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Academic literature on the topic 'Fungi Mutante'
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Journal articles on the topic "Fungi Mutante"
1
Martínez, M., E. López-Solanilla, P. Rodríguez-Palenzuela, P. Carbonero, and I. Díaz. "Inhibition of Plant-Pathogenic Fungi by the Barley Cystatin Hv-CPI (Gene Icy) Is Not Associated with Its Cysteine-Proteinase Inhibitory Properties." Molecular Plant-Microbe Interactions® 16, no. 10 (2003): 876–83. http://dx.doi.org/10.1094/mpmi.2003.16.10.876.
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The recombinant barley cystatin Hv-CPI inhibited the growth of three phytopathogenic fungi (Botrytis cinerea, Colletotrichum graminicola, and Plectosphaerella cucumerina) and the saprotrophic fungus Trichoderma viride. Several mutants of barley cystatin were generated by polymerase chain reaction approaches and both their anti-fungal and their cysteine-proteinase inhibitory properties investigated. Point mutants R38→G, Q63→L, and Q63→P diminished their capacity for inhibiting papain and cathepsin B, retaining their antifungal properties. However, mutant C68→G was more active for papain and cathepsin B than the wild type. These results indicate that in addition to the consensus cystatin-reactive site, Q63-V64-V65-A66-G67, the A37-R38-F39-A40-V41 region, common to all cereal cystatins, and the C68 residue are important for barley cystatin activity. On the other hand, the K92→P mutant is inactive as a fungicide, but still retains measurable inhibitory activity for papain and cathepsin B. Against B. cinerea, the antifungal effect of Hv-CPI and of its derived mutants does not always correlate with their activities as proteinase inhibitors, because the Q63→P mutant is inactive as a cystatin, while still inhibiting fungal growth, and the K92→P mutant shows the reciprocal effects. These data indicate that inhibition of plant-pathogenic fungi by barley cystatin is not associated with its cysteine-proteinase inhibitory activity. Moreover, these results are corroborated by the absence of inhibition of intra- and extramycelia-proteinase activities by barley cystatin and by other well-known inhibitors of cysteine-proteinase activity in the fungal zymograms of B. cinerea.
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Kawamura, Chie, Jouji Moriwaki, Norio Kimura, et al. "The Melanin Biosynthesis Genes of Alternaria alternata Can Restore Pathogenicity of the Melanin-Deficient Mutants of Magnaporthe grisea." Molecular Plant-Microbe Interactions® 10, no. 4 (1997): 446–53. http://dx.doi.org/10.1094/mpmi.1997.10.4.446.
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The phytopathogenic fungi Magnaporthe grisea and Alternaria alternata produce melanin via the polyketide biosynthesis, and both fungi form melanized colonies. However, the site of melanin deposition and the role of melanin in pathogenicity differ between these two fungi. M. grisea accumulates melanin in appressoria, and their melanization is essential for host penetration. On the other hand, A. alternata produces colorless appressoria, and melanin is not relevant to host penetration. We examined whether the melanin biosynthesis genes of A. alternata could complement the melanin-deficient mutations of M. grisea. Melanin-deficient, nonpathogenic mutants of M. grisea, albino (Alb¯), rosy (Rsy¯), and buff (Buf¯), were successfully transformed with a cosmid clone pMBR1 that carries melanin biosynthesis genes ALM, BRM1, and BRM2 of A. alternata. This transformation restored the melanin synthesis of the Alb¯ and Buf¯ mutants, but not that of the Rsy¯ mutant. The melanin-restored transformants regained mycelial melanization, appressorium melanization, and pathogenicity to rice. Further, transformation of Alb¯ and Buf¯ mutants with subcloned ALM and BRM2 genes, respectively, also produced melanin-restored transformants. These results indicate that the Alternaria genes ALM and BRM2 can restore pathogenicity to the mutants Alb¯ and Buf¯, respectively, due to their function during appressorium development in M. grisea.
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Arganoza, M. T., J. Ohrnberger, J. Min, and R. A. Akins. "Suppressor mutants of Neurospora crassa that tolerate allelic differences at single or at multiple heterokaryon incompatibility loci." Genetics 137, no. 3 (1994): 731–42. http://dx.doi.org/10.1093/genetics/137.3.731.
