Premium
Embryonic development and pattern formation
Author(s) -
MorrissKay G. M.,
Sokolova N.
Publication year - 1996
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.10.9.8801178
Subject(s) - retinoic acid , biology , yolk sac , retinoid x receptor , retinoid , morphogenesis , embryogenesis , vitamin a deficiency , zebrafish , syncytiotrophoblast , microbiology and biotechnology , endocrinology , embryo , medicine , retinol , genetics , placenta , fetus , vitamin , gene , nuclear receptor , pregnancy , transcription factor
During embryogenesis, information encoded in the genome is translated into cell proliferation, morphogenesis, and early stages of differen‐tiation. Embryonic pattern arises from the spatial and temporal regulation and coordination of these events. The vitamin A (retinol) derivative retinoic acid (RA) is essential for normal development. Mammalian embryos are protected against vitamin A deficiency by maternal retinoid homeostasis until stored retinoids fall to very low levels. Retinol binding protein, which is synthesized in the yolk sac placenta of rodent embryos and in the syncytiotro‐ phoblast of the human placenta, is essential for access of retinol to the embryo. Synthesis and metabolism of RA may involve cytoplasmic binding proteins, but the observation that mutants lacking these proteins are normal or near‐normal suggests that they are not essential. Severe congenital vitamin A deficiency results in a spectrum of malformations including defects of the eye, lungs, cardiovascular system, and urogenital system. Extreme deficiency results as well in forelimb abnormalities and cleft face, but the embryos are not viable. Similar abnormalities are observed in embryos lacking two retinoid receptors, but loss of one receptor results in either normal development or mild abnormalities. Two single‐re‐ ceptor null mutants, RARγ‐/‐ and RXRα‐/‐, show regional pattern‐specific resistance to teratogenic levels of RA. Mutations leading to abnormality of the structure or regulation of RA signaling pathway genes may be an important cause of human congenital abnormality.—Morriss‐Kay, G. M., Sokolova, N. Embryonic development and pattern formation. FASEBJ. 10,961‐968 (1996)