The defective gut colonization of <i>Candida albicans hog1</i> MAPK mutants is restored by overexpressing the transcriptional regulator of the white opaque transition <i>WOR1</i>

The transcriptional master regulator of the white opaque transition of <i>Candida albicans WOR1</i> is important for the adaptation to the commensal lifestyle in the mammalian gut, a major source of invasive candidiasis. We have generated cells that overproduce Wor1 in mutants defective in the Hog1 MAP kinase, defective in several stress responses and unable to colonize the mice gut. <i>WOR1</i> overexpression allows <i>hog1</i> to be established as a commensal in the murine gut in a commensalism model and even compete with wild-type <i>C. albicans</i> cells for establishment. This increased fitness correlates with an enhanced ability to adhere to biotic surfaces as well as increased proteinase and phospholipase production and a decrease in filamentation in vitro. We also show that <i>hog1</i> WOR1^OE are avirulent in a systemic candidiasis model in mice.

白色念珠菌（Candida albicans）WOR1基因作为其白色-不透明形态转换的转录主调控因子，对哺乳动物肠道内的共生定植生活方式适应至关重要，而哺乳动物肠道本身正是侵袭性念珠菌病的主要传染源。我们构建了在Hog1丝裂原活化蛋白激酶（MAP kinase）缺陷、多项应激反应受损且无法定植小鼠肠道的突变株中过表达Wor1的细胞；WOR1过表达可使hog1突变株在小鼠肠道共生模型中成功建立共生定植状态，甚至可与野生型（wild-type）白色念珠菌细胞竞争定植能力，该适应性提升与生物表面黏附能力增强、蛋白酶与磷脂酶产量升高以及体外丝状化水平降低显著相关。我们还证实，hog1 WOR1过表达（overexpression, OE）株在小鼠系统性念珠菌病模型中无致病力。

搜集汇总

背景与挑战

背景概述

该数据集聚焦于白色念珠菌（Candida albicans）的hog1 MAPK突变体在肠道定植中的缺陷问题，通过过表达WOR1转录调节因子成功恢复其共生能力。研究发现，WOR1过表达不仅增强了突变体的粘附性和酶产生，还降低了菌丝形成，使其在小鼠模型中无毒力，揭示了WOR1在肠道适应中的关键作用。数据集包括实验数据、资助信息和相关元数据，适用于微生物学、细胞生物学和遗传学等领域的研究。