Sodium butyrate stimulates DNA repair in UV-irradiated normal and xeroderma pigmentosum human fibroblasts.

Smerdon, Michael J.; Lan, Shou‐Jen; Calza, R. E.; Reeves, Raymond

doi:10.1016/s0021-9258(18)33468-9

Cited by 110 publications

(25 citation statements)

References 47 publications

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“…A role for p300 in NER is suggested by interactions of p300 with the repair factors UV-DDB (Rapic-Otrin et al, 2002) and PCNA (Hasan et al, 2001), stimulation of repair by p300 in vitro (Frit et al, 2002), and enhancement of NER by the histone deacetylase inhibitor sodium butyrate (Ramanathan and Smerdon 1989). Based on genetic approaches (Smerdon et al, 1982;Mullenders et al, 1986),…”

Section: Recruitment Of Chromatin Remodelers To Stalled Rnapiiomentioning

confidence: 99%

RETRACTED: Cockayne Syndrome A and B Proteins Differentially Regulate Recruitment of Chromatin Remodeling and Repair Factors to Stalled RNA Polymerase II In Vivo

et al. 2006

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Restoration of UV-inhibited transcription requires removal of transcription-blocking DNA lesions by transcription-coupled repair (TCR). In mammals, TCR is dependent on CSA and CSB proteins; however, their functions are largely unknown. Here, we analyzed the composition of UV-stalled transcription elongation complexes from human cells. We show that CSB and CSA display differential roles in recruitment of TCR-specific factors and that assembly for TCR occurs without disruption of the UV-stalled RNA polymerase II (RNAPIIo). CSB fulfills a key role as a coupling factor to attract histone acetyltransferase p300, nucleotide excision repair (NER) proteins, and CSA-DDB1 E3-ubiquitin ligase complex with the COP9 signalosome. CSA is dispensable for attraction of NER proteins to lesion-stalled RNAPIIo, yet in cooperation with CSB is required to recruit XAB2, the nucleosomal binding protein HMGN1, and TFIIS. These results give insight into the nature and order of molecular events that take place during TCR in the context of chromosomal DNA.

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Section: Recruitment Of Chromatin Remodelers To Stalled Rnapiiomentioning

confidence: 99%

RETRACTED: Cockayne Syndrome A and B Proteins Differentially Regulate Recruitment of Chromatin Remodeling and Repair Factors to Stalled RNA Polymerase II In Vivo

et al. 2006

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“…Cell Culture and Labeling during Replicative Synthesis. Human diploid fibroblasts (strains AG1518 and IMR 90) were grown in culture as described in Smerdon et al (1982b). Cells, between passage 10 and passage 17, were split 1:3 and prelabeled for 1 week with 25-75 nCi/mL [14C]dThd (50 mCi/mmol; New England Nuclear), depending on the experiment.…”

Section: Methodsmentioning

confidence: 99%

A nonuniform distribution of excision repair synthesis in nucleosome core DNA

Lan¹,

Smerdon²

1985

Biochemistry

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We have investigated the distribution in nucleosome core DNA of nucleotides incorporated by excision repair synthesis occurring immediately after UV irradiation in human cells. We show that the differences previously observed for whole nuclei between the DNase I digestion profiles of repaired DNA (following its refolding into a nucleosome structure) and bulk DNA are obtained for isolated nucleosome core particles. Analysis of the differences obtained indicates that they could reflect a significant difference in the level of repair-incorporated nucleotides at different sites within the core DNA region. To test this possibility directly, we have used exonuclease III digestion of very homogeneous sized core particle DNA to "map" the distribution of repair synthesis in these regions. Our results indicate that in a significant fraction of the nucleosomes the 5' and 3' ends of the core DNA are markedly enhanced in repair-incorporated nucleotides relative to the central region of the core particle. A best fit analysis indicates that a good approximation of the data is obtained for a distribution where the core DNA is uniformly labeled from the 5' end to position 62 and from position 114 to the 3' end, with the 52-base central region being devoid of repair-incorporated nucleotides. This distribution accounts for all of the quantitative differences observed previously between repaired DNA and bulk DNA following the rapid phase of nucleosome rearrangement when it is assumed that linker DNA and the core DNA ends are repaired with equal efficiency and the nucleosome structure of newly repaired DNA is identical with that of bulk chromatin. Furthermore, the 52-base central region that is devoid of repair synthesis contains the lowest frequency cutting sites for DNase I in vitro, as well as the only "internal" locations where two (rather than one) histones interact with a 10-base segment of each DNA strand.

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“…Cell Culture and Labeling. Normal human diploid fibroblasts (strains AG1518 and IMR-90) were grown in culture as described by Smerdon et al (1982a). Cells between passage 10 and passage 18 were split 1:3 and labeled with 25-50 nCi/mL [14C]dThd (50 mCi/mmol; New England Nuclear) or 10 nCi/mL [3H]dThd (50-80 Ci/mmol; New England Nuclear) for 3-6 days.…”

Section: Methodsmentioning

confidence: 99%

Nucleosome rearrangement in vitro. 1. Two phases of salt-induced nucleosome migration in nuclei

Watkins¹,

Smerdon²

1985

Biochemistry

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We have investigated the salt- and temperature-induced rearrangement of nucleosomes in both intact and H1-depleted nuclei from human cells. In agreement with previous reports on the rearrangement of nucleosomes in isolated chromatin or chromatin fragments, we observed a decrease in the average nucleosome repeat length following incubation of nuclei at 37 degrees C in elevated salt concentrations. However, this decrease occurred in two distinct phases. First, incubation of H1-depleted nuclei at 37 degrees C for as little as 10 min in low-salt, isotonic buffer (containing 0.025 M KCl) resulted in a shift in the limiting repeat value from approximately 190 to 168 base pairs (bp). A similar shift was observed for intact nuclei incubated at 37 degrees C for 1 h in buffer containing near-physiological salt concentrations (i.e., 0.175 M KCl). This limiting repeat value was maintained in both intact and H1-depleted nuclei up to a salt concentration of 0.45 M KCl in the incubation buffer. Second, at salt concentrations of 0.625 M KCl, a limiting repeat of approximately 146 bp was obtained, and the nuclei had clearly lysed. During the first shift in repeat length, little additional exchange of nuclear proteins occurred compared to nuclei kept on ice in a low-salt buffer. This was the case even though the conditions used to monitor exchange were optimized by using a high DNA to chromatin ratio. On the other hand, a significant increase in the exchange of nuclear proteins, and formation of nucleosomes on the naked DNA, was observed during the shift in repeat length to 146 bp.(ABSTRACT TRUNCATED AT 250 WORDS)

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Sodium butyrate stimulates DNA repair in UV-irradiated normal and xeroderma pigmentosum human fibroblasts.

Cited by 110 publications

References 47 publications

RETRACTED: Cockayne Syndrome A and B Proteins Differentially Regulate Recruitment of Chromatin Remodeling and Repair Factors to Stalled RNA Polymerase II In Vivo

RETRACTED: Cockayne Syndrome A and B Proteins Differentially Regulate Recruitment of Chromatin Remodeling and Repair Factors to Stalled RNA Polymerase II In Vivo

A nonuniform distribution of excision repair synthesis in nucleosome core DNA

Nucleosome rearrangement in vitro. 1. Two phases of salt-induced nucleosome migration in nuclei

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