Show simple item record

dc.contributor.authorJoshi, Swati M
dc.contributor.authorPandey, Amit K.
dc.contributor.authorCapite, Nicole
dc.contributor.authorFortune, Sarah M.
dc.contributor.authorRubin, Eric J.
dc.contributor.authorSassetti, Christopher M.
dc.date2022-08-11T08:09:36.000
dc.date.accessioned2022-08-23T16:37:00Z
dc.date.available2022-08-23T16:37:00Z
dc.date.issued2006-07-27
dc.date.submitted2009-04-02
dc.identifier.citation<p>Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11760-5. Epub 2006 Jul 25. <a href="http://dx.doi.org/10.1073/pnas.0603179103">Link to article on publisher's site</a></p>
dc.identifier.issn0027-8424 (Print)
dc.identifier.doi10.1073/pnas.0603179103
dc.identifier.pmid16868085
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38915
dc.description.abstractWe have previously shown that approximately 5% of the genes encoded by the genome of Mycobacterium tuberculosis are specifically required for the growth or survival of this bacterium during infection. This corresponds to hundreds of genes, most of which have no identifiable function. As a unique approach to characterize these genes, we developed a method to rapidly delineate functional pathways by identifying mutations that modify each other's phenotype, i.e., "genetic interactions". Using this method, we have defined a complex set of interactions between virulence genes in this pathogen, and find that the products of unlinked genes associate to form multisubunit transporters that are required for bacterial survival in the host. These findings implicate a previously undescribed family of transport systems in the pathogenesis of tuberculosis, and identify genes that are likely to function in the metabolism of their substrates. This method can be readily applied to other organisms at either the single pathway level, as described here, or at the system level to define quantitative genetic interaction networks.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16868085&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1544243/
dc.subjectAnimals
dc.subjectBacterial Proteins
dc.subjectChromosome Mapping
dc.subjectDNA Transposable Elements
dc.subject*Genes, Bacterial
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMolecular Sequence Data
dc.subjectMycobacterium tuberculosis
dc.subjectReproducibility of Results
dc.subjectTuberculosis
dc.subjectVirulence
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleCharacterization of mycobacterial virulence genes through genetic interaction mapping
dc.typeJournal Article
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume103
dc.source.issue31
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1748
dc.identifier.contextkey808513
html.description.abstract<p>We have previously shown that approximately 5% of the genes encoded by the genome of Mycobacterium tuberculosis are specifically required for the growth or survival of this bacterium during infection. This corresponds to hundreds of genes, most of which have no identifiable function. As a unique approach to characterize these genes, we developed a method to rapidly delineate functional pathways by identifying mutations that modify each other's phenotype, i.e., "genetic interactions". Using this method, we have defined a complex set of interactions between virulence genes in this pathogen, and find that the products of unlinked genes associate to form multisubunit transporters that are required for bacterial survival in the host. These findings implicate a previously undescribed family of transport systems in the pathogenesis of tuberculosis, and identify genes that are likely to function in the metabolism of their substrates. This method can be readily applied to other organisms at either the single pathway level, as described here, or at the system level to define quantitative genetic interaction networks.</p>
dc.identifier.submissionpathoapubs/1748
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.source.pages11760-5


This item appears in the following Collection(s)

Show simple item record