Mating and Pathogenic Development of the Smut Fungus
            <i>Ustilago maydis</i>
            Are Regulated by One Mitogen-Activated Protein Kinase Cascade

Müller, Philip; Weinzierl, Gerhard; Brachmann, Andreas; Feldbrügge, Michael; Kahmann, Regine

doi:10.1128/ec.2.6.1187-1199.2003

Cited by 131 publications

(215 citation statements)

References 58 publications

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“…promoter were largely independent on the upstream components (i.e., pheromone and receptors) for conjugation tube formation when grown in arabinose-containing medium (Mü ller et al, 2003). As we observed previously after pheromone treatment, pcl12 expression was increased after fuz7DD induction ( Figure 7D).…”

Section: Absence Of Pcl12 Delays the Formation Of The Conjugation Tubesupporting

confidence: 68%

“…These data suggest that Pcl12 plays a role in the polar growth of the conjugation tube, although we cannot exclude some indirect effect such as the possibility that Pcl12 participate in pheromone sensing as it has been recently proposed for Myo5 and Yup1 (Weber et al, 2003;Fuchs et al, 2006). To address this issue, we took advantage of the fuz7DD allele, which encodes an activated version of the mitogenactivated protein kinase (MAPK) kinase involved in pheromone response (Banuett and Herskowitz, 1994;Mü ller et al, 2003), since cells expressing this allele under the arabinose-induced crg1 (D) Pcl12-induced filamentation is dependent on cdk5. Overexpression of pcl12 in cells carrying a wild-type cdk5 allele (control) or carrying a cdk5 ts allele.…”

Section: Absence Of Pcl12 Delays the Formation Of The Conjugation Tubementioning

confidence: 99%

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Polar Growth in the Infectious Hyphae of the PhytopathogenUstilago maydisDepends on a Virulence-Specific Cyclin

2007

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The maize smut fungus Ustilago maydis switches from yeast to hyphal growth to infect maize (Zea mays) plants. This switching is promoted by mating of compatible cells and seems to be required for plant penetration. Although many genes distinctively expressed during this dimorphic switch have been identified and shown to be essential for the infection process, none seems to be explicitly required for polar growth control. Here, we report the characterization of pcl12, encoding a cyclin that interacts specifically with Cdk5, an essential cyclin-dependent kinase with regulatory roles in morphogenesis in U. maydis. Pcl12 fulfills the requirements to be a virulence-specific regulator of polar growth in U. maydis. First, pcl12 expression is induced during the pathogenic development. Secondly, Pcl12 is sufficient to induce hyperpolarized growth in U. maydis cells, as haploid cells overexpressing pcl12 in axenic conditions produce filaments that were morphologically indistinguishable from those produced during the infection process. Finally, cells defective in pcl12 showed impaired polar growth during the formation of the b-dependent filament, the induction of the conjugation tubes, or the formation of a promycelium in spore germination. However, in spite of this pivotal role during morphogenesis, pcl12 mutants were virulent. We discuss the implications of these results for the role of polar growth during the infection process.

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Section: Absence Of Pcl12 Delays the Formation Of The Conjugation Tubesupporting

confidence: 68%

Section: Absence Of Pcl12 Delays the Formation Of The Conjugation Tubementioning

confidence: 99%

Polar Growth in the Infectious Hyphae of the PhytopathogenUstilago maydisDepends on a Virulence-Specific Cyclin

2007

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“…In U. maydis, the Fuz7/Ubc5 MEK and Kpp4/Ubc4 both are required for transcriptional responses to pheromone, filamentous growth, mating, and pathogenicity (Banuett and Herskowitz, 1994;Andrews et al, 2000;Muller et al, 2003). However, unlike M. grisea, U. maydis has at least two MAPK genes, Kpp2 and Kpp6, that function downstream from Ubc4 and Fuz7 (Andrews et al, 2000;Muller et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…However, unlike M. grisea, U. maydis has at least two MAPK genes, Kpp2 and Kpp6, that function downstream from Ubc4 and Fuz7 (Andrews et al, 2000;Muller et al, 2003). In the human pathogen Candida albicans, HST7 MEK and CEK1 MAPK are involved in yeasthyphal transition, fungal pathogenesis, and mating responses Yeast transformants containing the bait and prey constructs of PMK1, MST7, MST11, and MST50 as indicated (top panels) were patched on SD-Leu-Trp-His plates (bottom left, His).…”

