Dataset Information

Whole Genome Metabolism - Mannheimia succiniciproducens (strain MBEL55E)

ABSTRACT:

Whole Genome Metabolism of "Mannheimia succiniciproducens (strain MBEL55E)"

This is a whole genome metabolism model of Mannheimia succiniciproducens (strain MBEL55E).

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: BMID000000141499 .

Other models with the same genus include BMID000000019273 BMID000000019274 BMID000000019275 BMID000000019276 BMID000000019277 BMID000000019278 BMID000000019279 BMID000000019280 BMID000000019281 BMID000000019282 BMID000000019283 BMID000000019284 BMID000000019285 BMID000000019286 BMID000000019287 BMID000000106637 BMID000000106638 BMID000000106639 BMID000000106640 BMID000000106641 BMID000000106642 BMID000000106643 BMID000000106644 BMID000000106645 BMID000000106646 BMID000000106647 BMID000000106648 BMID000000106649 BMID000000106650 BMID000000106651 BMID000000106652 BMID000000106653 BMID000000106654 BMID000000106655 BMID000000106656 BMID000000106657 BMID000000106658 BMID000000106659 BMID000000106660 BMID000000106661 BMID000000106662 BMID000000106663 BMID000000106664 BMID000000106665 BMID000000106666 BMID000000106667 BMID000000106668 BMID000000106669 BMID000000106670 BMID000000106671 BMID000000106672 BMID000000106673 BMID000000106674 BMID000000106675 BMID000000106676 BMID000000106677 BMID000000106678 BMID000000106679 BMID000000106680 BMID000000106681 BMID000000106682 BMID000000106683 BMID000000106684 BMID000000106685 BMID000000106686 BMID000000106687 BMID000000106688 BMID000000106689 BMID000000106690 BMID000000106691 BMID000000106692 BMID000000106693 BMID000000106694 BMID000000106695 BMID000000106696 BMID000000106697 BMID000000106698 BMID000000106699 BMID000000106700 BMID000000106701 BMID000000106702 BMID000000106703 BMID000000106704 BMID000000106705 BMID000000106706 BMID000000106707 BMID000000106708 BMID000000106709 BMID000000106710 BMID000000106711 BMID000000142234 BMID000000142633 BMID000000142755 .

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: BMID000000141499 | biostudies-other |

SECONDARY ACCESSION(S): 24180668

REPOSITORIES: biostudies-other

ACCESS DATA

Publications

Path2Models: large-scale generation of computational models from biochemical pathway maps.

Büchel Finja F Rodriguez Nicolas N Swainston Neil N Wrzodek Clemens C Wrzodek Clemens C Czauderna Tobias T Keller Roland R Mittag Florian F Schubert Michael M Glont Mihai M Golebiewski Martin M van Iersel Martijn M Keating Sarah S Rall Matthias M Wybrow Michael M Hermjakob Henning H Hucka Michael M Kell Douglas B DB Müller Wolfgang W Mendes Pedro P Zell Andreas A Chaouiya Claudine C Saez-Rodriguez Julio J Schreiber Falk F Laibe Camille C Dräger Andreas A Le Novère Nicolas N

BMC systems biology 20131101

<h4>Background</h4>Systems biology projects and omics technologies have led to a growing number of biochemical pathway models and reconstructions. However, the majority of these models are still created de novo, based on literature mining and the manual processing of pathway data.<h4>Results</h4>To increase the efficiency of model creation, the Path2Models project has automatically generated mathematical models from pathway representations using a suite of freely available software. Data sources ...[more]

PMID: 24180668

Publication: 1/2

Similar Datasets

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 - Mannheimia succiniciproducens (strain MBEL55E)

Publications

Path2Models: large-scale generation of computational models from biochemical pathway maps.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets