Dataset Information

Whole Genome Metabolism - Nocardia farcinica (strain IFM 10152)

ABSTRACT:

Whole Genome Metabolism of "Nocardia farcinica (strain IFM 10152)"

This is a whole genome metabolism model of Nocardia farcinica (strain IFM 10152).

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: BMID000000141699 .

Other models with the same genus include BMID000000016635 BMID000000016636 BMID000000016637 BMID000000016638 BMID000000016639 BMID000000016640 BMID000000016641 BMID000000016642 BMID000000016643 BMID000000016644 BMID000000016645 BMID000000016646 BMID000000016647 BMID000000016648 BMID000000016649 BMID000000016650 BMID000000096528 BMID000000096529 BMID000000096530 BMID000000096531 BMID000000096532 BMID000000096533 BMID000000096534 BMID000000096535 BMID000000096536 BMID000000096537 BMID000000096538 BMID000000096539 BMID000000096540 BMID000000096541 BMID000000096542 BMID000000096543 BMID000000096544 BMID000000096545 BMID000000096546 BMID000000096547 BMID000000096548 BMID000000096549 BMID000000096550 BMID000000096551 BMID000000096552 BMID000000096553 BMID000000096554 BMID000000096555 BMID000000096556 BMID000000096557 BMID000000096558 BMID000000096559 BMID000000096560 BMID000000096561 BMID000000096562 BMID000000096563 BMID000000096564 BMID000000096565 BMID000000096566 BMID000000096567 BMID000000096568 BMID000000096569 BMID000000096570 BMID000000096571 BMID000000096572 BMID000000096573 BMID000000096574 BMID000000096575 BMID000000096576 BMID000000096577 BMID000000096578 BMID000000096579 BMID000000096580 BMID000000096581 BMID000000096582 BMID000000096583 BMID000000096584 BMID000000096585 BMID000000096586 BMID000000096587 BMID000000096588 BMID000000096589 BMID000000096590 BMID000000096591 BMID000000096592 BMID000000096593 BMID000000096594 BMID000000096595 BMID000000096596 BMID000000096597 BMID000000096598 BMID000000096599 BMID000000096600 BMID000000096601 BMID000000096602 BMID000000096603 BMID000000096604 BMID000000096605 BMID000000096606 BMID000000096607 BMID000000096608 BMID000000096609 BMID000000096610 BMID000000096611 BMID000000096612 BMID000000096613 BMID000000096614 BMID000000096615 BMID000000096616 BMID000000096617 BMID000000096618 BMID000000096619 BMID000000096620 BMID000000141036 BMID000000142082 .

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: BMID000000141699 | biostudies-other |

SECONDARY ACCESSION(S): 24180668

REPOSITORIES: biostudies-other

ACCESS DATA

Publications

The complete genomic sequence of Nocardia farcinica IFM 10152.

Ishikawa Jun J Yamashita Atsushi A Mikami Yuzuru Y Hoshino Yasutaka Y Kurita Haruyo H Hotta Kunimoto K Shiba Tadayoshi T Hattori Masahira M

Proceedings of the National Academy of Sciences of the United States of America 20041004 41

We determined the genomic sequence of Nocardia farcinica IFM 10152, a clinical isolate, and revealed the molecular basis of its versatility. The genome consists of a single circular chromosome of 6,021,225 bp with an average G+C content of 70.8% and two plasmids of 184,027 (pNF1) and 87,093 (pNF2) bp with average G+C contents of 67.2% and 68.4%, respectively. The chromosome encoded 5,674 putative protein-coding sequences, including many candidate genes for virulence and multidrug resistance as w ...[more]

PMID: 15466710

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 - Nocardia farcinica (strain IFM 10152)

Publications

The complete genomic sequence of Nocardia farcinica IFM 10152.

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