Vastardis H, Karimbux N, Guthua S W, Seidman J G, Seidman C E
Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Nat Genet. 1996 Aug;13(4):417-21. doi: 10.1038/ng0896-417.
We demonstrate that a mutation in the homeobox gene, MSX1, causes a common developmental anomaly, familial tooth agenesis. Genetic linkage analyses in a family with autosomal dominant agenesis of second premolars and third molars identified a locus on chromosome 4p, where the MSX1 gene resides. Sequence analyses demonstrated an Arg31Pro missense mutation in the homeodomain of MSX1 in all affected family members. Arg 31 is a highly conserved homeodomain residue that interacts with the ribose phosphate backbone of target DNA. We propose that the Arg31 Pro mutatrion comprises MSX1 interactions, and suggest that MSX1 functions are critical for normal development of specific human teeth.
我们证明,同源框基因MSX1中的突变会导致一种常见的发育异常——家族性牙齿缺失。对一个患有常染色体显性遗传的第二前磨牙和第三磨牙缺失的家族进行的遗传连锁分析确定了4号染色体短臂上的一个位点,MSX1基因就位于该位点。序列分析表明,所有受影响的家族成员中,MSX1的同源结构域存在一个Arg31Pro错义突变。Arg 31是一个高度保守的同源结构域残基,它与靶DNA的核糖磷酸主链相互作用。我们认为Arg31Pro突变破坏了MSX1的相互作用,并表明MSX1的功能对于特定人类牙齿的正常发育至关重要。