Song W J, Sternberg L R, Kasten-Sportès C, Keuren M L, Chung S H, Slack A C, Miller D E, Glover T W, Chiang P W, Lou L, Kurnit D M
Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA.
Genomics. 1996 Dec 15;38(3):331-9. doi: 10.1006/geno.1996.0636.
The presence of an extra copy of human chromosome 21 (trisomy 21), especially region 21q22.2, causes many phenotypes in Down syndrome, including mental retardation. To study genes potentially responsible for some of these phenotypes, we cloned a human candidate gene (DYRK) from 21q22.2 and its murine counterpart (Dyrk) that are homologous to the Drosophila minibrain (mnb) gene required for neurogenesis and to the rat Dyrk gene (dual specificity tyrosine phosphorylation regulated kinase). The three mammalian genes are highly conserved, >99% identical at the protein level over their 763-amino-acid (aa) open reading frame; in addition, the mammalian genes are 83% identical over 414 aa to the smaller 542-aa mnb protein. The predicted human DYRK and murine Dyrk proteins both contain a nuclear targeting signal sequence, a protein kinase domain, a putative leucine zipper motif, and a highly conserved 13-consecutive-histidine repeat. Fluorescence in situ hybridization and regional mapping data localize DYRK between markers D21S336 and D21S337 in the 21q22.2 region. Northern blot analysis indicated that both human and murine genes encode approximately 6-kb transcripts. PCR screening of cDNA libraries derived from various human and murine tissues indicated that DYRK and Dyrk are expressed both during development and in the adult. In situ hybridization of Dyrk to mouse embryos (13, 15, and 17 days postcoitus) indicates a differential spatial and temporal pattern of expression, with the most abundant signal localized in brain gray matter, spinal cord, and retina. The observed expression pattern is coincident with many of the clinical findings in trisomy 21. Its chromosomal locus (21q22. 2), its homology to the mnb gene, and the in situ hybridization expression patterns of the murine Dyrk combined with the fact that transgenic mice for a YAC to which DYRK maps are mentally deficient suggest that DYRK may be involved in the abnormal neurogenesis found in Down syndrome.
人类21号染色体额外拷贝(21三体,尤其是21q22.2区域)的存在会导致唐氏综合征的多种表型,包括智力迟钝。为了研究可能导致其中一些表型的基因,我们从21q22.2克隆了一个人类候选基因(DYRK)及其小鼠对应基因(Dyrk),它们与神经发生所需的果蝇小脑袋(mnb)基因以及大鼠Dyrk基因(双特异性酪氨酸磷酸化调节激酶)同源。这三个哺乳动物基因高度保守,在其763个氨基酸的开放阅读框中,蛋白质水平上的同一性>99%;此外,哺乳动物基因在414个氨基酸上与较小的542个氨基酸的mnb蛋白有83%的同一性。预测的人类DYRK和小鼠Dyrk蛋白都包含一个核定位信号序列、一个蛋白激酶结构域、一个假定的亮氨酸拉链基序以及一个高度保守的13个连续组氨酸重复序列。荧光原位杂交和区域定位数据将DYRK定位在21q22.2区域的标记D21S336和D21S337之间。Northern印迹分析表明,人类和小鼠基因都编码约6kb的转录本。对来自各种人类和小鼠组织的cDNA文库进行PCR筛选表明,DYRK和Dyrk在发育过程中和成年期均有表达。Dyrk对小鼠胚胎(交配后13、15和17天)的原位杂交表明其表达具有不同时空模式,最丰富的信号定位于脑灰质、脊髓和视网膜。观察到的表达模式与21三体的许多临床发现一致。其染色体定位(21q22.2)、与mnb基因的同源性、小鼠Dyrk的原位杂交表达模式,再加上与DYRK定位的YAC转基因小鼠存在智力缺陷这一事实,表明DYRK可能参与了唐氏综合征中发现的异常神经发生。