Dataset Information

Whole Genome Metabolism - Proteus mirabilis (strain HI4320)

ABSTRACT:

Whole Genome Metabolism of "Proteus mirabilis (strain HI4320)"

This is a whole genome metabolism model of Proteus mirabilis (strain HI4320).

This model has been automatically generated by the SuBliMinaL Toolbox and libAnnotationSBML using information coming from from KEGG (release 66, April 2013, accessed via the resource's web services interface) and, where relevant, augmented with metabolic pathway information extracted from MetaCyc (version 17.0, March 2013).

This model has been produced by the path2models project and is currently hosted on BioModels Database and identified by: BMID000000141829 .

Other models with the same genus include BMID000000014263 BMID000000014264 BMID000000014265 BMID000000014266 BMID000000014267 BMID000000014268 BMID000000014269 BMID000000014270 BMID000000014271 BMID000000014272 BMID000000014273 BMID000000014274 BMID000000014275 BMID000000014276 BMID000000014277 BMID000000014278 BMID000000086948 BMID000000086949 BMID000000086950 BMID000000086951 BMID000000086952 BMID000000086953 BMID000000086954 BMID000000086955 BMID000000086956 BMID000000086957 BMID000000086958 BMID000000086959 BMID000000086960 BMID000000086961 BMID000000086962 BMID000000086963 BMID000000086964 BMID000000086965 BMID000000086966 BMID000000086967 BMID000000086968 BMID000000086969 BMID000000086970 BMID000000086971 BMID000000086972 BMID000000086973 BMID000000086974 BMID000000086975 BMID000000086976 BMID000000086977 BMID000000086978 BMID000000086979 BMID000000086980 BMID000000086981 BMID000000086982 BMID000000086983 BMID000000086984 BMID000000086985 BMID000000086986 BMID000000086987 BMID000000086988 BMID000000086989 BMID000000086990 BMID000000086991 BMID000000086992 BMID000000086993 BMID000000086994 BMID000000086995 BMID000000086996 BMID000000086997 BMID000000086998 BMID000000086999 BMID000000087000 BMID000000087001 BMID000000087002 BMID000000087003 BMID000000087004 BMID000000087005 BMID000000087006 BMID000000087007 BMID000000087008 BMID000000087009 BMID000000087010 BMID000000087011 BMID000000087012 BMID000000087013 BMID000000087014 BMID000000087015 BMID000000087016 BMID000000087017 BMID000000087018 BMID000000087019 BMID000000087020 BMID000000087021 BMID000000087022 BMID000000087023 BMID000000087024 BMID000000087025 BMID000000087026 BMID000000087027 .

To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

SUBMITTER: Path2Models project

PROVIDER: BMID000000141829 | biostudies-other |

SECONDARY ACCESSION(S): 24180668

REPOSITORIES: biostudies-other

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Publications

Complete genome sequence of uropathogenic Proteus mirabilis, a master of both adherence and motility.

Pearson Melanie M MM Sebaihia Mohammed M Churcher Carol C Quail Michael A MA Seshasayee Aswin S AS Luscombe Nicholas M NM Abdellah Zahra Z Arrosmith Claire C Atkin Becky B Chillingworth Tracey T Hauser Heidi H Jagels Kay K Moule Sharon S Mungall Karen K Norbertczak Halina H Rabbinowitsch Ester E Walker Danielle D Whithead Sally S Thomson Nicholas R NR Rather Philip N PN Parkhill Julian J Mobley Harry L T HL

Journal of bacteriology 20080328 11

The gram-negative enteric bacterium Proteus mirabilis is a frequent cause of urinary tract infections in individuals with long-term indwelling catheters or with complicated urinary tracts (e.g., due to spinal cord injury or anatomic abnormality). P. mirabilis bacteriuria may lead to acute pyelonephritis, fever, and bacteremia. Most notoriously, this pathogen uses urease to catalyze the formation of kidney and bladder stones or to encrust or obstruct indwelling urinary catheters. Here we report t ...[more]

PMID: 18375554

Publication: 1/2

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Project description:tRNAs are encoded by a large gene family, usually with several isogenic tRNAs interacting with the same codon. Mutations in the anticodon region of other tRNAs can overcome specific tRNA deficiencies. Phylogenetic analysis suggests that such mutations have occurred in evolution, but the driving force is unclear. We show that in yeast suppressor mutations in other tRNAs are able to overcome deficiency of the essential TRT2-encoded tRNAThrCGU at high temperature (40°C). Surprisingly, these tRNA suppressor mutations were obtained after whole-genome transformation with DNA from thermotolerant Kluyveromyces marxianus or Ogataea polymorpha strains, but from which the mutations did apparently not originate. We suggest that transient presence of donor DNA in the host facilitates proliferation at high temperature and thus increases the chances for occurrence of spontaneous mutations suppressing defective growth at high temperature. Whole-genome sequence analysis of three transformants revealed only four to five non-synonymous mutations of which one causing TRT2 anticodon stem stabilization and two anticodon mutations in non-threonyl-tRNAs, tRNALysCUU and tRNAeMetCAU, were causative. Both anticodon mutations suppressed lethality of TRT2 deletion and apparently caused the respective tRNAs to become novel substrates for threonyl-tRNA synthetase. LC-MS/MS data could not detect any significant mistranslation and RT-qPCR results contradicted induction of the unfolded protein response. We suggest that stress conditions have been a driving force in evolution for the selection of anticodon-switching mutations in tRNAs as revealed by phylogenetic analysis. Importance of the work In this work we have identified for the first time the causative elements in a eukaryotic organism introduced by applying whole-genome transformation and responsible for the selectable trait of interest, i.e. high temperature tolerance. Surprisingly, the whole-genome transformants contained just a few SNPs, which were unrelated to the sequence of the donor DNA. In each of three independent transformants, we have identified a SNP in a tRNA, either stabilizing the essential tRNAThrCGU at high temperature or switching the anticodon of tRNALysCUU or tRNAeMetCAU into CGU, which is apparently enough for in vivo recognition by threonyl-tRNA synthetase. LC-MS/MS analysis indeed indicated absence of significant mistranslation. Phylogenetic analysis showed that similar mutations have occurred throughout evolution and we suggest that stress conditions may have been a driving force for their selection. The low number of SNPs introduced by whole-genome transformation may favor its application for improvement of industrial yeast strains.

Dataset Information

Whole Genome Metabolism - Proteus mirabilis (strain HI4320)

Publications

Complete genome sequence of uropathogenic Proteus mirabilis, a master of both adherence and motility.

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