Dataset Information

Whole Genome Metabolism - Salinispora arenicola (strain CNS-205)

ABSTRACT:

Whole Genome Metabolism of "Salinispora arenicola (strain CNS-205)"

This is a whole genome metabolism model of Salinispora arenicola (strain CNS-205).

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: BMID000000140763 .

Other models with the same genus include BMID000000016782 BMID000000016783 BMID000000016784 BMID000000016785 BMID000000016786 BMID000000016787 BMID000000016788 BMID000000016789 BMID000000016790 BMID000000016791 BMID000000016792 BMID000000016793 BMID000000016794 BMID000000016795 BMID000000016796 BMID000000016797 BMID000000097159 BMID000000097160 BMID000000097161 BMID000000097162 BMID000000097163 BMID000000097164 BMID000000097165 BMID000000097166 BMID000000097167 BMID000000097168 BMID000000097169 BMID000000097170 BMID000000097171 BMID000000097172 BMID000000097173 BMID000000097174 BMID000000097175 BMID000000097176 BMID000000097177 BMID000000097178 BMID000000097179 BMID000000097180 BMID000000097181 BMID000000097182 BMID000000097183 BMID000000097184 BMID000000097185 BMID000000097186 BMID000000097187 BMID000000097188 BMID000000097189 BMID000000097190 BMID000000097191 BMID000000097192 BMID000000097193 BMID000000097194 BMID000000097195 BMID000000097196 BMID000000097197 BMID000000097198 BMID000000097199 BMID000000097200 BMID000000097201 BMID000000097202 BMID000000097203 BMID000000097204 BMID000000097205 BMID000000097206 BMID000000097207 BMID000000097208 BMID000000097209 BMID000000097210 BMID000000097211 BMID000000097212 BMID000000097213 BMID000000097214 BMID000000097215 BMID000000097216 BMID000000097217 BMID000000097218 BMID000000097219 BMID000000097220 BMID000000097221 BMID000000097222 BMID000000097223 BMID000000097224 BMID000000097225 BMID000000097226 BMID000000097227 BMID000000097228 BMID000000097229 BMID000000097230 BMID000000097231 BMID000000097232 BMID000000097233 BMID000000097234 BMID000000097235 BMID000000097236 BMID000000097237 BMID000000097238 BMID000000097239 BMID000000097240 BMID000000097241 BMID000000097242 BMID000000097243 BMID000000097244 BMID000000097245 BMID000000097246 BMID000000097247 BMID000000097248 BMID000000017415 BMID000000017416 BMID000000017417 BMID000000017418 BMID000000017419 BMID000000017420 BMID000000017421 BMID000000017422 BMID000000017423 BMID000000017424 BMID000000017425 BMID000000017426 BMID000000017427 BMID000000017428 BMID000000017429 BMID000000100019 BMID000000100020 BMID000000100021 BMID000000100022 BMID000000100023 BMID000000100024 BMID000000100025 BMID000000100026 BMID000000100027 BMID000000100028 BMID000000100029 BMID000000100030 BMID000000100031 BMID000000100032 BMID000000100033 BMID000000100034 BMID000000100035 BMID000000100036 BMID000000100037 BMID000000100038 BMID000000100039 BMID000000100040 BMID000000100041 BMID000000100042 BMID000000100043 BMID000000100044 BMID000000100045 BMID000000100046 BMID000000100047 BMID000000100048 BMID000000100049 BMID000000100050 BMID000000100051 BMID000000100052 BMID000000100053 BMID000000100054 BMID000000100055 BMID000000100056 BMID000000100057 BMID000000100058 BMID000000100059 BMID000000100060 BMID000000100061 BMID000000100062 BMID000000100063 BMID000000100064 BMID000000100065 BMID000000100066 BMID000000100067 BMID000000100068 BMID000000100069 BMID000000100070 BMID000000100071 BMID000000100072 BMID000000100073 BMID000000100074 BMID000000100075 BMID000000100076 BMID000000100077 BMID000000100078 BMID000000100079 BMID000000100080 BMID000000100081 BMID000000100082 BMID000000100083 BMID000000100084 BMID000000100085 BMID000000100086 BMID000000100087 BMID000000100088 BMID000000100089 BMID000000100090 BMID000000100091 BMID000000100092 BMID000000100093 BMID000000100094 BMID000000100095 BMID000000100096 BMID000000100097 BMID000000100098 BMID000000100099 BMID000000100100 BMID000000100101 BMID000000100102 BMID000000100103 BMID000000100104 BMID000000100105 BMID000000100106 BMID000000141604 .

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: BMID000000140763 | 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 - Salinispora arenicola (strain CNS-205)

Publications

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

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