Massive gene decay in the leprosy bacillus

By S. Cole, K. Eiglmeier, Julian Parkhill, K. James, N. Thomson, P. Wheeler, N. Honoré, T. Garnier, C. Churcher, D. Harris and 34 more. Nature, 2001

1,729 citations recorded by the source corpus.

Subfields: Epidemiology, Infectious Diseases

View Paper: https://www.semanticscholar.org/paper/ffdcde17df8c16e4826cdae320c0d6d9adfcabb3

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In Epidemiology

In Infectious Diseases

Elhanan Borenstein

Citations in the corpus

Re-annotation of the genome sequence of Mycobacterium tuberculosis H37Rv. (2002, background): “This annotation also contains new comparisons with the recently completed genome sequence of Mycobacterium leprae (Cole et al., 2001).”
Ψ-Φ: Exploring the outer limits of bacterial pseudogenes (2004, background): “…genome of typhus bacterium Rickettsia prowazekii contains a large noncoding fraction, formed, in part, by recognizable and degraded pseudogenes (Andersson et al. 1998); and in Mycobacterium leprae, the causative agent of leprosy, pseudogenes constitute 27% of the 3.3-Mb genome (Cole et al. 2001).”
Toxin–antitoxin loci are highly abundant in free-living but lost from host-associated prokaryotes (2005, background): “M.leprae evolved from Mtb by massive reductive evolution and its extant genome contains a large number of pseudogenes, indicating that its genome is still undergoing decay ( 38 ).”
Silencing Essential Protein Secretion in Mycobacterium smegmatis by Using Tetracycline Repressors (2007, background): “Functional orthologues for 78% of essential M. tuberculosis genes have been retained in the genome of M. leprae, even though its genome has undergone extensive degeneration and contains functional orthologues of only 40% of all M. tuberculosis genes ( 8 , 37).”
Pathway to Synthesis and Processing of Mycolic Acids in Mycobacterium tuberculosis (2005, background): “as a minimal genome (22), the lack of fabD2 in M.”
From Q Fever to Coxiella burnetii Infection: a Paradigm Change (2016, background): “, hyperpathogenicity is driven by deletion of nonvirulence genes rather than by acquisition of virulence factors (152, 153).”