Document Type
Article
Publication Date
3-4-2021
Abstract
Organismal development is a process that requires a fine-tuned control of cell fate and identity, through timely regulation of lineage-specific genes. These processes are mediated by the concerted action of transcription factors and protein complexes that orchestrate the interaction between cis-regulatory elements (enhancers, promoters) and RNA Polymerase II to elicit transcription. A proper understanding of these dynamics is essential to elucidate the mechanisms underlying developmental diseases. Many developmental disorders, such as Coffin-Siris Syndrome, characterized by growth impairment and intellectual disability are associated with mutations in subunits of the SWI/SNF chromatin remodeler complex, which is an essential regulator of transcription. ARID1B and its paralog ARID1A encode for the two largest, mutually exclusive, subunits of the complex. Mutations in ARID1A and, especially, ARID1B are recurrently associated with a very wide array of developmental disorders, suggesting that these two SWI/SNF subunits play an important role in cell fate decision. In this mini-review we therefore discuss the available scientific literature linking ARID1A and ARID1B to cell fate determination, pluripotency maintenance, and organismal development.
Recommended Citation
Pagliaroli, Luca and Trizzino, Marco, "The Evolutionary Conserved SWI/SNF Subunits ARID1A and ARID1B Are Key Modulators of Pluripotency and Cell-Fate Determination" (2021). Department of Biochemistry and Molecular Biology Faculty Papers. Paper 181.
https://jdc.jefferson.edu/bmpfp/181
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
PubMed ID
33748136
Language
English
Comments
This article is the author’s final published version in Frontiers in Cell and Developmental Biology, Volume 9, March 2021, Article number 643361.
The published version is available at https://doi.org/10.3389/fcell.2021.643361. Copyright © Pagliaroli and Trizzino.
Publication made possible in part by support from the Jefferson Open Access Fund