The hgl1 gene is required for dimorphism and teliospore formation in the fungal pathogen Ustilago maydis

被引:45
作者
Dürrenberger, F
Laidlaw, RD
Kronstad, JW
机构
[1] Univ British Columbia, Dept Microbiol, Biotechnol Lab, Vancouver, BC V6T 1Z3, Canada
[2] Univ British Columbia, Fac Agr Sci, Vancouver, BC V6T 1Z3, Canada
关键词
D O I
10.1046/j.1365-2958.2001.02528.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
The fungal pathogen Ustilago maydis causes a dramatic disease in maize involving the induction of tumours and the formation of masses of black teliospores. In this fungus, mating between haploid, budding cells results in the formation of the infectious, filamentous cell type that invades host tissue. Mating and filamentous growth are governed by the mating-type loci and by cAMP signalling, perhaps in response to signals from maize. To dissect the involvement of cAMP signalling further, the constitutive filamentous phenotype of a mutant with a defect in the catalytic subunit of protein kinase A was used to isolate suppressor mutations that restore budding growth. One such mutation identified the hgl1 gene, which is shown to be required for both the switch between budding and filamentous growth and tellospore formation during infection. In addition, the hgl1 gene product may be a target of phosphorylation by protein kinase A, and transcript levels for the gene are elevated during mating. Thus, the hgl1 gene provides a connection between mating, cAMP signalling and two important aspects of virulence: filamentous growth and the formation of teliospores.
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页码:337 / 348
页数:12
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