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RETRACTED: The Chromatin-Remodeling Complex WINAC Targets a Nuclear Receptor to Promoters and Is Impaired in Williams Syndrome
Open accessAbstract
We identified a human multiprotein complex (WINAC) that directly interacts with the vitamin D receptor (VDR) through the Williams syndrome transcription factor (WSTF). WINAC has ATP-dependent chromatin-remodeling activity and contains both SWI/SNF components and DNA replication-related factors. The latter might explain a WINAC requirement for normal S phase progression. WINAC mediates the recruitment of unliganded VDR to VDR target sites in promoters, while subsequent binding of coregulators requires ligand binding. This recruitment order exemplifies that an interaction of a sequence-specific regulator with a chromatin-remodeling complex can organize nucleosomal arrays at specific local sites in order to make promoters accessible for coregulators. Furthermore, overexpression of WSTF could restore the impaired recruitment of VDR to vitamin D regulated promoters in fibroblasts from Williams syndrome patients. This suggests that WINAC dysfunction contributes to Williams syndrome, which could therefore be considered, at least in part, a chromatin-remodeling factor disease.
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“The linked interval for MommeD10 contains 52 genes and Baz1b was chosen as the best candidate because it contains a bromodomain (a domain commonly associated with chromatin remodelers) and has recently been shown to form at least two chromatin remodeling complexes and associate with replication foci and promoters [23-25].”
From A genome-wide screen for modifiers of transgene variegation identifies genes with critical roles in development (2008) · cites this paper as [24]
In the citing paper
“It has previously been shown that Baz1b is expressed in the mouse embryo from around 9.5 dpc and whole mount in situ at 11.5 dpc showed expression in limb buds, tail and brain [24].”
From A genome-wide screen for modifiers of transgene variegation identifies genes with critical roles in development (2008) · cites this paper as [24]
In the citing paper
“This is consistent with the fact that both genes encode proteins involved in histone modification and chromatin remodeling [21,23-25,30-33].”
From A genome-wide screen for modifiers of transgene variegation identifies genes with critical roles in development (2008) · cites this paper as [24]
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The biology of chromatin remodeling complexes.
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“Among the 28 genes lost by heterozygous deletion is the gene encoding WSTF, a transcription factor that recruits BRG1- and BRM-containing WINAC complexes to vitamin D-regulated promoters (121) and recruits hSNF2H in the WICH complex to heterochromatic replication foci (83).”
BackgroundVitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice
Bouillon, R., Carmeliet, G., Verlinden, L., van Etten, E., Verstuyf, A., Luderer, H. F., Lieben, L., Mathieu, C., & Demay, M. (2008) · Endocrine Reviews · doi:10.1210/er.2008-0004 · Cited by 1,783
Nonclassic Actions of Vitamin D
Bikle, D. D. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2008-1454 · Cited by 995
“ement in its promoter to which VDR binds indirectly (12).”
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Dioxin receptor is a ligand-dependent E3 ubiquitin ligase
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Self-citation
Metadata
- Authors
- Kitagawa, H., Fujiki, R., Yoshimura, K., Mezaki, Y., Uematsu, Y., Matsui, D., Ogawa, S., Unno, K., Okubo, M., Tokita, A., Nakagawa, T., Ito, T., Ishimi, Y., Nagasawa, H., Matsumoto, T., Yanagisawa, J., & Kato, S.
- Affiliations
- Institute for Quantitative Biosciences, The University of Tokyo (JP)
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2003-06
- Volume
- 113
- Issue
- 7
- Pages
- 905-917
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2150721910
- Cited by
- 268
- References
- 45
- Citations by year
- 2024: 3 · 2023: 3 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 6 · 2017: 2 · 2016: 5 · 2015: 5 · 2014: 7 · 2013: 13 · 2012: 12
- FWCI
- 9.01
- Type
- journal article
- Language
- en
- Status
- Retracted
- Update notices
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Neuroscience › Developmental Neuroscience › Williams Syndrome Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- chromatin remodeling complexes, Williams syndrome, vitamin D receptor, SWI/SNF complex, promoter accessibility, coregulators, nucleosome organization, S phase progression
- MeSH terms
- Animals, Binding Sites, Cell Nucleus, Chromatin, DNA Replication, Eukaryotic Cells, Fetus, Gene Expression Regulation, Genes, Regulator, Humans, Nuclear Proteins, Nucleosomes, Promoter Regions, Genetic, Transcription Factors, Transcriptional Activation, S Phase, Protein Structure, Tertiary, Receptors, Calcitriol, Williams Syndrome, Active Transport, Cell Nucleus, Macromolecular Substances, Multiprotein Complexes, Mice
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