Dataset Information

Whole Genome Metabolism - Amycolatopsis mediterranei (strain U-32)

ABSTRACT:

Whole Genome Metabolism of "Amycolatopsis mediterranei (strain U-32)"

This is a whole genome metabolism model of Amycolatopsis mediterranei (strain U-32).

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: BMID000000141093 .

Other models with the same genus include BMID000000012509 BMID000000012510 BMID000000012511 BMID000000012512 BMID000000012513 BMID000000012514 BMID000000012515 BMID000000012516 BMID000000012517 BMID000000012518 BMID000000012519 BMID000000012520 BMID000000012521 BMID000000012522 BMID000000012523 BMID000000012524 BMID000000012525 BMID000000079969 BMID000000079970 BMID000000079971 BMID000000079972 BMID000000079973 BMID000000079974 BMID000000079975 BMID000000079976 BMID000000079977 BMID000000079978 BMID000000079979 BMID000000079980 BMID000000079981 BMID000000079982 BMID000000079983 BMID000000079984 BMID000000079985 BMID000000079986 BMID000000079987 BMID000000079988 BMID000000079989 BMID000000079990 BMID000000079991 BMID000000079992 BMID000000079993 BMID000000079994 BMID000000079995 BMID000000079996 BMID000000079997 BMID000000079998 BMID000000079999 BMID000000080000 BMID000000080001 BMID000000080002 BMID000000080003 BMID000000080004 BMID000000080005 BMID000000080006 BMID000000080007 BMID000000080008 BMID000000080009 BMID000000080010 BMID000000080011 BMID000000080012 BMID000000080013 BMID000000080014 BMID000000080015 BMID000000080016 BMID000000080017 BMID000000080018 BMID000000080019 BMID000000080020 BMID000000080021 BMID000000080022 BMID000000080023 BMID000000080024 BMID000000080025 BMID000000080026 BMID000000080027 BMID000000080028 BMID000000080029 BMID000000080030 BMID000000080031 BMID000000080032 BMID000000080033 BMID000000080034 BMID000000080035 BMID000000080036 BMID000000080037 BMID000000080038 BMID000000080039 BMID000000080040 BMID000000080041 BMID000000080042 BMID000000080043 BMID000000080044 BMID000000080045 BMID000000080046 BMID000000080047 BMID000000080048 BMID000000080049 BMID000000080050 BMID000000080051 BMID000000080052 BMID000000080053 BMID000000080054 BMID000000080055 BMID000000080056 BMID000000080057 BMID000000080058 BMID000000080059 BMID000000080060 BMID000000080061 BMID000000080062 BMID000000080063 BMID000000140876 BMID000000142473 .

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: BMID000000141093 | 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

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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 - Amycolatopsis mediterranei (strain U-32)

Publications

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

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