both T-toxin mediated super virulence and basic pathogenic ability are affected. Deletion of ChLAE1 or ChVEL1 reduces tolerance to H2O2. Expression of CAT3, one of the three catalase genes, is reduced in the Chvel1 mutant. Chlae1 and Chvel1 mutants also show decreased aerial hyphal growth, increased asexual sporulation and female sterility. ChLAE1 OE strains are female sterile, while ChVEL1 OE strains are more fertile than WT. ChLae1 and ChVel1 repress expression of 1,8-dihydroxynaphthalene (DHN) melanin biosynthesis genes, and, accordingly, melanization is enhanced in Chlae1 and Chvel1 mutants, and reduced in OE strains. Thus, ChLae1 and ChVel1 positively regulate T-toxin biosynthesis, pathogenicity and super virulence, oxidative stress responses, sexual development, and aerial hyphal growth, and negatively control melanin biosynthesis and asexual differentiation.

Chihiro Tanaka - One of the best experts on this subject based on the ideXlab platform.

  • ChMCO1 of Cochliobolus heterostrophus is a new class of metallo-oxidase, playing an important role in DHN-melanization
    Mycoscience, 2010
    Co-Authors: Yoshimoto Saitoh, Kosuke Izumitsu, Atsushi Morita, Kiminori Shimizu, Chihiro Tanaka
    Abstract:

    A metallo-oxidase gene from a phytopathogenic filamentous fungus, Cochliobolus heterostrophus was cloned. Structural prediction of ChMco1 indicated that this protein lacks a transmembrane helix and is soluble, whereas other known fungal metallo-oxidases including Saccharomyces cerevisiae FET3 are localized to the cell membrane. The results of searches in fungal genomic databases and phylogenetic analysis of fungal metallo-oxidases revealed that ChMco1 and its allies are distinct homologues of Fet3 and unique to filamentous ascomycetous species including C. heterostrophus . We performed a functional analysis of ChMCO1 by generating null mutants for the ChMco1 gene. The ChMco1 null (∆ ChMco1 ) mutants clearly had reduced melanization, although they showed normal growth and conidiation. Results also show that ∆ ChMco1 mutants lost laccase activity. These results suggest that ChMCO1 is a novel class of metallo-oxidase that is necessary for laccase activity and melanization.

  • the mapkk kinase chste11 regulates sexual asexual development melanization pathogenicity and adaptation to oxidative stress in Cochliobolus heterostrophus
    Current Genetics, 2009
    Co-Authors: Kosuke Izumitsu, Yoshimoto Saitoh, Atsushi Morita, Akira Yoshimi, Daisuke Kubo, Chihiro Tanaka
    Abstract:

    All fungi use multiple mitogen-activated protein kinase (MAPK) cascades to respond to external signals to regulate specialized responses. In this study, we cloned and characterized a putative MAPKKK gene ChSte11, orthologous to yeast STE11, of Cochliobolus heterostrophus. ΔChste11 strains showed defects in conidiation, sexual development, melanization and the formation of appressoria. These mutants were significantly less virulent on corn plants than the wild type. Similar phenotypes were observed in mutants of Chk1-MAPK, a putative downstream protein kinase of ChSte11. These results suggested that ChSte11 regulates various morphological changes and pathogenicity via Chk1 MAPK. Both ΔChste11 and Δchk1 strains showed severe sensitivity to oxidative stress, hydrogen peroxide, and heavy metals, cupric or ferric cations. ΔBmhog1 strains, mutants of the HOG1-type MAPK, did not show sensitivity to these forms of stress. Our results strongly suggested that the Ste11-type MAPKKK regulates not only various morphological changes and pathogenicity, but also adaptations to stress via Chk1-type MAPK in filamentous fungi.

