WSTF–ISWI chromatin remodeling complex targets heterochromatic replication foci
Open accessAbstract
The Williams Syndrome Transcription Factor (WSTF), the product of the WBSCR9 gene, is invariably deleted in the haploinsufficiency Williams-Beuren Syndrome. Along with the nucleosome-dependent ATPase ISWI, WSTF forms a novel chromatin remodeling complex, WICH (WSTF-ISWI chromatin remodeling complex), which is conserved in vertebrates. The WICH complex was purified to homogeneity from Xenopus egg extract and was found to contain only WSTF and ISWI. In mouse cells, WSTF interacts with the SNF2H isoform of ISWI. WSTF accumulates in pericentric heterochromatin coincident with the replication of these structures, suggesting a role for WSTF in the replication of heterochromatin. Such a role is supported by the in vitro activity of both the mouse and frog WICH complexes: they are involved in the assembly of regular spaced nucleosomal arrays. In contrast to the related ISWI-interacting protein ACF1/WCRF180, WSTF binds stably to mitotic chromosomes. As dysfunction of other chromatin remodeling factors often has severe effects on development, haploinsufficiency of WSTF may explain some of the phenotypes associated with this disease.
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Both MommeD5 and MommeD10 genes encode proteins involved in histone modification and chromatin remodeling.
“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 [23]
Baz1b was chosen as the best candidate for MommeD10 because it contains a bromodomain and has been shown to form chromatin remodeling complexes and associate with replication foci and promoters.
“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 [23]
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- Authors
- Bozhenok, L., Wade, P. A., & Varga‐Weisz, P.
- Affiliations
- Marie Curie (GB)
- Emory University (US)
- Corresponding author
- Varga‐Weisz, Patrick
- Venue
- The EMBO Journal
- Published
- 2002-05-01
- Volume
- 21
- Issue
- 9
- Pages
- 2231-2241
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC125993
- OpenAlex
- W2153612581
- Cited by
- 236
- References
- 55
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 9 · 2023: 6 · 2022: 2 · 2021: 5 · 2020: 5 · 2019: 3 · 2018: 6 · 2017: 5 · 2016: 6 · 2015: 6 · 2014: 15 · 2013: 16 · 2012: 7
- FWCI
- 7.32
- Type
- journal article
- Language
- en
- Update notices
- erratum (2002-06-17)
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Marie Curie
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Neuroscience › Developmental Neuroscience › Williams Syndrome Research
- Keywords
- WSTF, ISWI, chromatin remodeling, pericentromeric heterochromatin, Williams syndrome, SNF2H, nucleosome assembly, metaphase chromosomes, haploinsufficiency
- MeSH terms
- Bromodomain Containing Proteins, Adenosine Triphosphatases, Animals, Female, HeLa Cells, Heterochromatin, Humans, Nucleosomes, Oocytes, Stem Cells, Transcription Factors, Xenopus, Gene Deletion, Replication Origin, Williams Syndrome, Macromolecular Substances, Mice
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