Ren Ping, Springer Deborah J, Behr Melissa J, Samsonoff William A, Chaturvedi Sudha, Chaturvedi Vishnu
Mycology Laboratory, Wadsworth Center, New York State Department of Health, 120 New Scotland Ave., Albany, New York 12201-2002, USA.
Eukaryot Cell. 2006 Jul;5(7):1065-80. doi: 10.1128/EC.00009-06.
Cryptococcus gattii is a primary pathogenic yeast, increasingly important in public health, but factors responsible for its host predilection and geographical distribution remain largely unknown. We have characterized C. gattii STE12alpha to probe its role in biology and pathogenesis because this transcription factor has been linked to virulence in many human and plant pathogenic fungi. A full-length STE12alpha gene was cloned by colony hybridization and sequenced using primer walk and 3' rapid amplification of cDNA ends strategies, and a ste12alpha delta gene knockout mutant was created by URA5 insertion at the homologous site. A semiquantitative analysis revealed delayed and poor mating in ste12alpha delta mutant; this defect was not reversed by exogenous cyclic AMP. C. gattii parent and mutant strains showed robust haploid fruiting. Among putative virulence factors tested, the laccase transcript and enzymatic activity were down regulated in the ste12alpha delta mutant, with diminished production of melanin. However, capsule, superoxide dismutase, phospholipase, and urease were unaffected. Similarly, Ste12 deficiency did not cause any auxotrophy, assimilation defects, or sensitivity to a large panel of chemicals and antifungals. The ste12alpha delta mutant was markedly attenuated in virulence in both BALB/c and A/Jcr mice models of meningoencephalitis, and it also exhibited significant in vivo growth reduction and was highly susceptible to in vitro killing by human neutrophils (polymorphonuclear leukocytes). In tests designed to simulate the C. gattii natural habitat, the ste12alpha delta mutant was poorly pigmented on wood agar prepared from two tree species and showed poor survival and multiplication in wood blocks. Thus, STE12alpha plays distinct roles in C. gattii morphogenesis, virulence, and ecological fitness.
加氏隐球菌是一种主要的致病性酵母,在公共卫生方面的重要性日益增加,但其宿主偏好和地理分布的决定因素仍 largely 未知。我们对加氏隐球菌 STE12α 进行了表征,以探究其在生物学和发病机制中的作用,因为该转录因子已与许多人类和植物致病真菌的毒力相关联。通过菌落杂交克隆了全长 STE12α 基因,并使用引物步移和 3' cDNA 末端快速扩增策略进行测序,通过在同源位点插入 URA5 创建了 ste12α 缺失基因敲除突变体。半定量分析显示 ste12α 缺失突变体的交配延迟且不佳;这种缺陷不能被外源性环磷酸腺苷逆转。加氏隐球菌亲本和突变体菌株表现出强大的单倍体结实。在所测试的假定毒力因子中,漆酶转录本和酶活性在 ste12α 缺失突变体中下调,黑色素生成减少。然而,荚膜、超氧化物歧化酶、磷脂酶和脲酶不受影响。同样,Ste12 缺乏不会导致任何营养缺陷、同化缺陷或对大量化学物质和抗真菌剂的敏感性。ste12α 缺失突变体在脑膜脑炎的 BALB/c 和 A/Jcr 小鼠模型中毒力明显减弱,并且在体内也表现出显著的生长减少,并且对人中性粒细胞(多形核白细胞)的体外杀伤高度敏感。在旨在模拟加氏隐球菌自然栖息地的测试中,ste12α 缺失突变体在由两种树种制备的木琼脂上色素沉着不良,并且在木块中存活和繁殖不佳。因此,STE12α 在加氏隐球菌形态发生、毒力和生态适应性中发挥着不同的作用。