@article{2299, keywords = {Animals, Armadillos, DNA, Bacterial, Energy Metabolism, Evolution, Molecular, Gene Transfer, Horizontal, Genome, Bacterial, Humans, leprosy, Molecular Sequence Data, Multigene Family, Mycobacterium leprae, Sequence Analysis, DNA}, author = {Cole S T and Eiglmeier K and Parkhill J and James K D and Thomson N R and Wheeler P R and Honoré N and Garnier T and Churcher C and Harris D and Mungall K and Basham D and Brown D and Chillingworth T and Connor R and Davies R M and Devlin K and Duthoy S and Feltwell T and Fraser A and Hamlin N and Holroyd S and Hornsby T and Jagels K and Lacroix C and Maclean J and Moule S and Murphy L and Oliver K and Quail M A and Rajandream M A and Rutherford K M and Rutter S and Seeger K and Simon S and Simmonds M and Skelton J and Squares R and Squares S and Stevens K and Taylor K and Whitehead S and Woodward J R and Barrell B G}, title = {Massive gene decay in the leprosy bacillus.}, abstract = {

Leprosy, a chronic human neurological disease, results from infection with the obligate intracellular pathogen Mycobacterium leprae, a close relative of the tubercle bacillus. Mycobacterium leprae has the longest doubling time of all known bacteria and has thwarted every effort at culture in the laboratory. Comparing the 3.27-megabase (Mb) genome sequence of an armadillo-derived Indian isolate of the leprosy bacillus with that of Mycobacterium tuberculosis (4.41 Mb) provides clear explanations for these properties and reveals an extreme case of reductive evolution. Less than half of the genome contains functional genes but pseudogenes, with intact counterparts in M. tuberculosis, abound. Genome downsizing and the current mosaic arrangement appear to have resulted from extensive recombination events between dispersed repetitive sequences. Gene deletion and decay have eliminated many important metabolic activities including siderophore production, part of the oxidative and most of the microaerophilic and anaerobic respiratory chains, and numerous catabolic systems and their regulatory circuits.

}, year = {2001}, journal = {Nature}, volume = {409}, pages = {1007-11}, month = {2001 Feb 22}, issn = {0028-0836}, url = {http://www.nature.com/nature/journal/v409/n6823/pdf/4091007a0.pdf}, doi = {10.1038/35059006}, language = {eng}, }