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The secretory Candida effector Sce1 licenses fungal virulence by masking the immunogenicβ-1,3-glucan and promoting apoptosis of the host cells
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作者 Hongyu Wu Li Wang +4 位作者 Wenjuan Wang Zhugui Shao Xin-Ming Jia Hui Xiao jiangye chen 《mLife》 CSCD 2023年第2期159-177,共19页
Candida albicans deploys a variety of mechanisms such as morphological switch and elicitor release to promote virulence.However,the intricate interactions between the fungus and the host remain poorly understood,and a... Candida albicans deploys a variety of mechanisms such as morphological switch and elicitor release to promote virulence.However,the intricate interactions between the fungus and the host remain poorly understood,and a comprehensive inventory of fungal virulence factors has yet to be established.In this study,we identified a C.albicans secretory effector protein Sce1,whose induction and secretion are associated with vagina‐simulative conditions and chlamydospore formation.Sequence alignment showed that Sce1 belongs to a Pir family in C.albicans,which is conserved across several fungi and primarily characterized as aβ‐glucan binding protein in the Saccharomyces cerevisiae.Mechanically,Sce1 is primarily localized to the cell wall in a cleaved form as an alkali‐labileβ‐1,3‐glucan binding protein and plays a role in maskingβ‐glucan in acidic environments and chlamydospores,a feature that might underline C.albicans'ability to evade host immunity.Further,a cleaved short form of Sce1 protein could be released into extracellular compartments and presented in bone marrow‐derived macrophages infected with chlamydospores.This cleaved short form of Sce1 also demonstrated a unique ability to trigger the caspases‐8/9‐dependent apoptosis in various host cells.Correspondingly,genetic deletion of SCE1 led to dampened vaginal colonization of C.albicans and diminished fungal virulence during systemic infection.The discovery of Sce1 as a versatile virulence effector that executes at various compartments sheds light on the fungus–host interactions and C.albicans pathogenesis. 展开更多
关键词 APOPTOSIS Candida albicans EFFECTOR immune evasion Β-GLUCAN
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白念珠菌14-3-3蛋白Bmh1在细胞生长和菌丝发育中的功能解析 被引量:1
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作者 尹华 陈江野 常鹏 《微生物学报》 CAS CSCD 北大核心 2018年第11期1926-1937,共12页
【目的】应用Tet-off启动子研究白念珠菌唯一的14-3-3蛋白Bmh1在白念珠菌生长和菌丝发育过程中的功能。【方法】在白念珠菌URA3+菌株SN152中,我们敲除了1个BMH1基因拷贝,并用Tet-off启动子替代另一个BMH1基因拷贝的启动子,得到了可以用... 【目的】应用Tet-off启动子研究白念珠菌唯一的14-3-3蛋白Bmh1在白念珠菌生长和菌丝发育过程中的功能。【方法】在白念珠菌URA3+菌株SN152中,我们敲除了1个BMH1基因拷贝,并用Tet-off启动子替代另一个BMH1基因拷贝的启动子,得到了可以用强力霉素(Doxycycline)控制Bmh1表达水平的菌株。然后我们通过斑点试验和形态学观察对该菌株的生长和菌丝发育表型进行了分析。通过在ras1、flo8、efg1、cph1、tec1等重要菌丝发育调控因子突变体中过表达Bmh1,我们初步研究了Bmh1在菌丝发育调控网络中的位置。最后,我们构建了一些不同C末端的Bmh1嵌合体并检测了其对白念珠菌生长和菌丝发育的影响。【结果】Doxycycline诱导Bmh1表达水平下调时严重抑制了细胞的生长。非Doxycycline诱导条件下Bmh1高表达强烈促进了细胞的菌丝发育。这一促进作用绕过了ras1、efg1、cph1和tec1等基因缺失的影响,却被flo8基因的缺失阻断。C末端缺失或更换异源C末端的所有Bmh1突变株在Doxycycline诱导时都能够正常生长,但是没有明显促进菌丝发育。【结论】验证了白念珠菌14-3-3蛋白Bmh1是细胞生长所必需的,证明了Tet-off启动子可以严密控制Bmh1的表达水平。Bmh1是一个菌丝发育的正调控因子,位于Ras1、Efg1、Cph1和Tec1的下游,Flo8的上游。Bmh1的保守结构域是细胞生长所必需的,而C末端则是生长非必需的。 展开更多
关键词 白念珠菌 14-3-3 Bmh1 菌丝发育
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