  • phylogenetic analysis of heavy metal atpases in fungi and characterization of the copper transporting atpase of Cochliobolus heterostrophus
    Fungal Biology, 2009
    Co-Authors: Yoshimoto Saitoh, Kosuke Izumitsu, Chihiro Tanaka
    Abstract:

    We performed a phylogenetic analysis of heavy-metal ATPases (HMAs) in fungi and found that HMAs can be divided into three groups, A, B, and C. Group A is predicted to deliver copper ions to copper-containing proteins, while Groups B and C are thought to function as cell-membrane copper-efflux pumps. Furthermore, Groups B and C consist of fungal-specific HMAs, while Group A consists of fungal orthologues that have been well conserved in eukaryotes. We also cloned and characterized a Group A-type HMA gene (i.e., ChCcc2) of the filamentous plant pathogen, Cochliobolus heterostrophus. Mutation of ChCcc2 severely affected growth, pigmentation, conidiation, and colonial morphology. Activity of the copper-containing protein, laccase, was also lost in ChCcc2 mutants, suggesting that ChCCC2 plays an important role in growth and morphology by activating various copper-containing proteins in C. heterostrophus.

  • characterization of the bmr1 gene encoding a transcription factor for melanin biosynthesis genes in the phytopathogenic fungus bipolaris oryzae
    Fems Microbiology Letters, 2008
    Co-Authors: Junichi Kihara, Chihiro Tanaka, Akihiro Moriwaki, Nozomi Tanaka, Makoto Ueno, Sakae Arase
    Abstract:

    We isolated and characterized Bipolaris melanin regulation 1 gene (BMR1) encoding a transcription factor for melanin biosynthesis genes in the phytopathogenic fungus Bipolaris oryzae. Sequence analysis showed that the BMR1 gene encodes a putative protein of 1012 amino acids that has 99% sequence similarity to transcription factor Cmr1 of Cochliobolus heterostrophus. The predicted B. oryzae Bmr1 protein has two DNA-binding motifs, two Cys2His2 zinc finger domains, and a Zn(II)2Cys6 binuclear cluster domain at the N-terminal region of Bmr1. Targeted disruption of the BMR1 gene showed that BMR1 is essential for melanin biosynthesis in B. oryzae. The overexpression of the BMR1 gene led to more dark colonies than in the wild-type strain under dark conditions. Real-time PCR analysis showed that the BMR1 expression of the overexpression transformant was about 10-fold that of the wild type under dark conditions and of the expression of three melanin biosynthesis genes. These results indicated that BMR1 encodes the transcription factor of melanin biosynthesis genes in B. oryzae.

  • two component response regulators ssk1p and skn7p additively regulate high osmolarity adaptation and fungicide sensitivity in Cochliobolus heterostrophus
    Eukaryotic Cell, 2007
    Co-Authors: Kosuke Izumitsu, Akira Yoshimi, Chihiro Tanaka
    Abstract:

    Filamentous ascomycetous fungi possess many histidine kinases and two conserved response regulators, Ssk1p and Skn7p, in their two-component signaling systems. We previously reported that the fungus unique group III histidine kinase regulates high-osmolarity adaptation and iprodione/fludioxonil fungicide sensitivity by controlling the phosphorylation of Hog1-type mitogen-activated protein kinase (MAPK) in filamentous ascomycetes. Here, we have characterized the response regulator genes ChSsk1 and ChSkn7 in the southern corn leaf blight fungus Cochliobolus heterostrophus. Both ChSsk1- and ChSkn7-disrupted mutants showed little sensitivity to high-osmolarity stress and moderate resistance to the iprodione/fludioxonil fungicides. The phosphorylation of Hog1-type MAPK BmHog1p induced by high-osmolarity stress and fungicide treatments was only regulated by ChSsk1p, indicating that ChSkn7p has roles in high-osmolarity adaptation and fungicide sensitivity that are independent from the activation of BmHog1p. The Chssk1 Chskn7 double mutants clearly showed higher sensitivity to osmolar stress and higher resistance to fungicides than the single mutants. The dose responses of the double mutants fit well with those of the group III histidine kinase-deficient strain. These results suggest that in filamentous ascomycetes, the Ssk1- and Skn7-type response regulators control high-osmolarity adaptation and fungicide sensitivity additively with differential mechanisms under the regulation of the group III histidine kinase. This study provides evidence that filamentous fungi have a unique two-component signaling system that is different from that of yeast and is responsible for high-osmolarity adaptation and fungicide sensitivity.

Peter J Balintkurti - One of the best experts on this subject based on the ideXlab platform.

