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MAPK 突变体肠道定植缺陷可通过过表达白-不透明转化的转录调控因子得到恢复。

The defective gut colonization of MAPK mutants is restored by overexpressing the transcriptional regulator of the white opaque transition .

机构信息

Departamento de Microbiología y Parasitología, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain.

出版信息

Virulence. 2023 Dec;14(1):2174294. doi: 10.1080/21505594.2023.2174294.

Abstract

The transcriptional master regulator of the white opaque transition of 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. overexpression allows to be established as a commensal in the murine gut in a commensalism model and even compete with wild-type 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 WOR1 are avirulent in a systemic candidiasis model in mice.

摘要

作为 白色不透明转变的转录主控调节剂,对于适应哺乳动物肠道中的共生生活方式非常重要,而哺乳动物肠道是侵袭性念珠菌病的主要来源。我们已经生成了在 Hog1 MAP 激酶缺陷型突变体中过表达 Wor1 的细胞,这些突变体在多种应激反应中存在缺陷,并且无法在小鼠肠道中定植。过表达允许 在共生模型中作为共生菌定植于小鼠肠道中,甚至与野生型 细胞竞争定植。这种适应性的提高与增强对生物表面的粘附能力以及增加蛋白酶和磷脂酶的产生和体外丝状生长的减少相关。我们还表明, 在小鼠系统性念珠菌病模型中具有无毒力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2ad/9928469/88ee0c0d8c53/KVIR_A_2174294_F0001_OC.jpg

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