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DPY-30,一种在胚胎发育早期对秀丽隐杆线虫剂量补偿至关重要的核蛋白。

DPY-30, a nuclear protein essential early in embryogenesis for Caenorhabditis elegans dosage compensation.

作者信息

Hsu D R, Chuang P T, Meyer B J

机构信息

Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.

出版信息

Development. 1995 Oct;121(10):3323-34. doi: 10.1242/dev.121.10.3323.

Abstract

DPY-30 is an essential component of the C. elegans dosage compensation machinery that reduces X chromosome transcript levels in hermaphrodites (XX). DPY-30 is required for the sex-specific association of DPY-27 (a chromosome condensation protein homolog) with the hermaphrodite X chromosomes. Loss of dpy-30 activity results in XX-specific lethality. We demonstrate that dpy-30 encodes a novel nuclear protein of 123 amino acids that is present in both hermaphrodites and males (XO) throughout development. DPY-30 itself is not associated with the X chromosomes, nor is its pattern of expression perturbed by mutations in the gene hierarchy that controls dosage compensation. Therefore, DPY-30 is a ubiquitous factor that is likely to promote the hermaphrodite-specific association of DPY-27 with X by affecting the activity of a sex-specific dosage compensation gene. In XO animals, DPY-30 is required for developmental processes other than dosage compensation: coordinated movement, normal body size, correct tail morphology and mating behavior. We demonstrate that rescue of both the XX-specific lethality and the XO-specific morphological defects caused by dpy-30 mutations can be achieved by inducing dpy-30 transcripts either in the mother or in the embryo through the end of gastrulation. dpy-30 appears to be cotranscribed in an operon with a novel RNA-binding protein.

摘要

DPY-30是秀丽隐杆线虫剂量补偿机制的一个重要组成部分,该机制可降低雌雄同体(XX)中X染色体的转录水平。DPY-27(一种染色体凝聚蛋白同源物)与雌雄同体X染色体的性别特异性结合需要DPY-30。dpy-30活性的丧失导致XX特异性致死。我们证明,dpy-30编码一种由123个氨基酸组成的新型核蛋白,在整个发育过程中存在于雌雄同体和雄性(XO)中。DPY-30本身不与X染色体相关,其表达模式也不会因控制剂量补偿的基因层次结构中的突变而受到干扰。因此,DPY-30是一种普遍存在的因子,可能通过影响性别特异性剂量补偿基因的活性来促进DPY-27与X的雌雄同体特异性结合。在XO动物中,DPY-30是剂量补偿以外的发育过程所必需的:协调运动、正常体型、正确的尾部形态和交配行为。我们证明,通过在母亲或胚胎中诱导dpy-30转录本直至原肠胚形成结束,可以挽救由dpy-30突变引起的XX特异性致死和XO特异性形态缺陷。dpy-30似乎与一种新型RNA结合蛋白在一个操纵子中共同转录。

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