ATP chromatin remodelling

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Cells have multiple remodelling complexes, most of which are multisubunit complexes. Remodelling complexes are grouped into 4 families; INO80, SWI/SNF, CHD and ISWI<ref>Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).</ref><ref>S. Eustermann, K.Schall, D.Kostrewa, K. Lakomek, M. Strauss, M. Moldt, K-P. Hopfner. Structural Basis for nucleosome remodelling by the INO80 complex. Nature 2018; 556(7701).</ref>. Although the different families 'slide, evict and edit'<ref>S. Eustermann, K.Schall, D.Kostrewa, K. Lakomek, M. Strauss, M. Moldt, K-P. Hopfner. Structural Basis for nucleosome remodelling by the INO80 complex. Nature 2018; 556(7701).</ref>. nucleosomes, ATP hydrolysis drives DNA translocation of the motor domains of these complexes.  
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[[Cells|Cells]] have multiple remodelling complexes, most of which are multisubunit complexes. Remodelling complexes are grouped into 4 families; INO80, SWI/SNF, CHD and ISWI<ref>Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).</ref><ref>S. Eustermann, K.Schall, D.Kostrewa, K. Lakomek, M. Strauss, M. Moldt, K-P. Hopfner. Structural Basis for nucleosome remodelling by the INO80 complex. Nature 2018; 556(7701).</ref>. Although the different families 'slide, evict and edit'<ref>S. Eustermann, K.Schall, D.Kostrewa, K. Lakomek, M. Strauss, M. Moldt, K-P. Hopfner. Structural Basis for nucleosome remodelling by the INO80 complex. Nature 2018; 556(7701).</ref>&nbsp;[[Nucleosomes|nucleosomes]], [[ATP hydrolysis|ATP hydrolysis]] drives [[DNA translocation|DNA translocation]] of the motor domains of these complexes.  
  
 
ATP depedant chromatin remodelling involves:  
 
ATP depedant chromatin remodelling involves:  
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*eviction  
 
*eviction  
 
*spacing  
 
*spacing  
*histone variant exchange
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*[[Histone|histone]] variant exchange
  
The first complex isolated was SWI/SNF in yeast<ref>S.Whitehall. CMB2001, lecture 4. 2018.</ref>, with the catalytic subunit being identified as SNF2.  
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The first complex isolated was SWI/SNF in [[Yeast|yeast]]<ref>S.Whitehall. CMB2001, lecture 4. 2018.</ref>, with the catalytic subunit being identified as SNF2.  
  
In humans, 3 homologues of SWI/SNF proteins have been identified; hbrm and BRG1, which are homologous of SNF2/SWI2 and hSNF5, which is a homologue of SNF5<ref>Muchardt C, Reyes JC, Bourachot B, Leguoy E, Yaniv M. The hbrm and BRG-1 proteins, components of the human SNF/SWI complex, are phosphorylated and excluded from the condensed chromosomes during mitosis. The EMBO Journal. 1996;15(13):3394–402.</ref>. Hbrm and BRG1 promote transcriptional activation via the glucocorticoid and retonic acid receptors<ref>Muchardt C, Reyes JC, Bourachot B, Leguoy E, Yaniv M. The hbrm and BRG-1 proteins, components of the human SNF/SWI complex, are phosphorylated and excluded from the condensed chromosomes during mitosis. The EMBO Journal. 1996;15(13):3394–402.</ref>. BRG1 has been found to activate or repress nuclear processes (transcription, elongation, DNA replication), using various mechanisms including being assembled with transcriptional promoters and histone-modifying enzyme complexes<ref>Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).</ref>.  
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In humans, 3 [[Homologues|homologues]] of SWI/SNF proteins have been identified; hbrm and BRG1, which are homologous of SNF2/SWI2 and hSNF5, which is a homologue of SNF5<ref>Muchardt C, Reyes JC, Bourachot B, Leguoy E, Yaniv M. The hbrm and BRG-1 proteins, components of the human SNF/SWI complex, are phosphorylated and excluded from the condensed chromosomes during mitosis. The EMBO Journal. 1996;15(13):3394–402.</ref>. Hbrm and BRG1 promote transcriptional activation via the glucocorticoid and retonic acid receptors<ref>Muchardt C, Reyes JC, Bourachot B, Leguoy E, Yaniv M. The hbrm and BRG-1 proteins, components of the human SNF/SWI complex, are phosphorylated and excluded from the condensed chromosomes during mitosis. The EMBO Journal. 1996;15(13):3394–402.</ref>. BRG1 has been found to activate or repress nuclear processes ([[DNA_transcription|transcription]], [[Elongation|elongation]], [[DNA_replication|DNA replication]]), using various mechanisms including being assembled with [[Transcriptional promoters|transcriptional promoters]] and [[Histone-modifying enzyme complexes|histone-modifying enzyme complexes]]<ref>Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).</ref>.  
  