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Abstract Allelic differences at any one of at least 11 heterokaryon incompatibility (het) loci in Neurospora crassa trigger an incompatibility response: localized cell death at sites of hyphal anastomosis. We have isolated spontaneous and insertional suppressor mutants that are heterokaryon-compatible in spite of allelic differences at one or at several het loci. Some intra- and extragenic mutants tolerated allelic differences only at single het loci. Multi-tolerant spontaneous mutants were isolated by selecting simultaneously for tolerance of differences at het-c, -d and -e, or at each of these plus mating-type. Some suppressor mutants were specific for only one allele at the affected het locus; others suppressed both alleles. Insertional mutations were isolated from banks of transformants, each having a plasmid integrated into a random position in the chromosome. One mutant tolerated allelic differences at het-d. A homologous cosmid from a Neurospora genomic bank complemented the mutant phenotype. A second insertional inactivation mutant was tolerant of het-c differences. Inactivation of the wild-type locus corresponding to the integration site was accomplished by repeat-induced point mutation (RIP). The RIP progeny, like the original mutant, were tolerant of differences at het-c. It may be possible to use such suppressor mutants as universal donors of hypovirulence in pathogenic fungi.
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Bonfante, Paola, Andrea Genre, Antonella Faccio, et al. "The Lotus japonicus LjSym4 Gene Is Required for the Successful Symbiotic Infection of Root Epidermal Cells." Molecular Plant-Microbe Interactions® 13, no. 10 (2000): 1109–20. http://dx.doi.org/10.1094/mpmi.2000.13.10.1109.
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The role of the Lotus japonicus LjSym4 gene during the symbiotic interaction with Mesorhizobium loti and arbuscular mycorrhizal (AM) fungi was analyzed with two mutant alleles conferring phenotypes of different strength. Ljsym4-1 and Ljsym4-2 mutants do not form nodules with M. loti.Normal root hair curling and infection threads are not observed, while a nodC-dependent deformation of root hair tips indicates that nodulation factors are still perceived by Ljsym4 mutants. Fungal infection attempts on the mutants generally abort within the epidermis, but Ljsym4-1 mutants allow rare, successful, infection events, leading to delayed arbuscule formation. On roots of mutants homozygous for the Ljsym4-2 allele, arbuscule formation was never observed upon inoculation with either of the two AM fungi, Glomus intraradices or Gigaspora margarita. The strategy of epidermal penetration by G. margarita was identical for Ljsym4-2 mutants and the parental line, with appressoria, hyphae growing between two epidermal cells, penetration of epidermal cells through their anticlinal wall. These observations define a novel, genetically controlled step in AM colonization. Although rhizobia penetrate the tip of root hairs and AM fungi access an entry site near the base of epidermal cells, the LjSym4 gene is necessary for the appropriate response of this cell type to both microsymbionts. We propose that LjSym4 is required for the initiation or coordinated expression of the host plant cell's accommodation program, allowing the passage of both microsymbionts through the epidermis layer.
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Egan, John D., María D. García-Pedrajas, David L. Andrews, and Scott E. Gold. "Calcineurin Is an Antagonist to PKA Protein Phosphorylation Required for Postmating Filamentation and Virulence, While PP2A Is Required for Viability in Ustilago maydis." Molecular Plant-Microbe Interactions® 22, no. 10 (2009): 1293–301. http://dx.doi.org/10.1094/mpmi-22-10-1293.
