Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.13.3 (histidine kinase)
 2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Two-component" histidine kinase (HSK1) is the primary regulator of resistance to sugar osmotic stress and sensitivity to dicarboximide or phenylpyrrole fungicides in the citrus fungal pathogen Alternaria alternata. On the other hand, the mitogen-activated protein kinase HOG1 confers resistance solely to salts and oxidative stress. We report here independent and shared functions of the SKN7-mediated signaling pathway with HSK1 and HOG1. SKN7, a putative transcription downstream regulator of HSK1, is primarily required for cellular resistance to oxidative and sugar-induced osmotic stress. SKN7, perhaps acting in parallel with HOG1, is required for resistance to H(2)O(2), tert-butyl hydroperoxide, and cumyl peroxide, but not to the superoxide-generating compounds - menadione, potassium superoxide, and diamide. Because of phenotypic commonalities, SKN7 is likely involved in resistance to sugar-induced osmotic stress via the HSK1 signaling pathway. However, mutants lacking SKN7 displayed wild-type sensitivity to NaCl and KCl salts. SKN7 is constitutively localized in the nucleus regardless of H(2)O(2) treatment. When compared to the wild type, skn7 mutants exhibited lower catalase, peroxidase, and superoxide dismutase activities and induced significantly fewer necrotic lesions on the susceptible citrus cultivar. The skn7 mutant exhibited fungicide resistance at levels between the hsk1 and the hog1 mutant strains. Skn7/hog1 double mutants exhibited fungicide resistance, similar to the strain with a single AaHSK1 gene mutation. Moreover, the A. alternata SKN7 plays a role in conidia formation. Conidia produced by the skn7 mutant are smaller and have fewer transverse septae than those produced by wild type. All altered phenotypes in the mutant were restored by introducing and expressing a wild-type copy of SKN7 under control of the endogenous promoter.
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PMID:Roles for SKN7 response regulator in stress resistance, conidiation and virulence in the citrus pathogen Alternaria alternata. 2290 11

The tangerine pathotype of Alternaria alternata is a necrotrophic fungal pathogen causing brown spot disease on a number of citrus cultivars. To better understand the dynamics of signal regulation leading to oxidative and osmotic stress response and fungal infection on citrus, phenotypic characterization of the yeast SSK1 response regulator homolog was performed. It was determined that SSK1 responds to diverse environmental stimuli and plays a critical role in fungal pathogenesis. Experiments to determine the phenotypes resulting from the loss of SSK1 reveal that the SSK1 gene product may be fulfilling similar regulatory roles in signaling pathways involving a HOG1 MAP kinase during ROS resistance, osmotic resistance, fungicide sensitivity and fungal virulence. The SSK1 mutants display elevated sensitivity to oxidants, fail to detoxify H2O2 effectively, induce minor necrosis on susceptible citrus leaves, and displays resistance to dicarboximide and phenylpyrrole fungicides. Unlike the SKN7 response regulator, SSK1 and HOG1 confer resistance to salt-induced osmotic stress via an unknown kinase sensor rather than the "two component" histidine kinase HSK1. SSK1 and HOG1 play a moderate role in sugar-induced osmotic stress. We also show that SSK1 mutants are impaired in their ability to produce germ tubes from conidia, indicating a role for the gene product in cell differentiation. SSK1 also is involved in multi-drug resistance. However, deletion of the yeast SHO1 (synthetic high osmolarity) homolog resulted in no noticeable phenotypes. Nonetheless, our results show that A. alternata can sense and react to different types of stress via SSK1, HOG1 and SKN7 in a cooperative manner leading to proper physiological and pathological functions.
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PMID:How the Pathogenic Fungus Alternaria alternata Copes with Stress via the Response Regulators SSK1 and SHO1. 2686 27