Genes that implement the hermaphrodite mode of dosage compensation in Caenorhabditis elegans.
Genes that implement the hermaphrodite mode of dosage compensation in Caenorhabditis elegans.
复制标题
在秀丽隐杆线虫中实现雌雄同体剂量补偿模式的基因。
DOI：
10.1093/genetics/121.1.57
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发表时间：
1989
期刊：
影响因子：
3.3
通讯作者：
Meyer,BJ
中科院分区：
文献类型：
--
作者：
Plenefisch,JD;DeLong,L;Meyer,BJ
我们报告了秀丽隐杆线虫的剂量补偿过程中的几个重要组成部分的遗传特征。基因dpy-26、dpy-27、dpy-28和新鉴定的基因dpy-29的突变破坏剂量补偿，导致XX动物中X连锁基因表达升高和不完全外显的母体效应XX特异性致死率。这些dpy突变似乎导致XX动物以适合于XO动物的水平表达每组X连锁基因。XO dpy动物基本上是野生型的。XX动物携带两个或多个dpy基因突变的活力和X连锁基因表达水平与仅携带单一突变的动物相同，这与这些基因在单一过程中共同作用（剂量补偿）的观点一致。为了确定dpd-28基因的潜在作用时间，我们用一个热敏等位基因进行了温度变化实验。致死的温度敏感期开始于受精后5小时的300细胞阶段，并延伸至约9小时，这一点远远超过了细胞增殖的结束。这一温度敏感期表明，剂量补偿在XX动物胚胎发育中期起作用，此时许多合子转录的基因是活跃的。虽然dpy基因的突变对野生型XX或XO动物的性表型没有影响，但它们对性别决定过程已经受到遗传干扰的动物确实有轻微的雌性化影响。性别决定的雌性化效应和dpy突变引起的剂量补偿的雄性化效应的相反方向与野生型dpy基因协调控制这两个过程是不一致的。相反，女性化效应很可能是dpy突变引起的剂量补偿中断的间接后果。基于累积的证据，对C. elegans涉及通过dpy基因的作用将XX动物中的X连锁基因表达降低到与XO动物中的相同。
We report a genetic characterization of several essential components of the dosage compensation process in Caenorhabditis elegans. Mutations in the genes dpy-26, dpy-27, dpy-28, and the newly identified gene dpy-29 disrupt dosage compensation, resulting in elevated X-linked gene expression in XX animals and an incompletely penetrant maternal-effect XX-specific lethality. These dpy mutations appear to cause XX animals to express each set of X-linked genes at a level appropriate for XO animals. XO dpy animals are essentially wild type. Both the viability and the level of X-linked gene expression in XX animals carrying mutations in two or more dpy genes are the same as in animals carrying only a single mutation, consistent with the view that these genes act together in a single process (dosage compensation). To define a potential time of action for the gene dpd-28 we performed reciprocal temperature-shift experiments with a heat sensitive allele. The temperature-sensitive period for lethality begins 5 hr after fertilization at the 300-cell stage and extends to about 9 hr, a point well beyond the end of cell proliferation. This temperature-sensitive period suggests that dosage compensation is functioning in XX animals by mid-embryogenesis, when many zygotically transcribed genes are active. While mutations in the dpy genes have no effect on the sexual phenotype of otherwise wild-type XX or XO animals, they do have a slight feminizing effect on animals whose sex-determination process is already genetically perturbed. The opposite directions of the feminizing effects on sex determination and the masculinizing effects on dosage compensation caused by the dpy mutations are inconsistent with the wild-type dpy genes acting to coordinately control both processes. Instead, the feminizing effects are most likely an indirect consequence of disruptions in dosage compensation caused by the dpy mutations. Based on the cumulative evidence, the likely mechanism of dosage compensation in C. elegans involves reducing X-linked gene expression in XX animals to equal that in XO animals via the action of the dpy genes.