SWI/SNF

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Image:SNF2-Like Family.jpg
Diagram indicating location of the SNF2 Subfamily of proteins and their relative similarity with other proteins organized by their conservation of NTP-binding motifs.
SWI/SNF (SWItch/Sucrose NonFermentable)[1][1] is a yeast nucleosome remodeling complex composed of several proteins - products of the SWI and SNF genes (SWI1, SWI2/SNF2, SWI3, SWI5, SWI6) as well as several other polypeptides.[1] It possesses a DNA-stimulated ATPase activity and can destabilize histone-DNA interactions in reconstituted nucleosomes in an ATP-dependent manner, though the exact nature of this structural change is unknown.

Family members

Below is a list of yeast SWI/SNF family members and human orthologs:[1]

yeast human function
SWI1 ARID1A, ARID1B contains LXXLL nuclear receptor binding motifs
SWI2/SNF2 SMARCA4 ATP dependent chromatin remodeling
SWI3 SMARCC1, SMARCC2 similar sequence, function unknown
SWP73 SMARCD1, SMARCD2, SMARCD3 similar sequence, function unknown
SWP61 ACTL6A, ACTL6b actin-like protein

Mechanism of Action

Two mechanisms for nucleosome remodeling by SWI/SNF have been proposed.[1] The first model contends that a unidirectional diffusion of a twist defect within the nucleosomal DNA results in a corkscrew-like propagation of DNA over the octamer surface that initiates at the DNA entry site of the nucleosome. The other is known as the "bulge" or "loop-recapture" mechanism and it involves the dissociation of DNA at the edge of the nucleosome with reassociation of DNA inside the nucleosome, forming a DNA bulge on the octamer surface. The DNA loop would then propagate across the surface of the histone octamer in a wave-like manner, resulting in the repositioning of DNA without changes in the total number of histone-DNA contacts.[1] A recent study[1] has provided strong evidence against the twist diffusion mechanism and has further strengthened the loop-recapture model, as proposed in the figure below.

Image:SWI-SNF Model.jpg
A study conducted by Zofall et al.[1] provided more evidence for the "bulge propagation" mechanism of nucleosome remodeling.

See also

References

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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