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The Evolutionary Conserved SWI/SNF Subunits ARID1A and ARID1B Are Key Modulators of Pluripotency and Cell-Fate Determination

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TLDR
A recent mini-review as mentioned in this paper discusses the available scientific literature linking ARID1A and ARID 1B to cell fate determination, pluripotency maintenance, and organismal development.
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.

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Journal ArticleDOI

Biomolecular and Genetic Prognostic Factors That Can Facilitate Fertility-Sparing Treatment (FST) Decision Making in Early Stage Endometrial Cancer (ES-EC): A Systematic Review

TL;DR: The aim of this review was to identify and summarise the currently established biomolecular and genetic prognostic factors that can facilitate decision making for FST in ES-EC and to make more confident decisions on FST on the basis of these factors.
Journal ArticleDOI

The BAF chromatin remodeling complexes: structure, function, and synthetic lethalities.

TL;DR: In this paper, the authors reviewed recent progress in understanding the composition, assembly, structure, and function of BAF complexes and the consequences of their disease-associated mutations, highlighting intra-complex subunit dependencies and synthetic lethal interactions.
Posted ContentDOI

Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest differentiation in ARID1B-related neurodevelopmental disorders

TL;DR: A novel BAF configuration is discovered, which includes ARID1B, SMARCA4, and eight additional subunits, which acts as a gate-keeper which ensures exit from pluripotency and commitment towards neural crest differentiation, by attenuating pluripOTency enhancers of the SOX2 network.
Journal ArticleDOI

ARID1A serves as a receivable biomarker for the resistance to EGFR-TKIs in non-small cell lung cancer.

TL;DR: In this paper, the authors proposed a series of mechanisms related to the resistance to EGFR-TKIs induced by ARID1A alterations or expression loss and the potential therapeutic strategies to overcome the resistance based on published studies.
References
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Journal ArticleDOI

Chromatin-Remodeling-Factor ARID1B Represses Wnt/β-Catenin Signaling

TL;DR: The data suggest that aberrations in chromatin-remodeling factors,such as ARID1B, might contribute to neurodevelopmental abnormalities and cancer through deregulation of developmental and oncogenic pathways, such as the Wnt/β-catenin signaling pathway.
Journal Article

Loss of ARID1A/BAF250a expression in ovarian endometriosis and clear cell carcinoma

TL;DR: The data suggest that a portion of benign ovarian endometriosis has already undergone genetic alterations that lead to aberrant protein expression, possibly conferring a higher risk for malignant transformation.
Journal ArticleDOI

Essential Roles for ARID1B in Dendritic Arborization and Spine Morphology of Developing Pyramidal Neurons.

TL;DR: It is demonstrated that ARID1B is required for neuronal differentiation in the developing brain, such as in dendritic arborization and synapse formation, and plays a critical role in the establishment of cognitive circuitry by regulating dendrite complexity.
Journal ArticleDOI

Arid1b Haploinsufficiency Causes Abnormal Brain Gene Expression and Autism-Related Behaviors in Mice.

TL;DR: The results suggest that Arid1b haploinsufficiency causes ASD-like phenotypes in mice, and that the candidate gene AT-rich interaction domain 1B (ARID1B) encodes a chromatin remodeling factor.
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