  • identification of a locus in maize controlling response to a host selective toxin derived from Cochliobolus heterostrophus causal agent of southern leaf blight
    Theoretical and Applied Genetics, 2018
    Co-Authors: Xie Xiaodong, Bode A Olukolu, Peter J Balintkurti
    Abstract:

    Key Message A host-selective, proteinaceous maize toxin was identified from the culture filtrate of the maize pathogen Cochliobolus heterostrophus. A dominant gene for toxin susceptibility was identified on maize chromosome 4.

  • identification of a locus in maize controlling response to a host selective toxin derived from Cochliobolus heterostrophus causal agent of southern leaf blight
    Theoretical and Applied Genetics, 2018
    Co-Authors: Xie Xiaodong, Bode A Olukolu, Peter J Balintkurti, Qin Yang
    Abstract:

    A host-selective, proteinaceous maize toxin was identified from the culture filtrate of the maize pathogen Cochliobolus heterostrophus. A dominant gene for toxin susceptibility was identified on maize chromosome 4. A toxic activity was identified from the culture filtrate (CF) of the fungus Cochliobolus heterostrophus, causal agent of the maize disease southern leaf blight (SLB) with differential toxicity on maize lines. Two independent mapping populations; a 113-line recombinant inbred line population and a 258-line association population, were used to map loci associated with sensitivity to the CF at the seedling stage. A major QTL on chromosome 4 was identified at the same locus using both populations. Mapping in the association population defined a 400 kb region that contained the sensitivity locus. By comparing CF-sensitivity of the parents of the RIL population with that of the F1 progeny, we determined that the sensitivity allele was dominant. No relationship was observed between CF-sensitivity in seedlings and SLB susceptibility in mature plants; however, a significant correlation (− 0.58) was observed between SLB susceptibility and CF-sensitivity in seedlings. The activity of the CF was light-dependent and was sensitive to pronase, indicating that the toxin was proteinaceous.

  • precise mapping of quantitative trait loci for resistance to southern leaf blight caused by Cochliobolus heterostrophus race o and flowering time using advanced intercross maize lines
    Genetics, 2007
    Co-Authors: Peter J Balintkurti, M L Carson, John C Zwonitzer, Randall J Wisser, Marco A Oropezarosas, James B Holland, Steven J Szalma
    Abstract:

    The intermated B73 × Mo17 (IBM) population, an advanced intercross recombinant inbred line population derived from a cross between the maize lines B73 (susceptible) and Mo17 (resistant), was evaluated in four environments for resistance to southern leaf blight (SLB) disease caused by Cochliobolus heterostrophus race O. Two environments were artificially inoculated, while two were not inoculated and consequently had substantially lower disease pressure. Four common SLB resistance quantitative trait loci (QTL) were identified in all environments, two in bin 3.04 and one each in bins 1.10 and 8.02/3. There was no significant correlation between disease resistance and days to anthesis. A direct comparison was made between SLB QTL detected in two populations, independently derived from the same parental cross: the IBM advanced intercross population and a conventional recombinant inbred line population. Several QTL for SLB resistance were detected in both populations, with the IBM providing between 5 and, in one case, 50 times greater mapping resolution.

  • analysis of quantitative trait loci for resistance to southern leaf blight in juvenile maize
    Phytopathology, 2006
    Co-Authors: Peter J Balintkurti, M L Carson
    Abstract:

    Balint-Kurti, P. J., and Carson, M. L. 2006. Analysis of quantitative trait loci for resistance to southern leaf blight in juvenile maize. Phytopathology 96:221-225. A set of 192 maize recombinant inbred lines (RILs), derived from a cross between the inbred lines Mo17 and B73, were evaluated as 3-weekold seedlings in the greenhouse for resistance to southern leaf blight, caused by Cochliobolus heterostrophus race O. Six significant (LOD >3.1) quantitative trait loci (QTL) were identified for disease resistance, located on chromosomes 1, 2, 3, 6, 7, and 8. Results were compared with a previous study that had used the same RIL population and pathogen isolate, but had examined resistance in mature rather than juvenile plants. There was a very weak but significant correlation between the overall resistance phenotypes of the RILs scored as mature and juvenile plants. Two QTL were found in similar positions on chromosomes 1 and 3 at both growth stages. Other QTL were specific to one growth stage or the other. Twenty-three of these RILs, together with the parental lines, were inoculated in the greenhouse with four C. heterostrophus isolates. Results indicated that the quantitative resistance observed was largely isolate nonspecific.

