Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging

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Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging. / Lee, Jong-Hyuk; Demarest, Tyler G.; Babbar, Mansi; Kim, Edward W.; Okur, Mustafa N.; De, Supriyo; Croteau, Deborah L.; Bohr, Vilhelm A.

In: Nucleic Acids Research, Vol. 47, No. 16, 2019, p. 8548-8562.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Lee, J-H, Demarest, TG, Babbar, M, Kim, EW, Okur, MN, De, S, Croteau, DL & Bohr, VA 2019, 'Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging', Nucleic Acids Research, vol. 47, no. 16, pp. 8548-8562. https://doi.org/10.1093/nar/gkz568

APA

Lee, J-H., Demarest, T. G., Babbar, M., Kim, E. W., Okur, M. N., De, S., Croteau, D. L., & Bohr, V. A. (2019). Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging. Nucleic Acids Research, 47(16), 8548-8562. https://doi.org/10.1093/nar/gkz568

Vancouver

Lee J-H, Demarest TG, Babbar M, Kim EW, Okur MN, De S et al. Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging. Nucleic Acids Research. 2019;47(16):8548-8562. https://doi.org/10.1093/nar/gkz568

Author

Lee, Jong-Hyuk ; Demarest, Tyler G. ; Babbar, Mansi ; Kim, Edward W. ; Okur, Mustafa N. ; De, Supriyo ; Croteau, Deborah L. ; Bohr, Vilhelm A. / Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging. In: Nucleic Acids Research. 2019 ; Vol. 47, No. 16. pp. 8548-8562.

Bibtex

@article{7e486c2298aa4daeae4cf27dcf6f2009,
title = "Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging",
abstract = "Cockayne syndrome is an accelerated aging disorder, caused by mutations in the CSA or CSB genes. In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction. Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results show striking enrichment of PAR at transcription start sites, depletion of heterochromatin and downregulation of H3K9me3-specific methyltransferases SUV39H1 and SETDB1. Induced-expression of SETDB1 in CSB-deficient cells downregulated PAR and normalized mitochondrial function. The results suggest that defects in CSB are strongly associated with loss of heterochromatin, downregulation of SETDB1, increased PAR in highly-transcribed regions, and mitochondrial dysfunction.",
author = "Jong-Hyuk Lee and Demarest, {Tyler G.} and Mansi Babbar and Kim, {Edward W.} and Okur, {Mustafa N.} and Supriyo De and Croteau, {Deborah L.} and Bohr, {Vilhelm A.}",
year = "2019",
doi = "10.1093/nar/gkz568",
language = "English",
volume = "47",
pages = "8548--8562",
journal = "Nucleic Acids Research",
issn = "0305-1048",
publisher = "Oxford University Press",
number = "16",

}

RIS

TY - JOUR

T1 - Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging

AU - Lee, Jong-Hyuk

AU - Demarest, Tyler G.

AU - Babbar, Mansi

AU - Kim, Edward W.

AU - Okur, Mustafa N.

AU - De, Supriyo

AU - Croteau, Deborah L.

AU - Bohr, Vilhelm A.

PY - 2019

Y1 - 2019

N2 - Cockayne syndrome is an accelerated aging disorder, caused by mutations in the CSA or CSB genes. In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction. Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results show striking enrichment of PAR at transcription start sites, depletion of heterochromatin and downregulation of H3K9me3-specific methyltransferases SUV39H1 and SETDB1. Induced-expression of SETDB1 in CSB-deficient cells downregulated PAR and normalized mitochondrial function. The results suggest that defects in CSB are strongly associated with loss of heterochromatin, downregulation of SETDB1, increased PAR in highly-transcribed regions, and mitochondrial dysfunction.

AB - Cockayne syndrome is an accelerated aging disorder, caused by mutations in the CSA or CSB genes. In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction. Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results show striking enrichment of PAR at transcription start sites, depletion of heterochromatin and downregulation of H3K9me3-specific methyltransferases SUV39H1 and SETDB1. Induced-expression of SETDB1 in CSB-deficient cells downregulated PAR and normalized mitochondrial function. The results suggest that defects in CSB are strongly associated with loss of heterochromatin, downregulation of SETDB1, increased PAR in highly-transcribed regions, and mitochondrial dysfunction.

U2 - 10.1093/nar/gkz568

DO - 10.1093/nar/gkz568

M3 - Journal article

C2 - 31276581

VL - 47

SP - 8548

EP - 8562

JO - Nucleic Acids Research

JF - Nucleic Acids Research

SN - 0305-1048

IS - 16

ER -

ID: 241370783