Section: Discussionmentioning

confidence: 99%

A Mitogen-Activated Protein Kinase Cascade Regulating Infection-Related Morphogenesis in Magnaporthe grisea

et al. 2005

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Many fungal pathogens invade plants by means of specialized infection structures called appressoria. In the rice (Oryza sativa) blast fungus Magnaporthe grisea, the pathogenicity mitogen-activated protein (MAP) kinase1 (PMK1) kinase is essential for appressorium formation and invasive growth. In this study, we functionally characterized the MST7 and MST11 genes of M. grisea that are homologous with the yeast MAP kinase kinase STE7 and MAP kinase kinase kinase STE11. Similar to the pmk1 mutant, the mst7 and mst11 deletion mutants were nonpathogenic and failed to form appressoria. When a dominant MST7 allele with S212D and T216E mutations was introduced into the mst7 or mst11 mutant, appressorium formation was restored in the resulting transformants. PMK1 phosphorylation also was detected in the vegetative hyphae and appressoria of transformants expressing the MST7 S212D T216E allele. However, appressoria formed by these transformants failed to penetrate and infect rice leaves, indicating that constitutively active MST7 only partially rescued the defects of the mst7 and mst11 mutants. The intracellular cAMP level was reduced in transformants expressing the MST7 S212D T216E allele. We also generated MST11 mutant alleles with the sterile alpha motif (SAM) and Ras-association (RA) domains deleted. Phenotype characterizations of the resulting transformants indicate that the SAM domain but not the RA domain is essential for the function of MST11. These data indicate that MST11, MST7, and PMK1 function as a MAP kinase cascade regulating infection-related morphogenesis in M. grisea. Although no direct interaction was detected between PMK1 and MST7 or MST11 in yeast two-hybrid assays, a homolog of yeast STE50 in M. grisea directly interacted with both MST7 and MST11 and may function as the adaptor protein for the MST11-MST7-PMK1 cascade.

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“…Cell cycle regulation could affect the transmission pathway or it could interfere with elements downstream of the signaling cascade. To address whether the cell cycle arrest is affecting the ability to transmit the signal, we introduced into those strains (mutant and WT) that carry the AM1 reporter a construction that expresses the fuz7 DD allele, encoding a hyperactive version of the pheromone cascade MAPK kinase (Muller et al, 2003) under the control of the crg1 promoter. We thus bypassed the requirement of the signal transmission upstream of the last step, the activation of the MAP kinase (Kpp2) by its cognate MAPK kinase (Fuz7).…”

Section: Cell Cycle Arrest Is Required For Appressorium Formationmentioning

confidence: 99%

Programmed cell cycle arrest is required for infection of corn plants by the fungus Ustilago maydis

2014

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Ustilago maydis is a plant pathogen that requires a specific structure called infective filament to penetrate the plant tissue. Although able to grow, this filament is cell cycle arrested on the plant surface. This cell cycle arrest is released once the filament penetrates the plant tissue. The reasons and mechanisms for this cell cycle arrest are unknown. Here, we have tried to address these questions. We reached three conclusions from our studies. First, the observed cell cycle arrest is the result of the cooperation of at least two distinct mechanisms: one involving the activation of the DNA damage response (DDR) cascade; and the other relying on the transcriptional downregulation of Hsl1, a kinase that modulates the G2/M transition. Second, a sustained cell cycle arrest during the infective filament step is necessary for the virulence in U. maydis, as a strain unable to arrest the cell cycle was severely impaired in its ability to infect corn plants. Third, production of the appressorium, a structure required for plant penetration, is incompatible with an active cell cycle. The inability to infect plants by strains defective in cell cycle arrest seems to be caused by their failure to induce the appressorium formation process. In summary, our findings uncover genetic circuits to arrest the cell cycle during the growth of this fungus on the plant surface, thus allowing the penetration into plant tissue.

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Mating and Pathogenic Development of the Smut Fungus Ustilago maydis Are Regulated by One Mitogen-Activated Protein Kinase Cascade

Cited by 131 publications

References 58 publications

Polar Growth in the Infectious Hyphae of the PhytopathogenUstilago maydisDepends on a Virulence-Specific Cyclin

Polar Growth in the Infectious Hyphae of the PhytopathogenUstilago maydisDepends on a Virulence-Specific Cyclin

A Mitogen-Activated Protein Kinase Cascade Regulating Infection-Related Morphogenesis in Magnaporthe grisea

Programmed cell cycle arrest is required for infection of corn plants by the fungus Ustilago maydis

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