The conserved and divergent roles of Prdm3 and Prdm16 in zebrafish and mouse craniofacial development.

The conserved and divergent roles of Prdm3 and Prdm16 in zebrafish and mouse craniofacial development. Dev Biol. 2020 Feb 07;: Authors: Shull LC, Sen R, Menzel J, Goyama S, Kurokawa M, Artinger KB Abstract The formation of the craniofacial skeleton is a highly dynamic process that requires proper orchestration of various cellular processes in cranial neural crest cell (cNCC) development, including cell migration, proliferation, differentiation, polarity and cell death. Alterations that occur during cNCC development result in congenital birth defects and craniofacial abnormalities such as cleft lip with or without cleft palate. While the gene regulatory networks facilitating neural crest development have been extensively studied, the epigenetic mechanisms by which these pathways are activated or repressed in a temporal and spatially regulated manner remain largely unknown. Chromatin modifers can precisely modify gene expression through a variety of mechanisms including histone modifications such as methylation. Here, we investigated the role of two members of the PRDM (Positive regulatory domain) histone methyltransferase family, Prdm3 and Prdm16 in craniofacial development using genetic models in zebrafish and mice. Loss of prdm3 or prdm16 in zebrafish causes craniofacial defects including hypoplasia of the craniofacial cartilage elements, undefined posterior ceratobranchials, and decreased mineralization of the parasphenoid. In mice...
Source: Developmental Biology - Category: Biology Authors: Tags: Dev Biol Source Type: research
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