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Ustilago maydis is a dimorphic basidiomycete and the causal agent of corn smut disease. It serves as a genetic model for understanding dimorphism, pathogenicity, and mating response in filamentous fungi. Previous studies indicated the importance of regulated cAMP-dependent protein kinase A (PKA) for filamentous growth and pathogenicity in U. maydis. The roles of two protein phosphatases that potentially act antagonistically to PKA were assessed. A reverse genetics approach to mutate the catalytic subunits of calcineurin (CN, protein phosphatase [PP]2B) and PP2A in U. maydis was employed. A mutation in the CN catalytic subunit ucn1 caused a dramatic multiple-budding phenotype and mating between two ucn1 mutants was severely reduced. The pathogenicity of ucn1 mutant strains was also severely reduced, even in a solopathogenic haploid strain. Importantly, mutations disrupting protein phosphorylation by PKA were epistatic to ucn1 mutation, indicating a major role of ucn1 as a PKA antagonistic phosphatase. Genetic and inhibitor studies indicated that the U. maydis PP2A catalytic subunit gene (upa2) was essential.
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Hallen, Heather E., and Frances Trail. "The L-Type Calcium Ion Channel Cch1 Affects Ascospore Discharge and Mycelial Growth in the Filamentous Fungus Gibberella zeae (Anamorph Fusarium graminearum)." Eukaryotic Cell 7, no. 2 (2007): 415–24. http://dx.doi.org/10.1128/ec.00248-07.
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ABSTRACT Cch1, a putative voltage-gated calcium ion channel, was investigated for its role in ascus development in Gibberella zeae. Gene replacement mutants of CCH1 were generated and found to have asci which did not forcibly discharge spores, although morphologically ascus and ascospore development in the majority of asci appeared normal. Additionally, mycelial growth was significantly slower, and sexual development was slightly delayed in the mutant; mutant mycelia showed a distinctive fluffy morphology, and no cirrhi were produced. Wheat infected with Δcch1 mutants developed symptoms comparable to wheat infected with the wild type; however, the mutants showed a reduced ability to protect the infected stalk from colonization by saprobic fungi. Transcriptional analysis of gene expression in mutants using the Affymetrix Fusarium microarray showed 2,449 genes with significant, twofold or greater, changes in transcript abundance across a developmental series. This work extends the role of CCH1 to forcible spore discharge in G. zeae and suggests that this channel has subtle effects on growth and development.
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Silby, Mark W., and H. Khris Mahanty. "The importance ofrecAmutant strains for the study of antifungal genes inPseudomonas aureofaciensPA147-2." Canadian Journal of Microbiology 46, no. 8 (2000): 744–48. http://dx.doi.org/10.1139/w00-053.
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Pseudomonas aureofaciens PA147-2 shows antifungal activity toward a variety of plant pathogenic fungi. We have been investigating the molecular mechanisms underlying the fungal inhibition, and during these studies it was observed that the use of pLAFR3-based cosmids for in trans complementation of mutants lacking antifungal activity is hindered by cosmid instability. It was hypothesised that the cosmid stability could be improved by inactivation of recA. The recA gene of PA147-2 was cloned and shown to complement recA mutants of E. coli, restoring RecA-dependent functions when expressed in trans. Two recA mutants of PA147-2 were constructed. Both of these mutants show sensitivity to DNA damage. Cosmid pPS2122 restores antifungal activity to a mutant by allele exchange, but is unstable in trans. The stability of pPS2122 is shown to be improved in a recA mutant of PA147-2 with respect to the wild type.Key words: antifungal, complementation, recA, Pseudomonas aureofaciens PA147-2.
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Nižnanský, Ľuboš, Ľudovít Varečka, and Svetlana Kryštofová. "Disruption of GABA shunt affects Trichoderma atroviride response to nutritional and environmental stimuli." Acta Chimica Slovaca 9, no. 2 (2016): 109–13. http://dx.doi.org/10.1515/acs-2016-0019.
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Abstract The fungus Trichoderma atroviride is a member of the genus Trichoderma to which belong many species known for high cellulase production, formation of various antibiotics, plant biocontrol and antagonistic activities against other fungi. Deletion of T. atroviride glutamate decarboxylase gene gad caused minor defects in germination, hyphal branching, slower growth and disruption of conidiation pattern. GABA can be used by fungi as a secondary carbon source and as a primary nitrogen source. We analyzed the effect of different nutrient compositions and environmental conditions (light and temperature) on growth and development of T. atroviride in strains defective in the functional GAD. The gad mutants grown on NH4NO3 as a sole carbon source grew slower and formed conidiation bands closer to each other which was clearly demonstrated during their cultivation in race tubes. The gad mutants exhibited slightly lower apical extension growth rate at the room temperature but their apical extension rate dropped significantly at 30 °C. Higher temperature had also inhibitory effect on gad mutant conidiation, whereas 30 °C seems optimal temperature for the parental strain. The optimal temperature for gad mutant conidiation was lower than in F534, about 25 °C.
