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脆性X智力低下基因1(FMR1)CGG重复序列的家族性传递。

Familial transmission of the FMR1 CGG repeat.

作者信息

Nolin S L, Lewis F A, Ye L L, Houck G E, Glicksman A E, Limprasert P, Li S Y, Zhong N, Ashley A E, Feingold E, Sherman S L, Brown W T

机构信息

Department of Human Genetics, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA.

出版信息

Am J Hum Genet. 1996 Dec;59(6):1252-61.

Abstract

To better define the nature of FMR1 CGG-repeat expansions, changes in allele sizes for 191 families with fragile X and for 33 families with gray-zone repeats (40-60) were analyzed. Expansion of the fragile X chromosome to the full mutation was seen in 13.4% of offspring from premutation mothers with 56-59 repeats, 20.6% of those with 60-69 repeats, 57.8% of those with 70-79 repeats, 72.9% of those with 80-89 repeats, and 97.3% of those with 90-199 repeats. For premutation fathers, the majority (62%) of their daughters had a larger repeat number, while a few had either a smaller (22%) or the same (16%) repeat number, compared with their fathers' sizes. However, daughters with a smaller repeat number were observed only if their fathers had > or = 80 repeats. Fifteen (39.5%) of 38 such daughters carried a smaller repeat than did their fathers. We observed that a similar repeat number was inherited more often than expected by chance, among the members of a sibship segregating fragile X. This familial clustering, observed in the offspring of both males and females with a premutation, implies there may be an additional factor, independent of parental repeat size, that influences CGG-repeat instability. Instability in gray-zone allele transmissions was observed in 25% of alleles with 50-60 CGGs but in <8% of those with 40-49 CGGs. Examination of gray-zone allele organization revealed that long tracts of pure CGGs (>34) are not always unstably transmitted. These results raise new questions regarding the familial factors that may determine transmission expansions.

摘要

为了更好地界定FMR1基因CGG重复序列扩增的本质,我们分析了191个脆性X综合征家庭以及33个具有灰色区域重复序列(40 - 60)家庭的等位基因大小变化。在重复序列为56 - 59的前突变母亲的后代中,13.4%的后代出现脆性X染色体扩增至完全突变;重复序列为60 - 69的母亲,其后代中20.6%出现完全突变;重复序列为70 - 79的母亲,其后代中57.8%出现完全突变;重复序列为80 - 89的母亲,其后代中72.9%出现完全突变;重复序列为90 - 199的母亲,其后代中97.3%出现完全突变。对于前突变父亲,与父亲的重复序列大小相比,其大多数女儿(62%)的重复序列数更大,少数女儿的重复序列数更小(22%)或相同(16%)。然而,只有当父亲的重复序列数≥80时,才会观察到重复序列数更小的女儿。在38个这样的女儿中,有15个(39.5%)的重复序列数比父亲的小。我们观察到,在分离脆性X基因的同胞兄弟姐妹中,相似的重复序列数比随机预期的更常被遗传。在具有前突变的男性和女性的后代中都观察到这种家族聚集现象,这意味着可能存在一个独立于父母重复序列大小的额外因素,影响CGG重复序列的不稳定性。在具有50 - 60个CGG的等位基因传递中,25%观察到灰色区域等位基因的不稳定性,但在具有40 - 49个CGG的等位基因中,不稳定性发生率小于8%。对灰色区域等位基因组织的检查显示,长片段的纯CGG(>³⁴)并不总是不稳定传递。这些结果引发了关于可能决定传递扩增的家族因素的新问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ee1/1914886/6d011eff58bc/ajhg00025-0087-a.jpg

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