Premium
Genetic susceptibility in the neural tube defects induced by ochratoxin A in the genetic arhinencephaly mouse, Pdn/Pdn
Author(s) -
Ohta Kenichi,
Maekawa Mizuho,
Katagiri Ryuichi,
Ueta Etsuko,
Naruse Ichiro
Publication year - 2006
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/j.1741-4520.2006.00117.x
Subject(s) - gli3 , fgf8 , neural tube , embryo , gene , gene expression , microbiology and biotechnology , biology , andrology , medicine , genetics , receptor , repressor , fibroblast growth factor
It is well known that ochratoxin A (OTA) induces neural tube defects (NTDs) in mice. In the present study, OTA was administered to the genetic polydactyly/arhinencephaly mouse ( Pdn/Pdn ) to investigate the synergistic effect between gene and environmental toxin. OTA treatment on day 7.5 of gestation increased NTDs in the Pdn/Pdn mouse. The responsible gene for Pdn/Pdn is Gli3 . So, it was speculated that specific susceptibility for OTA in the Pdn/Pdn mouse embryo may be due to the severe depression of Gli3 gene expression. As correlated genes, Gli3 , Shh and Fgf8 gene expressions were examined in the Pdn mouse embryo on day 9 of gestation after administration of OTA on day 7.5. No alteration of Shh expression was observed in the non‐treated Pdn/Pdn , and OTA‐treated +/+ and Pdn/Pdn . Fgf8 signal was observed at the anterior neural ridge (ANR) in the non‐treated +/+, and that was elongated in the non‐treated Pdn/Pdn , and further elongated and more intensive in the OTA‐treated Pdn/Pdn . It was suggested that Fgf8 gene expression was affected by the depression of Gli3 , and alteration of Fgf8 gene expression was accelerated by the toxicity of OTA in the Pdn/Pdn.