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Distinct functions for Aldh1 and Raldh2 in the control of ligand production for embryonic retinoid signaling pathways

Distinct functions for Aldh1 and Raldh2 in the control of ligand production for embryonic... During vertebrate embryogenesis retinoic acid (RA) synthesis must be spatiotemporally regulated in order to appropriately stimulate various retinoid signaling pathways. Various forms of mammalian aldehyde dehydrogenase (ALDH) have been shown to oxidize the vitamin A precursor retinal to RA in vitro. Here we show that injection of Xenopus embryos with mRNAs for either mouse Aldh1 or mouse Raldh2 stimulates RA synthesis at low and high levels, respectively, while injection of human ALDH3 mRNA is unable to stimulate any detectable level of RA synthesis. This provides evidence that some members of the ALDH gene family can indeed perform RA synthesis in vivo. Whole‐mount immunohistochemical analyses of mouse embryos indicate that ALDH1 and RALDH2 proteins are localized in distinct tissues. RALDH2 is detected at E7.5–E10.5 primarily in trunk tissue (paraxial mesoderm, somites, pericardium, midgut, mesonephros) plus transiently from E8.5–E9.5 in the ventral optic vesicle and surrounding frontonasal region. ALDH1 is first detected at E9.0–E10.5 primarily in cranial tissues (ventral mesencephalon, dorsal retina, thymic primordia, otic vesicles) and in the mesonephros. As previous findings indicate that embryonic RA is more abundant in trunk rather than cranial tissues, our findings suggest that Raldh2 and Aldh1 control distinct retinoid signaling pathways by stimulating high and low RA biosynthetic activities, respectively, in various trunk and cranial tissues. Dev. Genet. 25:353–364, 1999. © 1999 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genesis: the Journal of Genetics and Development Wiley

Distinct functions for Aldh1 and Raldh2 in the control of ligand production for embryonic retinoid signaling pathways

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References (91)

Publisher
Wiley
Copyright
"Copyright © 1999 Wiley Subscription Services, Inc., A Wiley Company"
ISSN
1526-954X
eISSN
1526-968X
DOI
10.1002/(SICI)1520-6408(1999)25:4<353::AID-DVG9>3.0.CO;2-G
pmid
10570467
Publisher site
See Article on Publisher Site

Abstract

During vertebrate embryogenesis retinoic acid (RA) synthesis must be spatiotemporally regulated in order to appropriately stimulate various retinoid signaling pathways. Various forms of mammalian aldehyde dehydrogenase (ALDH) have been shown to oxidize the vitamin A precursor retinal to RA in vitro. Here we show that injection of Xenopus embryos with mRNAs for either mouse Aldh1 or mouse Raldh2 stimulates RA synthesis at low and high levels, respectively, while injection of human ALDH3 mRNA is unable to stimulate any detectable level of RA synthesis. This provides evidence that some members of the ALDH gene family can indeed perform RA synthesis in vivo. Whole‐mount immunohistochemical analyses of mouse embryos indicate that ALDH1 and RALDH2 proteins are localized in distinct tissues. RALDH2 is detected at E7.5–E10.5 primarily in trunk tissue (paraxial mesoderm, somites, pericardium, midgut, mesonephros) plus transiently from E8.5–E9.5 in the ventral optic vesicle and surrounding frontonasal region. ALDH1 is first detected at E9.0–E10.5 primarily in cranial tissues (ventral mesencephalon, dorsal retina, thymic primordia, otic vesicles) and in the mesonephros. As previous findings indicate that embryonic RA is more abundant in trunk rather than cranial tissues, our findings suggest that Raldh2 and Aldh1 control distinct retinoid signaling pathways by stimulating high and low RA biosynthetic activities, respectively, in various trunk and cranial tissues. Dev. Genet. 25:353–364, 1999. © 1999 Wiley‐Liss, Inc.

Journal

Genesis: the Journal of Genetics and DevelopmentWiley

Published: Jan 1, 1999

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