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Effects of 13‐ cis ‐retinoic acid on hindbrain and craniofacial morphogenesis in long‐tailed macaques ( Macaca fascicularis )
Author(s) -
Makori Norbert,
Peterson Pamela E.,
Blankenship Thomas N.,
DillardTelm Lisa,
Hummler Hans,
Hendrickx Andrew G.
Publication year - 1998
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1111/j.1600-0684.1998.tb00073.x
Subject(s) - hindbrain , rhombomere , neural crest , craniofacial , retinoic acid , branchial arch , biology , cranial neural crest , anatomy , morphogenesis , craniofacial abnormality , endocrinology , medicine , embryo , microbiology and biotechnology , genetics , hox gene , gene expression , gene
Hindbrain and craniofacial development during early organogenesis was studied in normal and retinoic acid‐exposed Macaca fascicularis embryos. 13‐ cis ‐retinoic acid impaired hindbrain segmentation as evidenced by compression of rhombomeres 1 to 5. Immunolocalization with the Hoxb‐1 gene product along with quantitative measurements demonstrated that rhombomere 4 was particularly vulnerable to size reduction. Accompanying malformations of cranial neural crest cell migration patterns involved reduction and/or delay in pre‐ and post‐otic placode crest cell populations that contribute to the pharyngeal arches and provide the developmental framework for the craniofacial region. The first and second pharyngeal arches were partially fused and the second arch was markedly reduced in size. The otocyst was delayed in development and shifted rostrolaterally relative to the hindbrain. These combined changes in the hindbrain, neural crest, and pharyngeal arches contribute to the craniofacial malformations observed in the retinoic acid malformation syndrome manifested in the macaque fetus.