Cytoplasmic dynein light intermediate chain is required for discrete aspects of mitosis in Caenorhabditis elegans.
Cytoplasmic dynein light intermediate chain is required for discrete aspects of mitosis in Caenorhabditis elegans.
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DOI：
10.1091/mbc.12.10.2921
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发表时间：
2001-10
影响因子：
3.3
通讯作者：
John H. Yoder;Min Han
中科院分区：
文献类型：
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作者：
John H. Yoder;Min Han
我们描述的dli-1，秀丽隐杆线虫同源细胞质动力蛋白轻中间链（LIC），细胞质动力蛋白马达复合物的亚基的表型表征。dli-1功能缺失突变纯合的动物在晚期幼虫细胞谱系中表现出随机的分裂失败，导致合子不育。DLI-1是有丝分裂期间动力蛋白功能所必需的。通过RNA介导的基因干扰（RNAi）耗尽dli-1基因产物揭示了早期胚胎的需要。单细胞dli-1（RNAi）胚胎表现出失败的细胞分裂尝试，导致各种有丝分裂缺陷。具体而言，原核迁移，中心体分离，中心体协会与男性原核包膜缺陷dli-1（RNAi）胚胎。然而，在这些胚胎中，减数分裂纺锤体的形成不受影响。DLI-1，像它的脊椎动物同系物，含有一个推定的核苷酸结合结构域类似于那些发现在ATP结合盒转运蛋白家族的ATP酶以及其他核苷酸结合和水解蛋白。已知核苷酸结合所需的保守赖氨酸残基中的氨基酸取代赋予dli-1突变体背景中的完全拯救，表明这不是DLI-1功能的必需结构域。
We describe phenotypic characterization of dli-1, the Caenorhabditis elegans homolog of cytoplasmic dynein light intermediate chain (LIC), a subunit of the cytoplasmic dynein motor complex. Animals homozygous for loss-of-function mutations in dli-1 exhibit stochastic failed divisions in late larval cell lineages, resulting in zygotic sterility. dli-1 is required for dynein function during mitosis. Depletion of the dli-1 gene product through RNA-mediated gene interference (RNAi) reveals an early embryonic requirement. One-cell dli-1(RNAi) embryos exhibit failed cell division attempts, resulting from a variety of mitotic defects. Specifically, pronuclear migration, centrosome separation, and centrosome association with the male pronuclear envelope are defective in dli-1(RNAi) embryos. Meiotic spindle formation, however, is not affected in these embryos. DLI-1, like its vertebrate homologs, contains a putative nucleotide-binding domain similar to those found in the ATP-binding cassette transporter family of ATPases as well as other nucleotide-binding and -hydrolyzing proteins. Amino acid substitutions in a conserved lysine residue, known to be required for nucleotide binding, confers complete rescue in a dli-1 mutant background, indicating this is not an essential domain for DLI-1 function.