G蛋白信号调节因子Crg1的突变增加了新型隐球菌的毒力。
Mutation of the regulator of G protein signaling Crg1 increases virulence in Cryptococcus neoformans.
作者信息
Wang Ping, Cutler Jim, King Jill, Palmer Daniel
机构信息
Department of Pediatrics, Research Institute for Children, Children's Hospital, 200 Henry Clay Ave., New Orleans, LA 70118, USA.
出版信息
Eukaryot Cell. 2004 Aug;3(4):1028-35. doi: 10.1128/EC.3.4.1028-1035.2004.
Abstract
The regulator of G protein signaling homolog Crg1 was found to be a key regulator of pheromone-responsive mating in the opportunistic human fungal pathogen Cryptococcus neoformans. A mutation in the CRG1 gene has greatly increased virulence in the prevalently distributed MATalpha strains of the fungus. Mouse survival time was shortened by 40%, and the lethal dosage was 100-fold less than that of wild-type strains. In addition, the increased virulence of crg1 mutant strains was dependent on the transcription factor homolog Ste12alpha but not on the mitogen-activated protein kinase homolog Cpk1. The enhanced mating due to CRG1 mutation, however, was still dependent on Cpk1. Interestingly, crg1 mutants of MATalpha cells produced dark melanin pigment under normally inhibitory conditions, which may relate to the mechanism for increased virulence.
摘要
G蛋白信号调节同源物Crg1被发现是机会性人类真菌病原体新生隐球菌中信息素反应性交配的关键调节因子。CRG1基因突变极大地增加了该真菌普遍存在的MATα菌株的毒力。小鼠存活时间缩短了40%，致死剂量比野生型菌株少100倍。此外，crg1突变株毒力的增加依赖于转录因子同源物Ste12α，而不依赖于丝裂原活化蛋白激酶同源物Cpk1。然而，由于CRG1突变导致的交配增强仍依赖于Cpk1。有趣的是，MATα细胞的crg1突变体在正常抑制条件下产生深色黑色素，这可能与毒力增加的机制有关。
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