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. 2022 Jan 3;12:763392. doi: 10.3389/fendo.2021.763392

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Copyright © 2022 Busby, Chen, Godfrey, Rehan, Wildman, Smith and Hassan

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Working model: BAF45A led PBAF chromatin remodeling activity regulates transcriptional activation in mineralized cells. The model shows that the BAF45A is an integral subunit of the mammalian PBAF chromatin remodeling complex. BAF45a, with the help of PBRM1, ARID2, BRD7, and BAF155, evict nucleosome and promote chromatin accessibility to initiates transcription. Depletion, mutation, or complete knockout of Baf45a in osteoblasts and odontoblasts destabilizes or switches the PBAF complex composition. Recruitment of such defective PBAF complex inhibits relevant bone or tooth tissue-specific transcriptional events and gene expression. Finally, this inappropriate remodeling preventing the maturation of osteo or odonto-progenitor cells. Further biochemical assessment of BAF45A function with other PBAF subunits in vivo will help to understand chromatin remodeling in mineralized tissues better.