ATP chromatin remodelling: Difference between revisions

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<references /><ref>Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).</ref>&nbsp;Cells have multiple remodelling complexes, most of which are multisubunit complexes. Remodelling complexes are grouped into 4 famillies; INO80, SWI/SNF, CHD and ISWI<ref name="1">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 famillies 'slide, evict and edit'&nbsp;<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.&nbsp;
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 name="1">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.  


ATP depedant chromatin remodelling involves:  
ATP depedant chromatin remodelling involves:  


*sliding&nbsp;
*sliding  
*unwrapping nucleosomes&nbsp;
*unwrapping nucleosomes  
*eviction&nbsp;
*eviction  
*spacing&nbsp;
*spacing  
*histone variant exchange&nbsp;
*histone variant exchange


The first complex isolated was SWI/SNF in yeast&nbsp;<ref>S.Whitehall. CMB2001, lecture 4. 2018.</ref>, with the catalytic subunit being identified as SNF2.&nbsp;
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.  


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&nbsp;<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&nbsp;<ref>Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).</ref>.&nbsp;
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>.  


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%)"&nbsp;<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>.&nbsp;
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>.  


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.&nbsp;
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.  
 
=== References ===
 
<references />

Revision as of 17:36, 18 October 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].Cite error: Invalid <ref> tag; name cannot be a simple integer. Use a descriptive title. Although the different families 'slide, evict and edit'[2]. nucleosomes, ATP hydrolysis drives DNA translocation of the motor domains of these complexes.

ATP depedant chromatin remodelling involves:

  • sliding
  • unwrapping nucleosomes
  • eviction
  • spacing
  • histone variant exchange

The first complex isolated was SWI/SNF in yeast[3], 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[4]. Hbrm and BRG1 promote transcriptional activation via the glucocorticoid and retonic acid receptors[5]. 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[6].

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[7]. " 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%)"[8]. 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)[9].

ATP dependant complexes work synergestically with HAT complexes; as HAT and ATP-dependant complexes are commonly recruited to the same promoters[10], 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.Whitehall. CMB2001, lecture 4. 2018.
  4. ↑ 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.
  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. ↑ Trotter KW, Archer TK. The BRG1 transcriptional coregulator. Nuclear Receptor Signaling. 2008;6(1).
  7. ↑ S.Whitehall. CMB2001, Lecture 4. 2018
  8. ↑ Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1)
  9. ↑ Shain AH, Pollack JR. The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers. PLoS ONE. 2013;8(1).
  10. ↑ S.WHitehall. CMB2001, lecture 4. 2018.
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