par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3.

par-6, a gene involved in the establishment of asymmetry in early C. elegans embryos, mediates the asymmetric localization of PAR-3.
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DOI:
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发表时间:
1996-10
期刊:
影响因子:
4.6
通讯作者:
Jennifer L. Watts;Bijan Etemad-Moghadam;Su Guo;Lynn Boyd;Bruce W. Draper;Craig C. Mello;J. Priess;K. Kemphues
Jennifer L. Watts;Bijan Etemad-Moghadam;Su Guo;Lynn Boyd;Bruce W. Draper;Craig C. Mello;J. Priess;K. Kemphues
中科院分区:
生物学2区
文献类型:
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作者:
Jennifer L. Watts;Bijan Etemad-Moghadam;Su Guo;Lynn Boyd;Bruce W. Draper;Craig C. Mello;J. Priess;K. Kemphues

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秀丽隐杆线虫单细胞胚胎中不对称的产生是建立前后轴和确保早期卵裂球正确识别的必要条件。具有分割缺陷表型(par)的母体效应致死突变已经确定了参与这一过程的几个基因。我们已经发现了一个新的基因,par-6,它与其他par基因一起作用,在早期胚胎中适当地定位细胞质成分。par6胚胎的早期表型包括卵裂球大小相等,P颗粒和SKN-1蛋白定位不正确,二次分裂切割模式异常。总的来说,这种表型与先前描述的par-3基因突变引起的表型非常相似。我们的遗传和免疫定位结果揭示了这种相似性的可能基础;par6通过par3在细胞外周定位或维持par3蛋白而起作用。此外,我们发现功能丧失的par-6突变是par-2功能丧失突变的显性旁路抑制因子。
The generation of asymmetry in the one-cell embryo of Caenorhabditis elegans is necessary to establish the anterior-posterior axis and to ensure the proper identity of early blastomeres. Maternal-effect lethal mutations with a partitioning defective phenotype (par) have identified several genes involved in this process. We have identified a new gene, par-6, which acts in conjunction with other par genes to properly localize cytoplasmic components in the early embryo. The early phenotypes of par-6 embryos include the generation of equal-sized blastomeres, improper localization of P granules and SKN-1 protein, and abnormal second division cleavage patterns. Overall, this phenotype is very similar to that caused by mutations in a previously described gene, par-3. The probable basis for this similarity is revealed by our genetic and immunolocalization results; par-6 acts through par-3 by localizing or maintaining the PAR-3 protein at the cell periphery. In addition, we find that loss-of-function par-6 mutations act as dominant bypass suppressors of loss-of-function mutations in par-2.