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酪氨酸酶中保守的半胱氨酸到丝氨酸突变是实验小鼠经典白化病突变的原因。

Conserved cysteine to serine mutation in tyrosinase is responsible for the classical albino mutation in laboratory mice.

作者信息

Yokoyama T, Silversides D W, Waymire K G, Kwon B S, Takeuchi T, Overbeek P A

机构信息

Howard Hughes Medical Institute, Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.

出版信息

Nucleic Acids Res. 1990 Dec 25;18(24):7293-8. doi: 10.1093/nar/18.24.7293.

Abstract

Albinism, due to a lack of melanin pigment, is one of the oldest known mutations in mice. Tyrosinase (monophenol oxygenase, EC 1.14.18.1) is the first enzyme in the pathway for melanin synthesis, and the gene encoding this enzyme has been mapped to the mouse albino (c) locus. We have used mouse tyrosinase cDNA clones and genomic sequencing to study the albino mutation in laboratory mice. Within the tyrosinase gene coding sequences, a G to C transversion at nucleotide 308, causing a cysteine to serine mutation at amino acid 103, is sufficient to abrogate pigment production in transgenic mice. This same base pair change is fully conserved in classical albino strains of laboratory mice. These results indicate that a conserved mutation in the tyrosinase coding sequences is responsible for the classical albino mutation in laboratory mice, and also that most albino laboratory mouse strains have been derived from a common ancestor.

摘要

白化病是由于缺乏黑色素色素,是小鼠中已知最古老的突变之一。酪氨酸酶(单酚氧化酶,EC 1.14.18.1)是黑色素合成途径中的第一个酶,编码该酶的基因已被定位到小鼠白化病(c)位点。我们使用小鼠酪氨酸酶cDNA克隆和基因组测序来研究实验室小鼠中的白化病突变。在酪氨酸酶基因编码序列内,核苷酸308处的G到C颠换,导致氨基酸103处的半胱氨酸到丝氨酸突变,足以消除转基因小鼠中的色素产生。这种相同的碱基对变化在实验室小鼠的经典白化病品系中完全保守。这些结果表明,酪氨酸酶编码序列中的保守突变是实验室小鼠经典白化病突变的原因,并且大多数白化病实验室小鼠品系都来自一个共同的祖先。

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