O C Yoder - One of the best experts on this subject based on the ideXlab platform.

  • two polyketide synthase encoding genes are required for biosynthesis of the polyketide virulence factor t toxin by Cochliobolus heterostrophus
    Molecular Plant-microbe Interactions, 2006
    Co-Authors: Scott E Baker, Scott Kroken, O C Yoder, Patrik Inderbitzin, Thipa Asvarak, Liang Shi, Gillian B Turgeon
    Abstract:

    Cochliobolus heterostrophus race T, causal agent of southern corn leaf blight, requires T-toxin (a family of C35 to C49 polyketides) for high virulence on T-cytoplasm maize. Production of T-toxin is controlled by two unlinked loci, Tox1A and Tox1B, carried on 1.2 Mb of DNA not found in race O, a mildly virulent form of the fungus that does not produce T-toxin, or in any other Cochliobolus spp. or closely related fungus. PKS1, a polyketide synthase (PKS)-encoding gene at Tox1A, and DEC1, a decarboxylase-encoding gene at Tox1B, are necessary for T-toxin production. Although there is evidence that additional genes are required for T-toxin production, efforts to clone them have been frustrated because the genes are located in highly repeated, A+T-rich DNA. To overcome this difficulty, ligation specificity-based expression analysis display (LEAD), a comparative amplified fragment length polymorphism/gel fractionation/capillary sequencing procedure, was applied to cDNAs from a near-isogenic pair of race T (Tox1+) and race O (Tox1-) strains. This led to discovery of PKS2, a second PKS-encoding gene that maps at Tox1A and is required for both T-toxin biosynthesis and high virulence to maize. Thus, the carbon chain of each T-toxin family member likely is assembled by action of two PKSs, which produce two polyketides, one of which may act as the starter unit for biosynthesis of the mature T-toxin molecule.

  • activation of an ap1 like transcription factor of the maize pathogen Cochliobolus heterostrophus in response to oxidative stress and plant signals
    Eukaryotic Cell, 2005
    Co-Authors: Sophie Lev, Ruthi Hadar, O C Yoder, Scott E Baker, Paolo Amedeo, Benjamin A. Horwitz
    Abstract:

    Redox sensing is a ubiquitous mechanism regulating cellular activity. Fungal pathogens face reactive oxygen species produced by the host plant's oxidative burst in addition to endogenous reactive oxygen species produced during aerobic metabolism. An array of preformed and induced detoxifying enzymes, including superoxide dismutase, catalases, and peroxidases, could allow fungi to infect plants despite the oxidative burst. We isolated a gene (CHAP1) encoding a redox-regulated transcription factor in Cochliobolus heterostrophus, a fungal pathogen of maize. CHAP1 is a bZIP protein that possesses two cysteine-rich domains structurally and functionally related to Saccharomyces cerevisiae YAP1. Deletion of CHAP1 in C. heterostrophus resulted in decreased resistance to oxidative stress caused by hydrogen peroxide and menadione, but the virulence of chap1 mutants was unaffected. Upon activation by oxidizing agents or plant signals, a green fluorescent protein (GFP)-CHAP1 fusion protein became localized in the nucleus. Expression of genes encoding antioxidant proteins was induced in the wild type but not in chap1 mutants. Activation of CHAP1 occurred from the earliest stage of plant infection, in conidial germ tubes on the leaf surface, and persisted during infection. Late in the course of infection, after extensive necrotic lesions were formed, GFP-CHAP1 redistributed to the cytosol in hyphae growing on the leaf surface. Localization of CHAP1 to the nucleus may, through changes in the redox state of the cell, provide a mechanism linking extracellular cues to transcriptional regulation during the plant-pathogen interaction.

