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结核分枝杆菌同基因菌株中IS6110介导的缺失多态性

IS6110-mediated deletion polymorphism in isogenic strains of Mycobacterium tuberculosis.

作者信息

Sampson S L, Richardson M, Van Helden P D, Warren R M

机构信息

Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA.

出版信息

J Clin Microbiol. 2004 Feb;42(2):895-8. doi: 10.1128/JCM.42.2.895-898.2004.

DOI:10.1128/JCM.42.2.895-898.2004
PMID:14766883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC344511/
Abstract

Previous studies have described IS6110-mediated polymorphism as an important driving force in Mycobacterium tuberculosis genome evolution and have provided indirect evidence for IS6110-driven deletion events. This study provides the first description of an IS6110-mediated deletion event in truly isogenic strains. We also provide further support for the hypothesis that the region from Rv1754 to Rv1765 is a hot spot for IS6110 insertion and deletion events.

摘要

先前的研究已将IS6110介导的多态性描述为结核分枝杆菌基因组进化中的一个重要驱动力，并为IS6110驱动的缺失事件提供了间接证据。本研究首次描述了在真正的同基因菌株中发生的IS6110介导的缺失事件。我们还进一步支持了以下假说，即从Rv1754到Rv1765的区域是IS6110插入和缺失事件的热点。

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