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减数分裂基因沉默复合物 MTREC/NURS 将核外切酶复合物招募到 YTH-RNA 结合蛋白 Mmi1 上。

Meiotic gene silencing complex MTREC/NURS recruits the nuclear exosome to YTH-RNA-binding protein Mmi1.

机构信息

Laboratory of Cell Responses, National Institute for Basic Biology, Myodaiji, Okazaki, Aichi, Japan.

National Institute for Fusion Science, Toki, Gifu, Japan.

出版信息

PLoS Genet. 2020 Feb 3;16(2):e1008598. doi: 10.1371/journal.pgen.1008598. eCollection 2020 Feb.

DOI:10.1371/journal.pgen.1008598
PMID:32012158
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7018101/
Abstract

Accurate target recognition in transcript degradation is crucial for regulation of gene expression. In the fission yeast Schizosaccharomyces pombe, a number of meiotic transcripts are recognized by a YTH-family RNA-binding protein, Mmi1, and selectively degraded by the nuclear exosome during mitotic growth. Mmi1 forms nuclear foci in mitotically growing cells, and the nuclear exosome colocalizes to such foci. However, it remains elusive how Mmi1 and the nuclear exosome are connected. Here, we show that a complex called MTREC (Mtl1-Red1 core) or NURS (nuclear RNA silencing) that consists of a zinc-finger protein, Red1, and an RNA helicase, Mtl1, is required for the recruitment of the nuclear exosome to Mmi1 foci. Physical interaction between Mmi1 and the nuclear exosome depends on Red1. Furthermore, a chimeric protein involving Mmi1 and Rrp6, which is a nuclear-specific component of the exosome, suppresses the ectopic expression phenotype of meiotic transcripts in red1Δ cells and mtl1 mutant cells. These data indicate that the primary function of MTREC/NURS in meiotic transcript elimination is to link Mmi1 to the nuclear exosome physically.

摘要

准确识别转录物降解中的靶标对于基因表达的调控至关重要。在裂殖酵母 Schizosaccharomyces pombe 中,许多减数分裂转录物被 YTH 家族 RNA 结合蛋白 Mmi1 识别,并在有丝分裂生长期间被核 exosome 选择性降解。Mmi1 在有丝分裂生长的细胞中形成核斑点,核 exosome 与这些斑点共定位。然而,Mmi1 和核 exosome 是如何连接的仍然难以捉摸。在这里,我们表明,一种称为 MTREC(Mtl1-Red1 核心)或 NURS(核 RNA 沉默)的复合物,由一个锌指蛋白 Red1 和一个 RNA 解旋酶 Mtl1 组成,对于核 exosome 向 Mmi1 斑点的募集是必需的。Mmi1 和核 exosome 之间的物理相互作用依赖于 Red1。此外,涉及 Mmi1 和 Rrp6 的嵌合蛋白,Rrp6 是 exosome 的核特异性成分,可抑制 red1Δ 细胞和 mtl1 突变细胞中减数分裂转录物的异位表达表型。这些数据表明,MTREC/NURS 在减数分裂转录物消除中的主要功能是将 Mmi1 与核 exosome 物理连接。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/5206658ecf05/pgen.1008598.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/78adaf5475e8/pgen.1008598.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/e5c4a205dbc2/pgen.1008598.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/165b2cd60802/pgen.1008598.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/29f6f63d2a57/pgen.1008598.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/8f2493e44223/pgen.1008598.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/5206658ecf05/pgen.1008598.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/78adaf5475e8/pgen.1008598.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/e5c4a205dbc2/pgen.1008598.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/165b2cd60802/pgen.1008598.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/29f6f63d2a57/pgen.1008598.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/8f2493e44223/pgen.1008598.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/7018101/5206658ecf05/pgen.1008598.g006.jpg

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