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Retinoic acid given at late embryonic stage depresses sonic hedgehog and Hoxd‐4 expression in the pharyngeal area and induces skeletal malformation in flounder ( Paralichthys olivaceus ) embryos
Author(s) -
Suzuki Tohru,
Oohara Ichiro,
Kurokawa Tadahide
Publication year - 1999
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1046/j.1440-169x.1999.00420.x
Subject(s) - retinoic acid , flounder , paralichthys , sonic hedgehog , biology , stage (stratigraphy) , olive flounder , medicine , endocrinology , fish <actinopterygii> , anatomy , andrology , microbiology and biotechnology , fishery , genetics , signal transduction , gene , paleontology
During the development of pharyngeal cartilages, signal molecules, including sonic hedgehog ( shh ) and various growth factors, as well as Hox genes are expressed in the pharyngeal area. To elucidate whether shh and Hoxd‐4 function in pharyngeal cartilage formation in teleost jaw and gill primordia, spatial and temporal patterns of shh expression in flounder ( Paralichthys olivaceus ) embryonic pharynx were examined. The effects of retinoic acid (RA) on shh and Hoxd‐4 expression and the patterning of pharyngeal cartilages were analyzed. At the prim‐5 stage, when cartilage precursor cells aggregate in the pharyngeal primordia, pharyngeal endoderm expressed shh in two domains, in portions of the mandibular and hyoid primordia and in the gill primordia. After a further 40 h, shh domains expanded at the posterior edge of the endoderm of each mandibular, hyoid and gill primordium, concurrent with the growth of the primordia. A new shh expression domain appeared at the endodermal border of the mouth. Retinoic acid treatment depressed shh and Hoxd‐4 expression, and also reduced the amount of expansion of the shh expression domains. Pharyngeal cartilages that formed in these embryos were malformed; their growth direction was shifted posteriorly and size was reduced. This provides the possibility that shh and Hoxd‐4 regulate the growth and direction of pharyngeal cartilage precursor cells and that RA disturbs their expression, causing skeletal malformation.