Dataset Information

Whole Genome Metabolism - Coccidioides immitis (strain RS)

ABSTRACT:

Whole Genome Metabolism of "Coccidioides immitis (strain RS)"

This is a whole genome metabolism model of Coccidioides immitis (strain RS).

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: BMID000000141846 .

Other models with the same genus include BMID000000007799 BMID000000007800 BMID000000007801 BMID000000007802 BMID000000007803 BMID000000007804 BMID000000007805 BMID000000007806 BMID000000007807 BMID000000007808 BMID000000007809 BMID000000007810 BMID000000007811 BMID000000007812 BMID000000007813 BMID000000007814 BMID000000007815 BMID000000007816 BMID000000007817 BMID000000007818 BMID000000007819 BMID000000007820 BMID000000007821 BMID000000007822 BMID000000007823 BMID000000007824 BMID000000007825 BMID000000007826 BMID000000007827 BMID000000007828 BMID000000007829 BMID000000060884 BMID000000060885 BMID000000060886 BMID000000060887 BMID000000060888 BMID000000060889 BMID000000060890 BMID000000060891 BMID000000060892 BMID000000060893 BMID000000060894 BMID000000060895 BMID000000060896 BMID000000060897 BMID000000060898 BMID000000060899 BMID000000060900 BMID000000060901 BMID000000060902 BMID000000060903 BMID000000060904 BMID000000060905 BMID000000060906 BMID000000060907 BMID000000060908 BMID000000060909 BMID000000060910 BMID000000060911 BMID000000060912 BMID000000060913 BMID000000060914 BMID000000060915 BMID000000060916 BMID000000060917 BMID000000060918 BMID000000060919 BMID000000060920 BMID000000060921 BMID000000060922 BMID000000060923 BMID000000060924 BMID000000060925 BMID000000060926 BMID000000060927 BMID000000060928 BMID000000060929 BMID000000060930 BMID000000060931 BMID000000060932 BMID000000060933 BMID000000060934 BMID000000060935 BMID000000060936 BMID000000060937 BMID000000060938 BMID000000060939 BMID000000060940 BMID000000060941 BMID000000060942 BMID000000060943 BMID000000060944 BMID000000060945 BMID000000060946 BMID000000060947 BMID000000060948 BMID000000060949 BMID000000060950 BMID000000060951 BMID000000060952 BMID000000060953 BMID000000060954 BMID000000060955 BMID000000060956 BMID000000060957 BMID000000060958 BMID000000020664 BMID000000020665 BMID000000020666 BMID000000020667 BMID000000020668 BMID000000020669 BMID000000020670 BMID000000020671 BMID000000020672 BMID000000020673 BMID000000020674 BMID000000020675 BMID000000020676 BMID000000020677 BMID000000020678 BMID000000020679 BMID000000020680 BMID000000020681 BMID000000020682 BMID000000020683 BMID000000020684 BMID000000020685 BMID000000020686 BMID000000020687 BMID000000020688 BMID000000020689 BMID000000020690 BMID000000020691 BMID000000020692 BMID000000020693 BMID000000020694 BMID000000112606 BMID000000112607 BMID000000112608 BMID000000112609 BMID000000112610 BMID000000112611 BMID000000112612 BMID000000112613 BMID000000112614 BMID000000112615 BMID000000112616 BMID000000112617 BMID000000112618 BMID000000112619 BMID000000112620 BMID000000112621 BMID000000112622 BMID000000112623 BMID000000112624 BMID000000112625 BMID000000112626 BMID000000112627 BMID000000112628 BMID000000112629 BMID000000112630 BMID000000112631 BMID000000112632 BMID000000112633 BMID000000112634 BMID000000112635 BMID000000112636 BMID000000112637 BMID000000112638 BMID000000112639 BMID000000112640 BMID000000112641 BMID000000112642 BMID000000112643 BMID000000112644 BMID000000112645 BMID000000112646 BMID000000112647 BMID000000112648 BMID000000112649 BMID000000112650 BMID000000112651 BMID000000112652 BMID000000112653 BMID000000112654 BMID000000112655 BMID000000112656 BMID000000112657 BMID000000112658 BMID000000112659 BMID000000112660 BMID000000112661 BMID000000112662 BMID000000112663 BMID000000112664 BMID000000112665 BMID000000112666 BMID000000112667 BMID000000112668 BMID000000112669 BMID000000112670 BMID000000112671 BMID000000112672 BMID000000112673 BMID000000112674 BMID000000112675 BMID000000112676 BMID000000112677 BMID000000112678 BMID000000112679 BMID000000140573 .

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: BMID000000141846 | biostudies-other |

SECONDARY ACCESSION(S): 24180668

REPOSITORIES: biostudies-other

ACCESS DATA

Publications

Comparative genomic analyses of the human fungal pathogens Coccidioides and their relatives.

Sharpton Thomas J TJ Stajich Jason E JE Rounsley Steven D SD Gardner Malcolm J MJ Wortman Jennifer R JR Jordar Vinita S VS Maiti Rama R Kodira Chinnappa D CD Neafsey Daniel E DE Zeng Qiandong Q Hung Chiung-Yu CY McMahan Cody C Muszewska Anna A Grynberg Marcin M Mandel M Alejandra MA Kellner Ellen M EM Barker Bridget M BM Galgiani John N JN Orbach Marc J MJ Kirkland Theo N TN Cole Garry T GT Henn Matthew R MR Birren Bruce W BW Taylor John W JW

Genome research 20090828 10

While most Ascomycetes tend to associate principally with plants, the dimorphic fungi Coccidioides immitis and Coccidioides posadasii are primary pathogens of immunocompetent mammals, including humans. Infection results from environmental exposure to Coccidiodies, which is believed to grow as a soil saprophyte in arid deserts. To investigate hypotheses about the life history and evolution of Coccidioides, the genomes of several Onygenales, including C. immitis and C. posadasii; a close, nonpatho ...[more]

PMID: 19717792

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 - Coccidioides immitis (strain RS)

Publications

Comparative genomic analyses of the human fungal pathogens Coccidioides and their relatives.

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