Omar Noor Fatin, Widiasih Widiyanto Tria, Utami Setyowati Triastuti, Niimi Masakazu, Niimi Kyoko, Toh-E Akio, Kajiwara Susumu
School of Life Science and Technology, Tokyo Institute of Technology.
Medical Mycology Research Center, Chiba University.
J Gen Appl Microbiol. 2021 Nov 25;67(5):195-206. doi: 10.2323/jgam.2021.02.001. Epub 2021 Jul 3.
We clarified the roles of VPH1 in Cryptococcus neoformans serotype D by examining the detailed phenotypes of VPH1-deficient cells (Δvph1) in terms of their capability to grow in acidic and alkaline pH, at a high temperature, and under high osmotic conditions, in addition to the involvement of VPH1 in copper (Cu) homeostasis and the expression of some C. neoformans virulence factors. Δvph1 could grow well on minimal medium (YNB) but exhibited hypersensitivity to 20 μM Cu due to the failure to induce Cu-detoxifying metallothionein genes (CMT1 and CMT2). In contrast, Δvph1 exhibited defective growth on rich medium (YPD), and the induction of Cu transporter genes (CTR1 and CTR4) did not occur in this medium, implying that this strain was incapable of the uptake of Cu ions for growth. However, the addition of excess Cu promoted CTR gene expression and supported Δvph1 growth. These results suggested that the lack of the VPH1 gene disturbed Cu homeostasis in C. neoformans. Moreover, the loss of Vph1 function influenced the urease activity of C. neoformans.
我们通过研究VPH1缺陷细胞（Δvph1）在酸性和碱性pH值、高温及高渗条件下的生长能力，以及VPH1在铜（Cu）稳态中的作用和新型隐球菌某些毒力因子的表达，阐明了VPH1在新型隐球菌D血清型中的作用。Δvph1在基本培养基（YNB）上能良好生长，但由于无法诱导铜解毒金属硫蛋白基因（CMT1和CMT2），对20 μM铜表现出超敏反应。相反，Δvph1在丰富培养基（YPD）上生长有缺陷，且在该培养基中不会诱导铜转运蛋白基因（CTR1和CTR4）的表达，这意味着该菌株无法摄取铜离子用于生长。然而，添加过量铜可促进CTR基因表达并支持Δvph1生长。这些结果表明，VPH1基因的缺失扰乱了新型隐球菌中的铜稳态。此外，Vph1功能的丧失影响了新型隐球菌的脲酶活性。
