Paternal chromosome incorporation into the zygote nucleus is controlled by maternal haploid in Drosophila
Paternal chromosome incorporation into the zygote nucleus is controlled by maternal haploid in Drosophila
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DOI：
10.1006/dbio.2000.0152
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发表时间：
2001-03-15
影响因子：
2.7
通讯作者：
Couble, P
中科院分区：
文献类型：
--
作者：
Loppin, B;Berger, F;Couble, P
母体单倍体（mh）是一种严格的母体效应突变，其导致产生单倍体雌核发育胚胎（卵子受精，但只有母体染色体参与发育）。我们对mh卵的受精和早期发育进行了细胞学分析，以阐明父本染色体消除的机制。在mb卵中，与野生型卵一样，雄性和雌性原核迁移并并置，第一个有丝分裂纺锤体形成，双亲染色体集合在中期板上。与对照卵相反，mb父本姐妹染色单体在第一次分裂后期不能分离。因此，在末期，父本染色质伸展并形成桥。在最初的三次胚胎分裂中，受损的父亲染色体逐渐从围绕母亲染色体的纺锤体中消失。大多数mb胚胎不能在非整倍体核的有害存在下存活，并迅速阻止其发育。其余的mb胚胎发育为单倍体雌核发育胚胎，并在孵化前死亡。mb表型非常类似于ms（3）K81突变体雄性受精卵的早期发育缺陷，以及在含有内共生细菌沃尔巴克氏体的果蝇不相容杂交产生的卵中观察到的早期发育缺陷。(C)北京：科学出版社.
maternal haploid (mh) is a strict maternal effect mutation that causes the production of haploid gynogenetic embryos (eggs are fertilized but only maternal chromosomes participate in development). We conducted a cytological analysis of fertilization and early development in mh eggs to elucidate the mechanism of paternal chromosome elimination. In mb eggs, as in wild-type eggs, male and female pronuclei migrate and appose, the first mitotic spindle forms, and both parental sets of chromosomes congress on the metaphase plate. In contrast to control eggs, mb paternal sister chromatids fail to separate in anaphase of the first division. As a consequence the paternal chromatin stretches and forms a bridge in telophase. During the first three embryonic divisions, damaged paternal chromosomes are progressively eliminated from the spindles that organize around maternal chromosomes. A majority of mb embryos do not survive the deleterious presence of aneuploid nuclei and rapidly arrest their development. The rest of mb embryos develop as haploid gynogenetic embryos and die before hatching. The mb phenotype is highly reminiscent of the early developmental defects observed in eggs fertilized by ms(3)K81 mutant males and in eggs produced in incompatible crosses of Drosophila harboring the endosymbiont bacteria Wolbachia. (C) 2001 Academic Press.