Identification of recessive maternal-effect mutations in the zebrafish using a gynogenesis-based method.

Identification of recessive maternal-effect mutations in the zebrafish using a gynogenesis-based method.
复制标题

使用基于雌核发育的方法鉴定斑马鱼的隐性母体效应突变。

DOI:
10.1002/dvdy.20145
复制
发表时间:
2004
期刊:
Developmental dynamics : an official publication of the American Association of Anatomists.
影响因子:
--
通讯作者:
Nusslein-Volhard,Christiane
Nusslein-Volhard,Christiane
中科院分区:
--
文献类型:
--
作者:
Pelegri,Francisco;Dekens,MarcusPS;Schulte-Merker,Stefan;Maischein,Hans-Martin;Weiler,Catrin;Nusslein-Volhard,Christiane

文献摘要

相似文献

在动物物种中,早期发育过程是由母系因素驱动的。在这里,我们描述了一种正向遗传学方法来识别斑马鱼中编码这种母体因子的基因中的隐性突变。我们使用了一种基于母系发生的方法来鉴定14种隐性母系效应突变。这些突变在成年雌性体内的纯合性导致其后代无法生存。用DNA染料和膜标记物标记的胚胎共聚焦显微镜使我们能够进一步分析突变胚胎的核和细胞分裂缺陷。这些突变在早期发育过程中导致一系列缺陷,包括卵子激活、早期核事件、有丝分裂、细胞质分裂、轴向模式和原肠胚形成。我们的努力构成了一个系统的尝试,以确定母系效应基因在脊椎动物物种。我们已经确定的突变样本反映了早期发育中母体驱动功能的多样性,并强调了母体因素在这一过程中的重要性。科学通报,2004(1):1 - 3。©2004 Wiley‐Liss, Inc。
In animal species, early developmental processes are driven by maternally derived factors. Here, we describe a forward genetics approach to identify recessive mutations in genes encoding such maternal factors in the zebrafish. We used a gynogenesis‐based approach to identify 14 recessive maternal‐effect mutations. Homozygosity for these mutations in adult females leads to the inviability of their offspring. Confocal microscopy of embryos labeled with a DNA dye and a membrane marker allowed us to further analyze mutant embryos for defects in nuclear and cellular divisions. The mutations result in a range of defects in early developmental processes, including egg activation, early nuclear events, mitosis, cytokinesis, axial patterning, and gastrulation. Our effort constitutes a systematic attempt to identify maternal‐effect genes in a vertebrate species. The sample of mutations that we have identified reflects the diversity of maternally driven functions in early development and underscores the importance of maternal factors in this process. Developmental Dynamics 231:324–335, 2004. © 2004 Wiley‐Liss, Inc.