Bicaudal-C recruits CCR4-NOT deadenylase to target mRNAs and regulates oogenesis, cytoskeletal organization, and its own expression
Bicaudal-C recruits CCR4-NOT deadenylase to target mRNAs and regulates oogenesis, cytoskeletal organization, and its own expression
复制标题
DOI：
10.1016/j.devcel.2007.10.002
复制
发表时间：
2007-11-01
影响因子：
11.8
通讯作者：
Lasko, Paul
中科院分区：
文献类型：
--
作者：
Chicoine, Jarred;Benoit, Perrine;Lasko, Paul
Bicaudal-C（Bic-C）编码一种RNA结合蛋白，是果蝇胚胎形成模式所必需的。我们鉴定了一组与卵巢核糖核蛋白复合物中Bic-C相关的mRNA。这些mRNA富含在卵子发生和细胞骨架调节中起作用的mRNA，并且包括Bic-C RNA本身。Bic-C结合Bic-C 5'非翻译区的特定片段，并通过直接结合CCR 4核心去腺苷酶复合物的组分N 0 T3/5来负调节其自身的表达，从而促进去腺苷化。Bic-C过表达诱导过早的细胞质流，后组表型，Oskar和驱动蛋白重链缺陷：β Gal定位以及背附件缺陷。这些表型与Bic-C突变体的表型在很大程度上是相互的，并且它们影响Bic-C相关mRNA已知或预测调节的细胞过程。我们的结论是，Bic-C调控特定的生殖系mRNA的表达，通过控制其聚（A）尾长度。
Bicaudal-C (Bic-C) encodes an RNA-binding protein required maternally for patterning the Drosophila embryo. We identified a set of mRNAs that associate with Bic-C in ovarian ribonucleoprotein complexes. These mRNAs are enriched for mRNAs that function in oogenesis and in cytoskeletal regulation, and include Bic-C RNA itself. Bic-C binds specific segments of the Bic-C 5' untranslated region and negatively regulates its own expression by binding directly to NOT3/5, a component of the CCR4 core deadenylase complex, thereby promoting deadenylation. Bic-C overexpression induces premature cytoplasmic-streaming, a posterior-group phenotype, defects in Oskar and Kinesin heavy chain:beta Gal localization as well as dorsal-appendage defects. These phenotypes are largely reciprocal to those of Bic-C mutants, and they affect cellular processes that Bic-C-associated mRNAs are known, or predicted, to regulate. We conclude that Bic-C regulates expression of specific germline mRNAs by controlling their poly(A)-tail length.