  • whole genome analysis of two component signal transduction genes in fungal pathogens
    Eukaryotic Cell, 2003
    Co-Authors: Natalie L Catlett, O C Yoder, Gillian B Turgeon
    Abstract:

    Two-component phosphorelay systems are minimally comprised of a histidine kinase (HK) component, which autophosphorylates in response to an environmental stimulus, and a response regulator (RR) component, which transmits the signal, resulting in an output such as activation of transcription, or of a mitogen-activated protein kinase cascade. The genomes of the yeasts Saccharomyces cerevisiae, Schizosaccharomyces pombe, and Candida albicans encode one, three, and three HKs, respectively. In contrast, the genome sequences of the filamentous ascomycetes Neurospora crassa, Cochliobolus heterostrophus (Bipolaris maydis), Gibberella moniliformis (Fusarium verticillioides), and Botryotinia fuckeliana (Botrytis cinerea) encode an extensive family of two-component signaling proteins. The putative HKs fall into 11 classes. Most of these classes are represented in each filamentous ascomycete species examined. A few of these classes are significantly more prevalent in the fungal pathogens than in the saprobe N. crassa, suggesting that these groups contain paralogs required for virulence. Despite the larger numbers of HKs in filamentous ascomycetes than in yeasts, all of the ascomycetes contain virtually the same downstream histidine phosphotransfer proteins and RR proteins, suggesting extensive cross talk or redundancy among HKs.

  • a novel class of gene controlling virulence in plant pathogenic ascomycete fungi
    Proceedings of the National Academy of Sciences of the United States of America, 2003
    Co-Authors: Scott Kroken, Bee-na Lee, Barbara Robbertse, O C Yoder, Alice C L Churchill, Gillian B Turgeon
    Abstract:

    Insertional mutants of the fungal maize pathogen Cochliobolus heterostrophus were screened for altered virulence. One mutant had 60% reduction in lesion size relative to WT but no other detectable change in phenotype. Analysis of sequence at the insertion site revealed a gene (CPS1) encoding a protein with two AMP-binding domains. CPS1 orthologs were detected in all Cochliobolus spp. examined, in several other classes of ascomycete fungi, and in animals but not in basidiomycete fungi, bacteria, or plants. Phylogenetic analysis suggested that CPS1 represents a previously undescribed subset of adenylate-forming enzymes that have diverged from certain acyl-CoA ligases, which in bacteria are involved in biosynthesis of nonribosomal peptides or polyketide/peptide hybrids. Disruption of CPS1 caused reduced virulence of both race T and race O of C. heterostrophus on maize, of Cochliobolus victoriae on oats, and of Gibberella zeae on wheat. These results suggest that CPS1 functions as a general fungal virulence factor in plant pathogenic ascomycetes.

  • a decarboxylase encoded at the Cochliobolus heterostrophus translocation associated tox1b locus is required for polyketide t toxin biosynthesis and high virulence on t cytoplasm maize
    Molecular Plant-microbe Interactions, 2002
    Co-Authors: Mark S Rose, Sung-hwan Yun, O C Yoder, Thipa Asvarak, Gillian B Turgeon
    Abstract:

    Genes at two unlinked loci (Tox1A and Tox1B) are required for production of the polyketide T-toxin by Cochliobolus heterostrophus race T, a pathogenic fungus that requires T-toxin for high virulence to maize with T-cytoplasm. Previous work indicated that Tox1A encodes a polyketide synthase (PKS1) required for T-toxin biosynthesis and for high virulence. To identify genes at Tox1B, a wild-type race T cDNA library was screened for genes missing in the genome of a Tox1B deletion mutant. The library was probed, first with a 415-kb NotI restriction fragment from the genome of the Tox1B mutant, then with the corresponding 560-kb fragment from the genome of wild type. Two genes, DEC1 (similar to acetoacetate decarboxylase-encoding genes) and RED1 (similar to genes encoding members of the medium-chain dehydrogenase/reductase superfamily), were recovered. Targeted disruption of DEC1 drastically reduced both T-toxin production and virulence of race T to T-cytoplasm maize, whereas specific inactivation of RED1 had no apparent effect on T-toxin production (as determined by bioassay) or on virulence. DEC1 and RED1 map within 1.5 kb of each other on Tox1B chromosome 6;12 and are unique to the genome of race T, an observation consistent with the hypothesis that these genes were acquired by C. heterostrophus via a horizontal transfer event.