Stage and tissue‐specific expression of the alcohol dehydrogenase 1 (<i>Adh‐1</i>) gene during mouse development

Vonesch, Jean‐Luc; Nakshatri, Harikrishna; Philippe, Murielle; Chambon, Pierre; Dollé, Pascal

doi:10.1002/aja.1001990305

Cited by 49 publications

(22 citation statements)

References 68 publications

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“…Interestingly, RA participates in cell proliferation and polarity establishment in early eye development (Sen et al, 2005) and may have antiapoptotic activity in the adult CNS by inhibiting JNK (c-Jun N-terminal protein kinase) activation (Ahn et al, 2005) or by inhibiting microglial expression of tumor necrosis factor-␣ (Dheen et al, 2005). The high embryonic expression of CYP1B1 observed in our study suggests that it may be an important source of RA for RGCs during embryonic and early postnatal development, especially considering that alcohol dehydrogenase 1 and 4, two potent embryonic synthesizers of RA, are not expressed in the eye during RGC development (Vonesch et al, 1994;Ang et al, 1996a,b). Thus, CYP1B1 mutations may potentially lead to congenital glaucoma by disrupting normal RA production in RGCs and subsequently impairing RGC survival during development or in the adult.…”

Section: Cyp1b1 Enhances Rgc Survivalmentioning

confidence: 69%

Disease Gene Candidates Revealed by Expression Profiling of Retinal Ganglion Cell Development

Wang

Kunzevitzky²,

Dugas³

et al. 2007

J. Neurosci.

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To what extent do postmitotic neurons regulate gene expression during development or after injury? We took advantage of our ability to highly purify retinal ganglion cells (RGCs) to profile their pattern of gene expression at 13 ages from embryonic day 17 through postnatal day 21. We found that a large proportion of RGC genes are regulated dramatically throughout their postmitotic development, although the genes regulated through development in vivo generally are not regulated similarly by RGCs allowed to age in vitro. Interestingly, we found that genes regulated by developing RGCs are not generally correlated with genes regulated in RGCs stimulated to regenerate their axons. We unexpectedly found three genes associated with glaucoma, optineurin, cochlin, and CYP1B1 (cytochrome P450, family 1, subfamily B, polypeptide 1), previously thought to be primarily expressed in the trabecular meshwork, which are highly expressed by RGCs and regulated through their development. We also identified several other RGC genes that are encoded by loci linked to glaucoma. The expression of glaucoma-linked genes by RGCs suggests that, at least in some cases, RGCs may be directly involved in glaucoma pathogenesis rather than indirectly involved in response to increased intraocular pressure. Consistent with this hypothesis, we found that CYP1B1 overexpression potentiates RGC survival.

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Section: Cyp1b1 Enhances Rgc Survivalmentioning

confidence: 69%

Disease Gene Candidates Revealed by Expression Profiling of Retinal Ganglion Cell Development

Wang

Kunzevitzky²,

Dugas³

et al. 2007

J. Neurosci.

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“…The explanation for this discrepancy between the mouse and avian data may be that, in the VAD embryos, there is no dietary vitamin A. Thus, all the embryonic RA production pathways, including those mediated by retinol dehydrogenases, e.g., adh1 and adh4 (Rossant et al, 1991;Vonesch et al, 1994;Haselbeck and Duester, 1998), and retinaldehyde dehydrogenases such as Raldh1, 2 and 3 (Blentic et al, 2003;Fan et al, 2003) are blocked. In the hypomorphic raldh2 mouse mutants, only one RA-producing enzymatic pathway is partially blocked, perhaps resulting in a less severe effect upon Tbx1 expression.…”

Section: Discussionmentioning

confidence: 95%

Retinoic acid down‐regulates Tbx1 expression in vivo and in vitro

Roberts¹,

Ivins²,

James³

et al. 2005

Developmental Dynamics

105

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Both Tbx1 and retinoic acid (RA) are key players in embryonic pharyngeal development; loss of Tbx1 produces DiGeorge syndrome-like phenotypes in mouse models as does disruption of retinoic acid homeostasis. We have demonstrated that perturbation of retinoic acid levels in the avian embryo produces altered Tbx1 expression. In vitamin A-deficient quails, which lack endogenous retinoic acid, Tbx1 expression patterns were disrupted early in development and expression was subsequently lost in all tissues. "Gain-of-function" experiments where RA-soaked beads were grafted into the pharyngeal region produced localized down-regulation of Tbx1 expression. In these embryos, analysis of Shh and Foxa2, upstream control factors for Tbx1, suggested that the effect of RA was independent of this regulatory pathway. Real-time polymerase chain reaction analysis of retinoic acid-treated P19 cells showed a dosedependent repression of Tbx1 by retinoic acid. Repression of Tbx1 transcript levels was first evident after 8 -12 hr in culture in the presence of retinoic acid, and to achieve the highest levels of repression, de novo protein synthesis was required. Developmental Dynamics 232:928 -938, 2005.

