Ohio State University, Columbus, OH 43210, USA.
Ohio State University, Columbus, OH 43210, USA.
Curr Opin Microbiol. 2017 Dec;40:1-7. doi: 10.1016/j.mib.2017.10.003. Epub 2017 Oct 27.
Mammalian body temperature triggers differentiation of the fungal pathogen Histoplasma capsulatum into yeast cells. The Drk1 regulatory kinase and an interdependent network of Ryp transcription factors establish the yeast state. Beyond morphology, the differentiation-dependent expression program equips yeasts for invasion and survival within phagosomes. Yeast cells produce α-glucan and the Eng1 endoglucanase which hide yeasts from immune detection. Secretion of yeast phase-specific Sod3 and CatB detoxify phagocyte-derived reactive oxygen molecules. Histoplasma cells adapt to iron and zinc limitation in activated macrophages by production of siderophores and the Zrt2 transporter, respectively. Yeasts also respond to inflammation-associated hypoxia. Histoplasma pathogenicity thus relies on factors controlled by yeast differentiation as well as environment-dependent responses.
哺乳动物体温引发真菌病原体荚膜组织胞浆菌向酵母菌细胞分化。Drk1 调节激酶和相互依存的 Ryp 转录因子网络建立了酵母状态。除了形态，分化依赖性表达程序使酵母菌具备了在吞噬体中入侵和存活的能力。酵母菌产生α-葡聚糖和 Eng1 内切葡聚糖酶，使酵母菌躲避免疫检测。酵母阶段特异性 Sod3 和 CatB 的分泌可清除吞噬细胞衍生的活性氧分子。荚膜组织胞浆菌通过产生铁载体和 Zrt2 转运体分别适应激活巨噬细胞中的铁和锌限制。酵母菌还对与炎症相关的缺氧做出反应。因此，荚膜组织胞浆菌的致病性依赖于由酵母菌分化控制的因素以及环境依赖性反应。
