CAMP REGULATES MORPHOGENESIS IN THE FUNGAL PATHOGEN USTILAGO-MAYDIS
CAMP REGULATES MORPHOGENESIS IN THE FUNGAL PATHOGEN USTILAGO-MAYDIS
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DOI：
10.1101/gad.8.23.2805
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发表时间：
1994-12-01
影响因子：
10.5
通讯作者：
KRONSTAD, J
中科院分区：
文献类型：
--
作者：
GOLD, S;DUNCAN, G;KRONSTAD, J
玉米黑粉菌在交配相互作用和环境条件下表现出从出芽到丝状生长的二态转换。我们已经发现，破坏uac 1基因，编码腺苷酸环化酶，在组成型丝状表型的结果。芽是恢复的uac 1突变体后，在cAMP的存在下生长，或通过基因外抑制，因为在ubc 1基因突变。ubc 1基因编码cAMP依赖性蛋白激酶（PKA）的II型调节亚基;该基因的缺陷会减弱通常在交配和暴露于空气中时发生的丝状生长。野生型细胞在cAMP中的生长和ubc 1基因的突变也会导致母细胞和子细胞分离（胞质分裂）的缺陷，并改变芽位选择。这些结果表明cAMP和PKA在U.玉蜀黍;这种作用可能是常见的二型真菌病原体。
The fungal pathogen Ustilago maydis exhibits a dimorphic switch from budding to filamentous growth in response to mating interactions and environmental conditions. We have found that disruption of the uac1 gene, encoding adenylate cyclase, results in a constitutively filamentous phenotype. Budding is restored to the uac1 mutant upon growth in the presence of cAMP or by extragenic suppression because of a mutation in the ubc1 gene. The ubc1 gene encodes a type II regulatory subunit of cAMP-dependent protein kinase (PKA); defects in this gene attenuate the filamentous growth that normally occurs in response to mating and exposure to air. Growth of wild-type cells in cAMP and mutation of the ubc1 gene also cause defects in the separation of mother and daughter cells (cytokinesis) and alter bud site selection. These results indicate a key role for cAMP and PKA in morphogenesis in U. maydis; this role may be common among dimorphic fungal pathogens.