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“…These enzymes belong to a family that largely detoxifies xenobiotics and have kinetic characteristics more consistent with xenobiotic clearance than for producing endocrine factors (13). ADHI expression first appears at e10.5 and does not correlate well with sites of atRA synthesis in the mouse embryo, prompting the conclusion that its involvement appears unlikely in embryonic atRA biosynthesis (14). ADHIV shows more widespread expression than ADHI, but it is not expressed in diverse areas of atRA biosynthesis and use in the adult (15).…”

mentioning

confidence: 94%

Molecular Characterization of a Mouse Short Chain Dehydrogenase/Reductase Active with All-trans-retinol in Intact Cells, mRDH1

Zhang¹,

Chen²,

Smith³

et al. 2001

Journal of Biological Chemistry

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Metabolic activation of retinol (vitamin A) via sequential actions of retinol and retinal dehydrogenases produces the active metabolite all-trans-retinoic acid. This work reports cDNA cloning, enzymatic characterization, function in a reconstituted path of all-trans-retinoic acid biosynthesis in cell culture, and mRNA expression patterns in adult tissues and embryos of a mouse retinol dehydrogenase, RDH1. RDH1 represents a new member of the short chain dehydrogenase/reductase superfamily that differs from other mouse RDH in relative activity with all-trans and cis-retinols. RDH1 has a multifunctional catalytic nature, as do other short chain dehydrogenase/reductases. In addition to retinol dehydrogenase activity, RDH1 has strong 3␣-hydroxy and weak 17␤-hydroxy steroid dehydrogenase activities. RDH1 has widespread and intense mRNA expression in tissues of embryonic and adult mice. The mouse embryo expresses RDH1 as early as 7.0 days post-coitus, and expression is especially intense within the neural tube, gut, and neural crest at embryo day 10.5. Cells cotransfected with RDH1 and any one of three retinal dehydrogenase isozymes synthesize all-trans-retinoic acid from retinol, demonstrating that RDH1contributes to a path of all-trans-retinoic acid biosynthesis in intact cells. These characteristics are consistent with RDH1 functioning in a path of all-trans-retinoic acid biosynthesis starting early during embryogenesis. Naturally occurring retinoids (vitamin A and its metabolites) function beyond their well known contributions to vision, conception, growth, and epithelial differentiation. Vertebrates require retinoids for the development of numerous embryonic structures (e.g. limbs, nervous system, heart, kidney), the immune response, and control of intermediary metabolism (1-4). Retinol metabolites serve as endocrine factors that bind to and activate the RAR␣, -␤, and -␥, and the RXR␣, -␤, and -␥ members of the nuclear hormone receptor superfamily (5, 6). Mechanisms for the pleiotropic actions of retinoids are provided by the number of retinoid receptors, their many cell-specific isoforms (generated by differential promoter use and alternative splicing), and heterodimerization of RXR with several other nuclear receptors (7). Receptor expression patterns alone, however, do not explain fully the complex temporal and spatial effects of retinoids during embryogenesis and during postnatal development and growth (8).Metabolism activates vitamin A (retinol) by producing atRA, 1 an endogenous RAR ligand generated both centrally and locally (9, 10). Two sequential reactions produce atRA from all-trans-retinol; they are reversible and rate-limiting dehydrogenation into all-trans-retinal catalyzed by RDH and irreversible and perhaps rate-determining dehydrogenation of alltrans-retinal catalyzed by RALDH. Members of two classes of alcohol dehydrogenases have been proposed to serve as RDH (11,12). The medium chain dehydrogenases, ADH classes I and IV, convert retinol into retinal in vitro. These enzymes belong to a family that...

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Stage and tissue‐specific expression of the alcohol dehydrogenase 1 (Adh‐1) gene during mouse development

Cited by 49 publications

References 68 publications

Disease Gene Candidates Revealed by Expression Profiling of Retinal Ganglion Cell Development

Disease Gene Candidates Revealed by Expression Profiling of Retinal Ganglion Cell Development

Retinoic acid down‐regulates Tbx1 expression in vivo and in vitro

Molecular Characterization of a Mouse Short Chain Dehydrogenase/Reductase Active with All-trans-retinol in Intact Cells, mRDH1

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