title: The SskA and SrrA response regulators are implicated in oxidative stress responses of hyphae and asexual spores in the phosphorelay signaling network of Aspergillus nidulans.
abstract: Histidine-to-Aspartate (His-Asp) phosphorelay (or two-component) systems are common signal transduction mechanisms implicated in a wide variety of cellular responses to environmental stimuli in both prokaryotes and eukaryotes. For a model filamentous fungi, Aspergillus nidulans, in this study we first compiled a complete list of His-Asp phosphorelay components, including 15 genes for His-kinase (HK), four genes for response regulator (RR), and only one for histidine-containing phosphotransfer intermediate (HPt). For these RR genes, a set of deletion mutants was constructed so as to create a null allele for each. When examined these mutant strains under various conditions stressful for hyphal growth and asexual spore development, two of them (designated DeltasskA and DeltasrrA) showed a marked phenotype of hypersensitivity to oxidative stresses (particularly, to hydrogen peroxide). In this respect, expression of the vegetative-stage specific catB catalase gene was severely impaired in both mutants. Furthermore, conidia from DeltasskA were hypersensitive not only to treatment with H(2)O(2), but also to treatment at aberrantly low (4 degrees C) and high (50 degrees C) temperatures, resulting in reduced germination efficiency. In this respect, not only the catA catalase gene specific for asexual development, but also a set of genes encoding the enzymes for synthesis of certain stress tolerant compatible solutes, such as trehalose and glycerol, were markedly downregulated in conidia from DeltasskA. These results together are indicative of the physiological importance of the His-Asp phosphorelay signaling network involving the SskA and SrrA response regulators.
authors.affiliation: Laboratory of Molecular Microbiology, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan. t2706693@mbox.nagoya-u.ac.jp
authors.forename: Daisuke
authors.initials: D
authors.lastname: Hagiwara
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Asano
authors.forename: Junichiro
authors.initials: J
authors.lastname: Marui
authors.forename: Kentaro
authors.initials: K
authors.lastname: Furukawa
authors.forename: Kyoko
authors.initials: K
authors.lastname: Kanamaru
authors.forename: Masashi
authors.initials: M
authors.lastname: Kato
authors.forename: Keietsu
authors.initials: K
authors.lastname: Abe
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Takafumi
authors.initials: T
authors.lastname: Yamashino
authors.forename: Takeshi
authors.initials: T
authors.lastname: Mizuno
mesh_terms: D001224:Aspartic Acid / Q000502:physiology; D001233:Aspergillus nidulans / Q000235:genetics / Q000502:physiology*; D015139:Blotting, Southern; D002374:Catalase / Q000378:metabolism; D003470:Culture Media; D017931:DNA Primers; D005800:Genes, Fungal / Q000502:physiology*; D006639:Histidine / Q000502:physiology; D006861:Hydrogen Peroxide / Q000494:pharmacology; D025301:Hyphae / Q000235:genetics / Q000378:metabolism*; D017403:In Situ Hybridization; D009154:Mutation / Q000235:genetics / Q000502:physiology; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress / Q000235:genetics / Q000502:physiology*; D010957:Plasmids / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology*; D013172:Spores, Fungal / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D014170:Transformation, Genetic
chemical_list: D003470:Culture Media; D017931:DNA Primers; D016877:Oxidants; D001224:Aspartic Acid; D006639:Histidine; D006861:Hydrogen Peroxide; D002374:Catalase