Structural genomics of Mycobacterium tuberculosis.
TL;DRAbstract
In 1998 the genome sequence of Mycobacterium tuberculosis H37Rv was published1. M. tuberculosis is the primary causative agent of tuberculosis, a disease with a long history in humans, which still has a great impact on human mortality today. As part of the M. tuberculosis Structural Genomics Consortium we selected nine target genes (Rv0534c (menA); Rv0548c (menB); Rv0553 (menC); Rv0555 (menD); Rv0542c (menE); Rv3853 (menG); Rv0558 (ubiE); Rv0989c (grcC2) and Rv0990c) from M. tuberculosis, including all known members of the menaquinone biosynthesis pathway, for structural studies. \nAll nine genes were taken through the structural genomics “pipeline”, either becoming stuck at various “bottlenecks” or continuing successfully to structure solution. At the initial bioinformatics analysis step, eight of the nine targeted genes were deemed suitable for further study. PCR amplification and cloning of these genes into several different expression vectors followed. Expression of the gene p
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In 1998 the genome sequence of Mycobacterium tuberculosis H37Rv was published1. M. tuberculosis is the primary causative agent of tuberculosis, a disease with a long history in humans, which still has a great impact on human mortality today. As part of the M. tuberculosis Structural Genomics Consortium we selected nine target genes (Rv0534c (menA); Rv0548c (menB); Rv0553 (menC); Rv0555 (menD); Rv0542c (menE); Rv3853 (menG); Rv0558 (ubiE); Rv0989c (grcC2) and Rv0990c) from M. tuberculosis, including all known members of the menaquinone biosynthesis pathway, for structural studies. \nAll nine genes were taken through the structural genomics “pipeline”, either becoming stuck at various “bottlenecks” or continuing successfully to structure solution. At the initial bioinformatics analysis step, eight of the nine targeted genes were deemed suitable for further study. PCR amplification and cloning of these genes into several different expression vectors followed. Expression of the gene p
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