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导致蝙蝠白鼻综合征的真菌病原体对紫外线极度敏感。

Extreme sensitivity to ultraviolet light in the fungal pathogen causing white-nose syndrome of bats.

作者信息

Palmer Jonathan M, Drees Kevin P, Foster Jeffrey T, Lindner Daniel L

机构信息

Center for Forest Mycology Research, Northern Research Station, US Forest Service, Madison, WI, 53726, USA.

Department of Molecular, Cellular, and Biomedical Sciences, University of New Hampshire, Durham, NH, 03824, USA.

出版信息

Nat Commun. 2018 Jan 2;9(1):35. doi: 10.1038/s41467-017-02441-z.

Abstract

Bat white-nose syndrome (WNS), caused by the fungal pathogen Pseudogymnoascus destructans, has decimated North American hibernating bats since its emergence in 2006. Here, we utilize comparative genomics to examine the evolutionary history of this pathogen in comparison to six closely related nonpathogenic species. P. destructans displays a large reduction in carbohydrate-utilizing enzymes (CAZymes) and in the predicted secretome (~50%), and an increase in lineage-specific genes. The pathogen has lost a key enzyme, UVE1, in the alternate excision repair (AER) pathway, which is known to contribute to repair of DNA lesions induced by ultraviolet (UV) light. Consistent with a nonfunctional AER pathway, P. destructans is extremely sensitive to UV light, as well as the DNA alkylating agent methyl methanesulfonate (MMS). The differential susceptibility of P. destructans to UV light in comparison to other hibernacula-inhabiting fungi represents a potential "Achilles' heel" of P. destructans that might be exploited for treatment of bats with WNS.

摘要

蝙蝠白鼻综合征(WNS)由真菌病原体毁灭隐球菌引起,自2006年出现以来,已使北美冬眠蝙蝠数量锐减。在此,我们利用比较基因组学来研究该病原体与六个密切相关的非致病物种相比的进化史。毁灭隐球菌在碳水化合物利用酶(CAZymes)和预测的分泌组中大幅减少(约50%),且谱系特异性基因增加。该病原体在交替切除修复(AER)途径中失去了一种关键酶UVE1,已知该酶有助于修复紫外线(UV)诱导的DNA损伤。与无功能的AER途径一致,毁灭隐球菌对紫外线以及DNA烷化剂甲磺酸甲酯(MMS)极为敏感。与其他栖息于冬眠洞穴的真菌相比,毁灭隐球菌对紫外线的不同敏感性代表了毁灭隐球菌的一个潜在“阿喀琉斯之踵”,这可能被用于治疗患白鼻综合征的蝙蝠。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db1b/5750222/4a823319be60/41467_2017_2441_Fig1_HTML.jpg

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