Vitamin A and retinoid signaling: genomic and nongenomic effects

Tanoury, Ziad Al; Piskunov, Aleksandr; Rochette‐Egly, Cécile

doi:10.1194/jlr.r030833

Cited by 335 publications

(278 citation statements)

References 168 publications

(197 reference statements)

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“…As both receptors have essentially the same DNA recognition site (RGKTCA), a canonical retinoic acid response element (RARE) is usually two direct repeats of the recognition sequence, separated by a spacer region of variable length [68]. The use of chromatin immunoprecipitation (ChIP), however, with antibodies against RARs has demonstrated a much greater diversity of RAREs than previously appreciated, including direct repeats with no spacer [69].…”

Section: Interaction With Dnamentioning

confidence: 99%

Retinoic Acid and the Development of the Endoderm

Kelly

Drysdale

2015

JDB

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Retinoic acid (RA) is an important signaling molecule in the development of the endoderm and an important molecule in protocols used to generate endodermal cell types from stem cells. In this review, we describe the RA signaling pathway and its role in the patterning and specification of the extra embryonic endoderm and different endodermal organs. The formation of endoderm is an ancient evolutionary feature and RA signaling appears to have coevolved with the vertebrate lineage. Towards that end, we describe how RA participates in many regulatory networks required for the formation of extraembryonic structures as well as the organs of the embryo proper.

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Section: Interaction With Dnamentioning

confidence: 99%

Retinoic Acid and the Development of the Endoderm

Kelly

Drysdale

2015

JDB

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“…Activation of RA-responsive genes occurs through binding of RA to one of three RA receptors (RARs), RAR␣, RAR␤, or RAR␥, at defined genomic loci called retinoic acid response elements (RAREs). These binding events result in recruitment of transcriptional activators and subsequent transcription of downstream target genes (Al Tanoury et al, 2013). Previous studies have shown that RA transcriptional complexes associate with histone acetyltransferases, such as CBP/p300, which function through histone modification (Chakravarti et al, 1996;Hou et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Diencephalic Size Is Restricted by a Novel Interplay Between GCN5 Acetyltransferase Activity and Retinoic Acid Signaling

et al. 2017

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Diencephalic defects underlie an array of neurological diseases. Previous studies have suggested that retinoic acid (RA) signaling is involved in diencephalic development at late stages of embryonic development, but its roles and mechanisms of action during early neural development are still unclear. Here we demonstrate that mice lacking enzymatic activity of the acetyltransferase GCN5 ((Gcn5 hat/hat )), which were previously characterized with respect to their exencephalic phenotype, exhibit significant diencephalic expansion, decreased diencephalic RA signaling, and increased diencephalic WNT and SHH signaling. Using a variety of molecular biology techniques in both cultured neuroepithelial cells treated with a GCN5 inhibitor and forebrain tissue from (Gcn5 hat/hat ) embryos, we demonstrate that GCN5, RAR␣/␥, and the poorly characterized protein TACC1 form a complex in the nucleus that binds specific retinoic acid response elements in the absence of RA. Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. Intriguingly, RA signaling defects caused by in vitro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RAR␤. Last, we demonstrate that the diencephalic expansion and transcriptional defects seen in (Gcn5 hat/hat ) mutants can be rescued with gestational RA supplementation, supporting a direct link between GCN5, TACC1, and RA signaling in the developing diencephalon. Together, our studies identify a novel, nonhistone substrate for GCN5 whose modification regulates a previously undescribed, tissue-specific mechanism of RA signaling that is required to restrict diencephalic size during early forebrain development.

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“…RA signaling is mediated by RA receptors (RARs) that act as receptors and transcription factors to control gene transcription (Al Tanoury et al, 2013). RA is required for vasculogenesis in the early embryo (Lai et al, 2003;Bohnsack et al, 2004) and there is some evidence that it may have a role in angiogenesis and vessel maturation in the CNS.…”

Section: Introductionmentioning

confidence: 99%