Ghannoum M A, Spellberg B, Saporito-Irwin S M, Fonzi W A
Division of Infectious Diseases, Harbor-UCLA Research and Education Institute, St. John's Cardiovascular Research Center, Torrance 90509, USA.
Infect Immun. 1995 Nov;63(11):4528-30. doi: 10.1128/iai.63.11.4528-4530.1995.
Candida albicans mutants lacking PHR1 exhibit a pH-dependent morphogenic defect which is expressed at pH 7.5, a pH comparable to that of mammalian blood (S. M. Saporito-Irwin, C. E. Birse, P. S. Sypherd, and W. A. Fonzi, Mol. Cell. Biol. 15:601-613, 1995). The in vivo relevance of this expression pattern was tested in a mouse model of systemic candidiasis. A phr1/phr1 mutant was found to be less virulent than an isogenic Phr1+ strain and exhibited altered morphological development in vivo. These results indicate that PHR1 contributes to the virulence of C. albicans.
缺乏PHR1的白色念珠菌突变体表现出pH依赖性的形态发生缺陷,该缺陷在pH 7.5时表达,此pH与哺乳动物血液的pH相当(S. M. 萨波里托-欧文、C. E. 伯斯、P. S. 西弗德和W. A. 丰齐,《分子与细胞生物学》15:601 - 613,1995年)。在系统性念珠菌病的小鼠模型中测试了这种表达模式在体内的相关性。发现phr1/phr1突变体的毒力低于同基因的Phr1 +菌株,并且在体内表现出形态发育改变。这些结果表明PHR1有助于白色念珠菌的毒力。