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Histones rule! The FASEB conference on chromatin and transcription. July 7-12, 2001.

Wells WA - J. Cell Biol. (2001)

View Article: PubMed Central - PubMed

Affiliation: WELLSW@ROCKEFELLER.EDU

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The meeting covered all of chromatin biology, but talks kept returning to methyl modifications at lysine 4 (K4) and lysine 9 (K9) of histone H3... Indeed, an immunoprecipitation of the tumor suppressor and transcriptional repressor Rb brought down SUV39H1... The K9 modification has been associated with repressed chromatin, and Kouzarides found that both Rb and SUV39H1 are needed for in vivo repression of certain regulated genes... The exceptions to this rule are small regions with an opposite distribution of these modifications; these regions apparently include the active, pseudoautosomal regions of the inactive X... Jenuwein also reported that K9- methylated H3 covers much of the inactive X, but in addition he found the same variant in the heterochromatin around centromeres... Loss of this methylation causes chromosomes to pair incorrectly during spermatogenesis and stick together near their kinetochores, perhaps secondary to an opening up of the centric heterochromatin... Geneviève Almouzni (Institut Curie, Paris, France) found that the K9 staining at centric heterochromatin is lost following RNase treatment, raising the intriguing possibility that RNAs are critical to heterochromatin formation... Now that K9 modifications are known to be common to both impenetrably repressed heterochromatin and a dynamically repressed cell cycle promoter, it is not clear what makes the two types of repression distinct... At the very least there appears to be more than one way of translating K9 methylation into repression, as early evidence suggests that HP1 is not bound to the K9-methylated inactive X. ▪ References: Dramatic correlations and anticorrelations between different histone H3 modifications, as reported by Gary Felsenfeld (National Institutes of Health, Bethesda, MD), are yielding clues about how chromatin is divided into active and inactive regions... Felsenfeld used chromatin immunoprecipitation to track H3 methylation at lysines 4 (K4) and 9 (K9) and a double acetylation of H3 at lysines 9 and 14... He found that acetylation and K4 methylation, both modifications associated with gene activation, closely mirrored each other in different regions of the chicken β-globin locus... H1 binds to DNA as it enters and exits the nucleosome, thus locking the DNA in place... But now Peterson has found that phosphorylation by cyclin-dependent kinases may alleviate this locking, allowing SWI/SNF to do its job.

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Small DNA circles do not remodel.Peterson/Elsevier
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uro3: Small DNA circles do not remodel.Peterson/Elsevier


Histones rule! The FASEB conference on chromatin and transcription. July 7-12, 2001.

Wells WA - J. Cell Biol. (2001)

Small DNA circles do not remodel.Peterson/Elsevier
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196202&req=5

uro3: Small DNA circles do not remodel.Peterson/Elsevier

View Article: PubMed Central - PubMed

Affiliation: WELLSW@ROCKEFELLER.EDU

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

The meeting covered all of chromatin biology, but talks kept returning to methyl modifications at lysine 4 (K4) and lysine 9 (K9) of histone H3... Indeed, an immunoprecipitation of the tumor suppressor and transcriptional repressor Rb brought down SUV39H1... The K9 modification has been associated with repressed chromatin, and Kouzarides found that both Rb and SUV39H1 are needed for in vivo repression of certain regulated genes... The exceptions to this rule are small regions with an opposite distribution of these modifications; these regions apparently include the active, pseudoautosomal regions of the inactive X... Jenuwein also reported that K9- methylated H3 covers much of the inactive X, but in addition he found the same variant in the heterochromatin around centromeres... Loss of this methylation causes chromosomes to pair incorrectly during spermatogenesis and stick together near their kinetochores, perhaps secondary to an opening up of the centric heterochromatin... Geneviève Almouzni (Institut Curie, Paris, France) found that the K9 staining at centric heterochromatin is lost following RNase treatment, raising the intriguing possibility that RNAs are critical to heterochromatin formation... Now that K9 modifications are known to be common to both impenetrably repressed heterochromatin and a dynamically repressed cell cycle promoter, it is not clear what makes the two types of repression distinct... At the very least there appears to be more than one way of translating K9 methylation into repression, as early evidence suggests that HP1 is not bound to the K9-methylated inactive X. ▪ References: Dramatic correlations and anticorrelations between different histone H3 modifications, as reported by Gary Felsenfeld (National Institutes of Health, Bethesda, MD), are yielding clues about how chromatin is divided into active and inactive regions... Felsenfeld used chromatin immunoprecipitation to track H3 methylation at lysines 4 (K4) and 9 (K9) and a double acetylation of H3 at lysines 9 and 14... He found that acetylation and K4 methylation, both modifications associated with gene activation, closely mirrored each other in different regions of the chicken β-globin locus... H1 binds to DNA as it enters and exits the nucleosome, thus locking the DNA in place... But now Peterson has found that phosphorylation by cyclin-dependent kinases may alleviate this locking, allowing SWI/SNF to do its job.

Show MeSH