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人类凝血因子IX基因的缺失率及缺失模式。

The rates and patterns of deletions in the human factor IX gene.

作者信息

Ketterling R P, Vielhaber E L, Lind T J, Thorland E C, Sommer S S

机构信息

Department of Biochemistry and Molecular Biology, Mayo Clinic/Foundation, Rochester, MN 55905.

出版信息

Am J Hum Genet. 1994 Feb;54(2):201-13.

Abstract

Deletions are commonly observed in genes with either segments of highly homologous sequences or excessive gene length. However, in the factor IX gene and in most genes, deletions (of > or = 21 bp) are uncommon. We have analyzed DNA from 290 families with hemophilia B (203 independent mutations) and have found 12 deletions > 20 bp. Eleven of these are > 2 kb (range > 3-163 kb), and one is 1.1 kb. The junctions of the four deletions that are completely contained within the factor IX gene have been determined. A novel mutation occurred in patient HB128: the data suggest that a 26.8-kb deletion occurred between two segments of alternating purines and pyrimidines and that a 2.3-kb sense strand segment derived from the deleted region was inserted. For our sample of 203 independent mutations, we estimate the "baseline" rates of deletional mutation per base pair per generation as a function of size. The rate for large (> 2 kb) deletions is exceedingly low. For every mutational event in which a given base is at the junction of a large deletion, there are an estimated 58 microdeletions (< 20 bp) and 985 single-base substitutions at that base. Analysis of the nine reported deletion junctions in the factor IX gene literature reveals that (i) five are associated with inversions, orphan sequences, or sense strand insertions; (ii) four are simple deletions that display an excess of short direct repeats at their junctions; (iii) there is no dramatic clustering of junctions within the gene; and (iv) with the exception of alternating purines and pyrimidines, deletion junctions are not preferentially associated with repetitive DNA.

摘要

在具有高度同源序列片段或基因长度过长的基因中,缺失现象较为常见。然而,在因子IX基因以及大多数基因中,大于或等于21 bp的缺失并不常见。我们分析了290个血友病B家族的DNA(203个独立突变),发现了12个大于20 bp的缺失。其中11个大于2 kb(范围为大于3 - 163 kb),1个为1.1 kb。已经确定了完全包含在因子IX基因内的4个缺失的连接点。患者HB128发生了一种新的突变:数据表明,在交替嘌呤和嘧啶的两个片段之间发生了26.8 kb的缺失,并且来自缺失区域的2.3 kb有义链片段被插入。对于我们203个独立突变的样本,我们估计了每代每个碱基对的缺失突变“基线”率与大小的函数关系。大(大于2 kb)缺失的发生率极低。对于给定碱基位于大缺失连接点的每一个突变事件,估计在该碱基处有58个微缺失(小于20 bp)和985个单碱基替换。对因子IX基因文献中报道的9个缺失连接点的分析表明:(i)5个与倒位、孤儿序列或有义链插入有关;(ii)4个是简单缺失,在其连接点处显示出过量的短直接重复序列;(iii)基因内连接点没有明显的聚集;(iv)除了交替嘌呤和嘧啶外,缺失连接点与重复DNA没有优先关联。

相似文献

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Deletions with inversions: report of a mutation and review of the literature.
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The factor IX gene as a model for analysis of human germline mutations: an update.
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3
Deletions with inversions: report of a mutation and review of the literature.
Hum Mutat. 1993;2(1):53-7. doi: 10.1002/humu.1380020110.

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