作者: Ian Muchamore , Malcolm Maden , Ian J. McKay , Julian Lewis , Robb Krumlauf
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摘要: kreisler is a recessive mutation resulting in gross malformation of the inner ear homozygous mice. The defects are related to abnormalities hindbrain embryo, adjacent rudiments. At E9.5, neural tube posterior boundary between third and fourth rhombomeres, r3 r4, appears unsegmented, region that would normally correspond r4 unusually thick-walled contains many dying cells. absence morphological segmentation corresponds an altered pattern gene expression region, with major r4/5 minor anterior it. From patterns at E9.5 Krox-20, Hoxb-1 (Hox 2.9), Hoxb-2 2.8), Hoxa-3 1.5), Hoxd-4 4.2) cellular retinoic-acid binding protein I (CRABP I), it fundamental defect loss r5 r6. Correspondingly, glossopharyngeal ganglion nerve, associated r6 missing abducens which originates from r6, also absent. Examination Krox-20 stages as early E8.5 indicates fails ever be expressed its domain mutant. abnormal amount cell death seen only later. An interpretation cells become specified stage adopt character instead, producing excess disposed subsequently by death.