A MAP kinase encoded by the ubc3 gene of Ustilago maydis is required for filamentous growth and full virulence

被引:136
作者
Mayorga, ME [1 ]
Gold, SE [1 ]
机构
[1] Univ Georgia, Dept Plant Pathol, Athens, GA 30602 USA
关键词
D O I
10.1046/j.1365-2958.1999.01610.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ustilago maydis, the causal agent of corn smut disease, displays dimorphic growth in which it alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. We are interested in identifying the genetic determinants of filamentous growth and pathogenicity in U. maydis. To do this, we have taken a forward genetic approach. Previously, we. showed that haploid adenylate cyclase (uac1) mutants display a constitutively filamentous phenotype, Mutagenesis of a uac1 disruption strain allowed the isolation of a large number of budding suppressor mutants. These mutants are named ubc, for Ustilaglo bypass of cyclase, as they no longer require the production of cAMP to grow in the budding morphology. Complementation of one of these suppressor mutants led to the identification of ubc3, which is required for filamentous growth and encodes a MBP kinase most similar to those of the yeast pheromone response pathway. In addition to filamentous growth, the ubc3 gene is required for pheromone response and for full virulence. Mutations in the earlier identified fuz7 MAP kinase kinase also suppress the filamentous phenotype of the uac1 disruption mutant, adding evidence that both ubc3 and fuz7 are members of this same MAP kinase cascade. These results support an important interplay of the cAMP and MBP kinase signal transduction pathways in the control; of morphogenesis and pathogenicity in U. maydis.
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页码:485 / 497
页数:13
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