Dataset Information

Whole Genome Metabolism - Anaplasma phagocytophilum (strain HZ)

ABSTRACT:

Whole Genome Metabolism of "Anaplasma phagocytophilum (strain HZ)"

This is a whole genome metabolism model of Anaplasma phagocytophilum (strain HZ).

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: BMID000000140344 .

Other models with the same genus include BMID000000010592 BMID000000010593 BMID000000010594 BMID000000010595 BMID000000010596 BMID000000010597 BMID000000010598 BMID000000010599 BMID000000010600 BMID000000010601 BMID000000010602 BMID000000010603 BMID000000010604 BMID000000071809 BMID000000071810 BMID000000071811 BMID000000071812 BMID000000071813 BMID000000071814 BMID000000071815 BMID000000071816 BMID000000071817 BMID000000071818 BMID000000071819 BMID000000071820 BMID000000071821 BMID000000071822 BMID000000071823 BMID000000071824 BMID000000071825 BMID000000071826 BMID000000071827 BMID000000071828 BMID000000071829 BMID000000071830 BMID000000071831 BMID000000071832 BMID000000071833 BMID000000071834 BMID000000071835 BMID000000071836 BMID000000071837 BMID000000071838 BMID000000071839 BMID000000071840 BMID000000071841 BMID000000071842 BMID000000071843 BMID000000071844 BMID000000071845 BMID000000071846 BMID000000071847 BMID000000071848 BMID000000071849 BMID000000071850 BMID000000071851 BMID000000071852 BMID000000071853 BMID000000071854 BMID000000071855 BMID000000071856 BMID000000013937 BMID000000013938 BMID000000013939 BMID000000013940 BMID000000013941 BMID000000013942 BMID000000013943 BMID000000013944 BMID000000013945 BMID000000013946 BMID000000013947 BMID000000013948 BMID000000013949 BMID000000085427 BMID000000085428 BMID000000085429 BMID000000085430 BMID000000085431 BMID000000085432 BMID000000085433 BMID000000085434 BMID000000085435 BMID000000085436 BMID000000085437 BMID000000085438 BMID000000085439 BMID000000085440 BMID000000085441 BMID000000085442 BMID000000085443 BMID000000085444 BMID000000085445 BMID000000085446 BMID000000085447 BMID000000085448 BMID000000085449 BMID000000085450 BMID000000085451 BMID000000085452 BMID000000085453 BMID000000085454 BMID000000085455 BMID000000085456 BMID000000085457 BMID000000085458 BMID000000085459 BMID000000085460 BMID000000085461 BMID000000085462 BMID000000085463 BMID000000085464 BMID000000085465 BMID000000085466 BMID000000085467 BMID000000085468 BMID000000085469 BMID000000085470 BMID000000085471 BMID000000085472 BMID000000085473 BMID000000085474 BMID000000085475 BMID000000085476 BMID000000085477 BMID000000085478 BMID000000141665 BMID000000019677 BMID000000019678 BMID000000019679 BMID000000019680 BMID000000019681 BMID000000019682 BMID000000019683 BMID000000019684 BMID000000019685 BMID000000019686 BMID000000019687 BMID000000019688 BMID000000019689 BMID000000108300 BMID000000108301 BMID000000108302 BMID000000108303 BMID000000108304 BMID000000108305 BMID000000108306 BMID000000108307 BMID000000108308 BMID000000108309 BMID000000108310 BMID000000108311 BMID000000108312 BMID000000108313 BMID000000108314 BMID000000108315 BMID000000108316 BMID000000108317 BMID000000108318 BMID000000108319 BMID000000108320 BMID000000108321 BMID000000108322 BMID000000108323 BMID000000108324 BMID000000108325 BMID000000108326 BMID000000108327 BMID000000108328 BMID000000108329 BMID000000108330 BMID000000108331 BMID000000108332 BMID000000108333 BMID000000108334 BMID000000108335 BMID000000108336 BMID000000108337 BMID000000108338 BMID000000108339 BMID000000108340 BMID000000108341 BMID000000108342 BMID000000108343 BMID000000108344 BMID000000108345 BMID000000108346 BMID000000108347 BMID000000108348 BMID000000108349 BMID000000108350 BMID000000108351 BMID000000140954 BMID000000020932 BMID000000020933 BMID000000020934 BMID000000020935 BMID000000020936 BMID000000020937 BMID000000020938 BMID000000020939 BMID000000020940 BMID000000020941 BMID000000020942 BMID000000020943 BMID000000020944 BMID000000113732 BMID000000113733 BMID000000113734 BMID000000113735 BMID000000113736 BMID000000113737 BMID000000113738 BMID000000113739 BMID000000113740 BMID000000113741 BMID000000113742 BMID000000113743 BMID000000113744 BMID000000113745 BMID000000113746 BMID000000113747 BMID000000113748 BMID000000113749 BMID000000113750 BMID000000113751 BMID000000113752 BMID000000113753 BMID000000113754 BMID000000113755 BMID000000113756 BMID000000113757 BMID000000113758 BMID000000113759 BMID000000113760 BMID000000113761 BMID000000113762 BMID000000113763 BMID000000113764 BMID000000113765 BMID000000113766 BMID000000113767 BMID000000113768 BMID000000113769 BMID000000113770 BMID000000113771 BMID000000113772 BMID000000113773 BMID000000113774 BMID000000113775 BMID000000113776 BMID000000113777 BMID000000113778 BMID000000113779 BMID000000113780 BMID000000113781 BMID000000140278 .

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: BMID000000140344 | 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 - Anaplasma phagocytophilum (strain HZ)

Publications

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

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