China
Africa
Explore chapters and articles related to this topic
Introduction to Genomics
Published in Altuna Akalin, Computational Genomics with R, 2020
Furthermore, certain proteins can influence chromatin structure by interacting with histones. Some of these proteins, like those of the Polycomb Group (PcG) and CTCF, are discussed above in the insulators and silencer sections. In vertebrates and insects, PcGs are responsible for maintaining the silent state of developmental genes, and trithorax group proteins (trxG) for maintaining their active state (Henikoff, 2008; Schwartz and Pirrotta, 2007). PcGs and trxGs induce repressed or active states by catalyzing histone modifications or DNA methylation. Both the proteins bind PREs that can be on promoters or several kilobases away. Another protein that induces histone modifications is CTCF. CTCF is associated with boundaries between active and repressive histone marks (Phillips and Corces, 2009). This is due to the role of CTCF in regulating the 3D genome structure. Two CTCF binding sites that are far away from each other in linear distance can bind together in 3D space thus forming chromatin loops.
Retinoic acid signaling is critical for generation of pancreatic progenitors from human embryonic stem cells
Published in Growth Factors, 2023
Niloufer P. Dumasia, Aparna P. Khanna, Prasad S. Pethe
Signaling pathways including BMP4, TGFβ, hippo, and hedgehog are known to regulate gene expression patterns through the induction of cell-intrinsic epigenetic mechanisms such as HDACs, Polycomb group (PcG) proteins, and the Trithorax group proteins (Dumasia and Pethe 2020). As a response to signaling cues, epigenetic modifiers can alter the chromatin state and transcriptional responsiveness at developmental genes thereby affecting differentiation. We have previously shown that sonic hedgehog signaling regulates PcG proteins during pancreatic specification (Dumasia, Khanna, and Pethe 2021). The binding of RA to its nuclear receptors initiates interactions with various PcG protein subunits at developmentally significant genes (Gillespie and Gudas 2007; Kashyap et al. 2011; Laursen et al. 2013). During early differentiation of mESCs, PRC2 member Ezh2 is lost from target genes along with a decrease in Ezh2 mRNA as a response to RA treatment (Lee, Murdoch, and Fritsch 2007). Whether RA regulates gene expression via such PcG mechanisms during pancreatic differentiation from human embryonic stem cells (hESCs) is not known.