Dataset Information

Whole Genome Metabolism - Hodgkinia cicadicola (strain Dsem)

ABSTRACT:

Whole Genome Metabolism of "Hodgkinia cicadicola (strain Dsem)"

This is a whole genome metabolism model of Hodgkinia cicadicola (strain Dsem).

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: BMID000000141151 .

Other models with the same genus include BMID000000021241 BMID000000021242 BMID000000021243 BMID000000021244 BMID000000115184 BMID000000115185 BMID000000115186 BMID000000115187 BMID000000115188 BMID000000115189 BMID000000115190 BMID000000115191 BMID000000115192 BMID000000115193 BMID000000115194 BMID000000115195 BMID000000115196 BMID000000115197 BMID000000115198 BMID000000115199 BMID000000115200 BMID000000115201 .

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: BMID000000141151 | 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 - Hodgkinia cicadicola (strain Dsem)

Publications

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

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