![]() ![]() Chromatin accessibility and protein cooperativity may both play roles in restricting the cohort of bound locations under a given set of cellular conditions. While some characterization of RAR genomic binding has recently been carried out in mouse ES and human breast cancer cell lines, it is unknown which genes are targeted by RAR during neurogenesis, and how RAR binding targets are selected. However, the proposed independence of RAR binding from the presence of the ligand has only been confirmed at a small number of sites. In the presence of the retinoid ligand, RAR (often heterodimerized with RXR) recruits co-activators (Ncoa1 and Ncoa2), p300, and core components of the transcriptional machinery. It has been proposed that RARs are constitutively bound to target sites in the absence of retinoids, recruiting co-repressors such as Ncor1 and Ncor2. ![]() The response to RA during neuronal development is mediated by the action of retinoic acid receptor isoforms (collectively abbreviated here as RARs). Retinoic acid (RA) is the most commonly used neuralizing agent during in vitro embryonic stem (ES) cell differentiation since exposure to it results in a rapid transition from pluripotent embryoid bodies to committed neuronal precursors. In the developing neural tube, retinoid signaling initiates neural differentiation, specifies caudal hindbrain and rostral cervical spinal identity, and controls patterning and differentiation of spinal motor neurons and interneurons. Therefore, understanding how signal-responsive TFs are integrated into a dynamic cellular context will further our knowledge of the mechanisms guiding the acquisition of specific cellular identities. The effect of a signal on gene expression, and ultimately on cell fate, depends on where such TFs bind to the genome. While these external signals can take the form of steroid hormones, protein growth factors, or other molecules, their presence is typically communicated by signal-responsive transcription factors (TFs). Cellular competence, fate determination, and differentiation are influenced by the external signals cells receive. ![]()
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January 2023
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