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Disruption of transcriptional coactivator Sub1 leads to genome-wide re-distribution of clustered mutations induced by APOBEC in active yeast genes. / Lada, A.G.; Kliver, S.F.; Dhar, A.; Polev, D.E.; Masharsky, A.E.; Rogozin, I.B.; Pavlov, Y.I.

In: PLoS Genetics, Vol. 11, No. 5, 2015.

Research output: Contribution to journal › Article

Harvard

Lada, AG, Kliver, SF, Dhar, A, Polev, DE, Masharsky, AE, Rogozin, IB & Pavlov, YI 2015, 'Disruption of transcriptional coactivator Sub1 leads to genome-wide re-distribution of clustered mutations induced by APOBEC in active yeast genes', PLoS Genetics, vol. 11, no. 5. https://doi.org/10.1371/journal.pgen.1005217

APA

Lada, A. G., Kliver, S. F., Dhar, A., Polev, D. E., Masharsky, A. E., Rogozin, I. B., & Pavlov, Y. I. (2015). Disruption of transcriptional coactivator Sub1 leads to genome-wide re-distribution of clustered mutations induced by APOBEC in active yeast genes. PLoS Genetics, 11(5). https://doi.org/10.1371/journal.pgen.1005217

Vancouver

Lada AG, Kliver SF, Dhar A, Polev DE, Masharsky AE, Rogozin IB et al. Disruption of transcriptional coactivator Sub1 leads to genome-wide re-distribution of clustered mutations induced by APOBEC in active yeast genes. PLoS Genetics. 2015;11(5). https://doi.org/10.1371/journal.pgen.1005217

Author

Lada, A.G. ; Kliver, S.F. ; Dhar, A. ; Polev, D.E. ; Masharsky, A.E. ; Rogozin, I.B. ; Pavlov, Y.I. / Disruption of transcriptional coactivator Sub1 leads to genome-wide re-distribution of clustered mutations induced by APOBEC in active yeast genes. In: PLoS Genetics. 2015 ; Vol. 11, No. 5.

BibTeX

@article{f2d007367a3f402090daea0fb6175848,
title = "Disruption of transcriptional coactivator Sub1 leads to genome-wide re-distribution of clustered mutations induced by APOBEC in active yeast genes",
abstract = "Mutations in genomes of species are frequently distributed non-randomly, resulting in muta-tion clusters, including recently discovered kataegis in tumors. DNA editing deaminases play the prominent role in the etiology of these mutations. To gain insight into the enigmatic mechanisms of localized hypermutagenesis that lead to cluster formation, we analyzed the mutational single nucleotide variations (SNV) data obtained by whole-genome sequencing of drug-resistant mutants induced in yeast diploids by AID/APOBEC deaminase and base analog 6-HAP. Deaminase from sea lamprey, PmCDA1, induced robust clusters, while 6-HAP induced a few weak ones. We found that PmCDA1, AID, and APOBEC1 deaminases preferentially mutate the beginning of the actively transcribed genes. Inactivation of tran-scription initiation factor Sub1 strongly reduced deaminase-induced can1 mutation frequen-cy, but, surprisingly, did not decrease the total SNV load in genomes. However, the SNVs in the genomes of the sub1 clones were re-distributed, a",
keywords = "mutations, deaminases, sub1, kataegis",
author = "A.G. Lada and S.F. Kliver and A. Dhar and D.E. Polev and A.E. Masharsky and I.B. Rogozin and Y.I. Pavlov",
year = "2015",
doi = "10.1371/journal.pgen.1005217",
language = "English",
volume = "11",
journal = "PLoS Genetics",
issn = "1553-7390",
publisher = "Public Library of Science",
number = "5",

}

RIS

TY - JOUR

T1 - Disruption of transcriptional coactivator Sub1 leads to genome-wide re-distribution of clustered mutations induced by APOBEC in active yeast genes

AU - Lada, A.G.

AU - Kliver, S.F.

AU - Dhar, A.

AU - Polev, D.E.

AU - Masharsky, A.E.

AU - Rogozin, I.B.

AU - Pavlov, Y.I.

PY - 2015

Y1 - 2015

N2 - Mutations in genomes of species are frequently distributed non-randomly, resulting in muta-tion clusters, including recently discovered kataegis in tumors. DNA editing deaminases play the prominent role in the etiology of these mutations. To gain insight into the enigmatic mechanisms of localized hypermutagenesis that lead to cluster formation, we analyzed the mutational single nucleotide variations (SNV) data obtained by whole-genome sequencing of drug-resistant mutants induced in yeast diploids by AID/APOBEC deaminase and base analog 6-HAP. Deaminase from sea lamprey, PmCDA1, induced robust clusters, while 6-HAP induced a few weak ones. We found that PmCDA1, AID, and APOBEC1 deaminases preferentially mutate the beginning of the actively transcribed genes. Inactivation of tran-scription initiation factor Sub1 strongly reduced deaminase-induced can1 mutation frequen-cy, but, surprisingly, did not decrease the total SNV load in genomes. However, the SNVs in the genomes of the sub1 clones were re-distributed, a

AB - Mutations in genomes of species are frequently distributed non-randomly, resulting in muta-tion clusters, including recently discovered kataegis in tumors. DNA editing deaminases play the prominent role in the etiology of these mutations. To gain insight into the enigmatic mechanisms of localized hypermutagenesis that lead to cluster formation, we analyzed the mutational single nucleotide variations (SNV) data obtained by whole-genome sequencing of drug-resistant mutants induced in yeast diploids by AID/APOBEC deaminase and base analog 6-HAP. Deaminase from sea lamprey, PmCDA1, induced robust clusters, while 6-HAP induced a few weak ones. We found that PmCDA1, AID, and APOBEC1 deaminases preferentially mutate the beginning of the actively transcribed genes. Inactivation of tran-scription initiation factor Sub1 strongly reduced deaminase-induced can1 mutation frequen-cy, but, surprisingly, did not decrease the total SNV load in genomes. However, the SNVs in the genomes of the sub1 clones were re-distributed, a

KW - mutations

KW - deaminases

KW - sub1

KW - kataegis

U2 - 10.1371/journal.pgen.1005217

DO - 10.1371/journal.pgen.1005217

M3 - Article

VL - 11

JO - PLoS Genetics

JF - PLoS Genetics

SN - 1553-7390

IS - 5

ER -

ID: 3932226