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Mukherjee, Prasun K., Jagannathan Latha, Ruthi Hadar, and Benjamin A. Horwitz. "TmkA, a Mitogen-Activated Protein Kinase of Trichoderma virens, Is Involved in Biocontrol Properties and Repression of Conidiation in the Dark." Eukaryotic Cell 2, no. 3 (2003): 446–55. http://dx.doi.org/10.1128/ec.2.3.446-455.2003.
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ABSTRACT Trichoderma virens is a mycoparasitic fungus used in biocontrol of soilborne plant pathogens. It inhibits or kills plant-pathogenic fungi through production of antifungal antibiotics and parasitism of hyphae and sclerotia. Conidiation, or the production of asexual spores, an inducible process triggered by light or nutrient stress, is an important trait in survival and also development of formulation products. In many fungi, signaling pathways, including mitogen-activated protein kinase (MAPK) cascades, have been implicated in parasitism of host plants as well as in the production of asexual spores. Here, we have studied the role of a MAPK gene, that for TmkA, in conidiation and antagonistic properties of a biocontrol strain of T. virens. Through single- and double-crossover recombination, we obtained three tmkA loss-of-function mutants. The TmkA transcript was not detectable in these mutants. The mutants conidiated in the dark, although photoinduction was normal and the light sensitivities of the wild type and the mutant were the same. The mutants had, overall, normal colony morphology, but their radial growth rate was reduced by about 16%, with no decrease in biomass production. Against Rhizoctonia solani hyphae, the knockout mutants exhibited mycoparasitic coiling and lysis of host hyphae similar to that of the wild type. The mutants, however, were less effective in colonizing the sclerotia of R. solani. On Sclerotium rolfsii, the MAPK loss-of-function mutants had reduced antagonistic properties in confrontation assays and failed to parasitize the sclerotia. TmkA-dependent and -independent pathways are thus involved in antagonism against different hosts. Finally, in contrast to the case for other filamentous fungi studied so far, signaling through a MAPK represses, rather than induces, asexual sporulation.
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Cheng, V., H. U. Stotz, K. Hippchen, and A. T. Bakalinsky. "Genome-Wide Screen for Oxalate-Sensitive Mutants of Saccharomyces cerevisiae." Applied and Environmental Microbiology 73, no. 18 (2007): 5919–27. http://dx.doi.org/10.1128/aem.02843-06.
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ABSTRACT Oxalic acid is an important virulence factor produced by phytopathogenic filamentous fungi. In order to discover yeast genes whose orthologs in the pathogen may confer self-tolerance and whose plant orthologs may protect the host, a Saccharomyces cerevisiae deletion library consisting of 4,827 haploid mutants harboring deletions in nonessential genes was screened for growth inhibition and survival in a rich medium containing 30 mM oxalic acid at pH 3. A total of 31 mutants were identified that had significantly lower cell yields in oxalate medium than in an oxalate-free medium. About 35% of these mutants had not previously been detected in published screens for sensitivity to sorbic or citric acid. Mutants impaired in endosomal transport, the rgp1Δ, ric1Δ, snf7Δ, vps16Δ, vps20Δ, and vps51Δ mutants, were significantly overrepresented relative to their frequency among all verified yeast open reading frames. Oxalate exposure to a subset of five mutants, the drs2Δ, vps16Δ, vps51Δ, ric1Δ, and rib4Δ mutants, was lethal. With the exception of the rib4Δ mutant, all of these mutants are impaired in vesicle-mediated transport. Indirect evidence is provided suggesting that the sensitivity of the rib4Δ mutant, a riboflavin auxotroph, is due to oxalate-mediated interference with riboflavin uptake by the putative monocarboxylate transporter Mch5.