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分枝杆菌基因组中的简单序列重复

Simple sequence repeats in mycobacterial genomes.

作者信息

Sreenu Vattipally B, Kumar Pankaj, Nagaraju Javaregowda, Nagarajam Hampapathalu A

机构信息

Laboratory of Computational Biology, Centre for DNA Fingerprinting and Diagnostics, ECIL Road, Nacharam, Hyderabad 500 076, India.

出版信息

J Biosci. 2007 Jan;32(1):3-15. doi: 10.1007/s12038-007-0002-7.

Abstract

Simple sequence repeats (SSRs) or microsatellites are the repetitive nucleotide sequences of motifs of length 1-6 bp. They are scattered throughout the genomes of all the known organisms ranging from viruses to eukaryotes. Microsatellites undergo mutations in the form of insertions and deletions (INDELS) of their repeat units with some bias towards insertions that lead to microsatellite tract expansion. Although prokaryotic genomes derive some plasticity due to microsatellite mutations they have in-built mechanisms to arrest undue expansions of microsatellites and one such mechanism is constituted by post-replicative DNA repair enzymes MutL, MutH and MutS. The mycobacterial genomes lack these enzymes and as a null hypothesis one could expect these genomes to harbour many long tracts. It is therefore interesting to analyse the mycobacterial genomes for distribution and abundance of microsatellites tracts and to look for potentially polymorphic microsatellites. Available mycobacterial genomes, Mycobacterium avium, M. leprae, M. bovis and the two strains of M. tuberculosis (CDC1551 and H37Rv) were analysed for frequencies and abundance of SSRs. Our analysis revealed that the SSRs are distributed throughout the mycobacterial genomes at an average of 220-230 SSR tracts per kb. All the mycobacterial genomes contain few regions that are conspicuously denser or poorer in microsatellites compared to their expected genome averages. The genomes distinctly show scarcity of long microsatellites despite the absence of a post-replicative DNA repair system. Such severe scarcity of long microsatellites could arise as a result of strong selection pressures operating against long and unstable sequences although influence of GC-content and role of point mutations in arresting microsatellite expansions can not be ruled out. Nonetheless, the long tracts occasionally found in coding as well as non-coding regions may account for limited genome plasticity in these genomes.

摘要

简单序列重复(SSRs)或微卫星是长度为1 - 6个碱基对的基序的重复核苷酸序列。它们散布在从病毒到真核生物的所有已知生物体的基因组中。微卫星以其重复单元的插入和缺失(INDELS)形式发生突变,并且在插入方面存在一定偏向性,这会导致微卫星序列长度增加。虽然原核生物基因组由于微卫星突变而具有一定可塑性,但它们具有内在机制来阻止微卫星的过度扩展,其中一种机制由复制后DNA修复酶MutL、MutH和MutS构成。分枝杆菌基因组缺乏这些酶,因此,基于零假设,可以预期这些基因组含有许多长序列。因此,分析分枝杆菌基因组中微卫星序列的分布和丰度,并寻找潜在的多态性微卫星是很有趣的。我们分析了现有分枝杆菌基因组,包括鸟分枝杆菌、麻风分枝杆菌、牛分枝杆菌以及两株结核分枝杆菌(CDC1551和H37Rv)中SSRs的频率和丰度。我们的分析表明,SSRs分布在整个分枝杆菌基因组中,平均每千碱基有220 - 230个SSRs序列。与预期的基因组平均值相比,所有分枝杆菌基因组都有一些区域的微卫星明显更密集或更稀少。尽管缺乏复制后DNA修复系统,但这些基因组明显显示出长微卫星的稀缺。长微卫星如此严重的稀缺可能是由于针对长而不稳定序列的强大选择压力导致的,尽管不能排除GC含量的影响以及点突变在阻止微卫星扩展中的作用。尽管如此,在编码区和非编码区偶尔发现的长序列可能解释了这些基因组中有限的基因组可塑性。

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