Massive gene decay in the leprosy bacillus

@article{Cole2001MassiveGD,
  title={Massive gene decay in the leprosy bacillus},
  author={Stewart T. Cole and Karin Eiglmeier and Julian Parkhill and Keith D. James and Nicholas R. Thomson and Paul Robert Wheeler and Nadine Honoré and Thierry Garnier and Carol M. Churcher and David E Harris and Karen L. Mungall and D. Basham and D. Brown and Tracey Chillingworth and R. Connor and Robin M. Davies and Kieran Devlin and St{\'e}phanie Duthoy and Theresa Feltwell and Audrey Fraser and Nancy Hamlin and Simon Holroyd and T. Hornsby and Kay Jagels and C{\'e}line Masoni Lacroix and J. M. Maclean and Sharon Moule and Lee D Murphy and Karen Oliver and Michael A. Quail and Marie-Ad{\`e}le Rajandream and Kim M. Rutherford and Simon R. Rutter and Kathy Seeger and Sylvie Simon and Mark Simmonds and Jason Skelton and Rob Squares and Steven Squares and Kim Stevens and K. Taylor and Sally Whitehead and John Robert Woodward and Bart Barrell},
  journal={Nature},
  year={2001},
  volume={409},
  pages={1007-1011}
}
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… Expand
The decaying genome of Mycobacterium leprae.
TLDR
Reductive evolution, gene decay and genome downsizing have eliminated entire metabolic pathways, together with their regulatory circuits and accessory functions, particularly those involved in catabolism, and may explain the unusually long generation time and account for the inability to culture the leprosy bacillus. Expand
Mycobacterium leprae's evolution and environmental adaptation.
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The complete sequencing and the comparative genome analysis show that M. leprae underwent a genome reductive evolution process, as result of lifestyle change and adaptation to different environments; some of lost genes are homologous to those of host cells. Expand
Mycobacterium leprae and Leprosy: A Compendium
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Entire sequencing of the bacterial genome revealed numerous pseudogenes (inactive reading frames with functional counterparts in M. tuberculosis) which might be responsible for the very limited metabolic activity of M. leprae, which has affinity to the peripheral nerves and are likely to cause neuropathy. Expand
Phylogenomics and antimicrobial resistance of the leprosy bacillus Mycobacterium leprae
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Comparative and phylogenetic analysis of 154 genomes from 25 countries provides insight into the pathogen’s evolution and antimicrobial resistance, uncovering lineages and phylogeographic trends, with the most ancestral strains linked to the Far East. Expand
M. leprae genome sequence.
TLDR
The completion of the Mycobacterium leprae genome sequence will enable testing of hypotheses that have immediate practical applications, such as drug discovery, diagnostic tools and vaccines, and will be invaluable in understanding the molecular basis for the complicated pathogenic mechanisms of leprosy. Expand
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The very low reactivity of the unique truncated hemoglobin retained by M. leprae could account for the susceptibility of this exceptionally slow‐growing microbe to NO. Expand
Biological Implications of Mycobacterium leprae Gene Expression during Infection
TLDR
Results suggest that M. leprae actively catabolizes fatty acids for energy, produces a large number of secretory proteins, utilizes the full array of sigma factors available, produces several proteins involved in iron transport, storage and regulation in the absence of recognizable genes encoding iron scavengers and transcribes several genes associated with virulence in M. tuberculosis. Expand
History and Phylogeography of Leprosy
TLDR
Comparative genomics of four different strains from India, Brazil, Thailand, and the USA revealed remarkable conservation of the ~3.27-megabase genome yet uncovered 215 polymorphic sites, mainly single-nucleotide polymorphisms (SNP), and a handful of new pseudogenes that helped retrace the evolution of M. leprae and the dissemination of leprosy. Expand
Mycobacterium leprae: genes, pseudogenes and genetic diversity.
TLDR
Comparative genomics of four different strains revealed remarkable conservation of the genome yet uncovered 215 polymorphic sites, mainly single nucleotide polymorphisms, and a handful of new pseudogenes, which helped retrace the evolution of M. leprae. Expand
Review Article Nitric Oxide and Mycobacterium leprae Pathogenicity
TLDR
Comparative genomics has unraveled massive gene decay in M. leprae, linking the strictly parasitic lifestyle with the reductive genome evolution, and could account for the susceptibility of this exceptionally slow-growing microbe to NO. Expand
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