As SWI/SNF plays a key role in the cell cycle, it has been indicated to be a potent tumour suppressor. Mutations within subunits of these complexes have been linked to more than 20% of human cancers<ref>S.Whitehall. CMB2001, Lecture 4. 2018</ref>. " The cancers with the highest SWI/SNF mutation rates were ovarian clear cell carcinoma (75%), clear cell renal cell carcinoma (57%), hepatocellular carcinoma (40%), gastric cancer (36%), melanoma (34%), and pancreatic cancer (26%)"<ref>Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1)</ref>. Common mutations within the subunits found to lead to cancer include epigenic silencing, rearrangement and deletions which lead to inactivation of SWI/SNF subunit(s)<ref>Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1).</ref>.  
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As SWI/SNF plays a key role in the [[Cell cycle|cell cycle]], it has been indicated to be a potent [[Tumour suppressor|tumour suppressor]]. [[Mutation|Mutations]] within subunits of these complexes have been linked to more than 20% of human [[Cancer|cancers]]<ref>S.Whitehall. CMB2001, Lecture 4. 2018</ref>. "The cancers with the highest SWI/SNF mutation rates were [[Ovarian clear cell carcinoma|ovarian clear cell carcinoma]] (75%), clear cell renal cell carcinoma (57%), hepatocellular carcinoma (40%), gastric cancer (36%), [[Melanoma|melanoma]] (34%), and pancreatic cancer (26%)"<ref>Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1)</ref>. Common mutations within the subunits found to lead to cancer include epigenic silencing, rearrangement and [[Deletion_mutation|deletions]] which lead to inactivation of SWI/SNF subunit(s)<ref>Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1).</ref>.  
  
ATP dependant complexes work synergestically with HAT complexes; as HAT and ATP-dependant complexes are commonly recruited to the same promoters<ref>S.WHitehall. CMB2001, lecture 4. 2018.</ref>, which results in a cascade of reactions leading to enhanced production of the pre-initiation complex.  
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ATP dependant complexes work synergestically with [[HAT complexes|HAT complexes]]; as HAT and ATP-dependant complexes are commonly recruited to the same promoters<ref>S.WHitehall. CMB2001, lecture 4. 2018.</ref>, which results in a [[Cascade_reaction|cascade]] of reactions leading to enhanced production of the [[Pre-Initiation_Complex|pre-initiation complex]].  
  
 
=== References  ===
 
=== References  ===
  
 
<references />
 
<references />

Latest revision as of 10:42, 24 November 2018

Cells have multiple remodelling complexes, most of which are multisubunit complexes. Remodelling complexes are grouped into 4 families; INO80, SWI/SNF, CHD and ISWI[1][2]. Although the different families 'slide, evict and edit'[3] nucleosomes, ATP hydrolysis drives DNA translocation of the motor domains of these complexes.

ATP depedant chromatin remodelling involves:

The first complex isolated was SWI/SNF in yeast[4], with the catalytic subunit being identified as SNF2.

In humans, 3 homologues of SWI/SNF proteins have been identified; hbrm and BRG1, which are homologous of SNF2/SWI2 and hSNF5, which is a homologue of SNF5[5]. Hbrm and BRG1 promote transcriptional activation via the glucocorticoid and retonic acid receptors[6]. BRG1 has been found to activate or repress nuclear processes (transcription, elongation, DNA replication), using various mechanisms including being assembled with transcriptional promoters and histone-modifying enzyme complexes[7].

As SWI/SNF plays a key role in the cell cycle, it has been indicated to be a potent tumour suppressor. Mutations within subunits of these complexes have been linked to more than 20% of human cancers[8]. "The cancers with the highest SWI/SNF mutation rates were ovarian clear cell carcinoma (75%), clear cell renal cell carcinoma (57%), hepatocellular carcinoma (40%), gastric cancer (36%), melanoma (34%), and pancreatic cancer (26%)"[9]. Common mutations within the subunits found to lead to cancer include epigenic silencing, rearrangement and deletions which lead to inactivation of SWI/SNF subunit(s)[10].

ATP dependant complexes work synergestically with HAT complexes; as HAT and ATP-dependant complexes are commonly recruited to the same promoters[11], which results in a cascade of reactions leading to enhanced production of the pre-initiation complex.

References

  1. Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).
  2. S. Eustermann, K.Schall, D.Kostrewa, K. Lakomek, M. Strauss, M. Moldt, K-P. Hopfner. Structural Basis for nucleosome remodelling by the INO80 complex. Nature 2018; 556(7701).
  3. S. Eustermann, K.Schall, D.Kostrewa, K. Lakomek, M. Strauss, M. Moldt, K-P. Hopfner. Structural Basis for nucleosome remodelling by the INO80 complex. Nature 2018; 556(7701).
  4. S.Whitehall. CMB2001, lecture 4. 2018.
  5. Muchardt C, Reyes JC, Bourachot B, Leguoy E, Yaniv M. The hbrm and BRG-1 proteins, components of the human SNF/SWI complex, are phosphorylated and excluded from the condensed chromosomes during mitosis. The EMBO Journal. 1996;15(13):3394–402.
  6. Muchardt C, Reyes JC, Bourachot B, Leguoy E, Yaniv M. The hbrm and BRG-1 proteins, components of the human SNF/SWI complex, are phosphorylated and excluded from the condensed chromosomes during mitosis. The EMBO Journal. 1996;15(13):3394–402.
  7. Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).
  8. S.Whitehall. CMB2001, Lecture 4. 2018
  9. Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1)
  10. Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1).
  11. S.WHitehall. CMB2001, lecture 4. 2018.
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