可的松诱导的小鼠腭裂。对胚胎反应性状的遗传控制的探索。
Cortisone-induced cleft palate in the mouse. A search for the genetic control of the embryonic response trait.
作者信息
Biddle F G, Fraser R C
出版信息
Genetics. 1977 Feb;85(2):289-302. doi: 10.1093/genetics/85.2.289.
Abstract
The cause of the difference in the mean tolerance (ED50) to cortisone-induced cleft palate between the embryos of the A/J and C57BL/6J strains appears to be due to a small number of genes. A single major gene effect and a polygenic model, in the sense of many equal and additive genes, have been ruled out. The embryonic tolerance of C57BL/6J is greater than and dominant to that of A/J; two or three loci, possibly with independent effects, appear to explain the variability. A component of the variation in embryonic response may be associated with or linked to the major histocompatibility locus (H-2). No evidence was found to support the hypothesis of X-chromosome linked susceptibility to cortisone-induced cleft palate.
摘要
A/J和C57BL/6J品系胚胎对可的松诱导腭裂的平均耐受性（半数有效剂量，ED50）存在差异，其原因似乎是少数基因所致。单一主基因效应以及多基因模型（即许多等效和累加基因）已被排除。C57BL/6J的胚胎耐受性大于A/J，且对A/J具有显性作用；两个或三个位点可能具有独立效应，似乎可以解释这种变异性。胚胎反应变异的一个组成部分可能与主要组织相容性位点（H-2）相关或连锁。未发现证据支持X染色体连锁的对可的松诱导腭裂易感性的假说。
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