Tudor domain containing protein 5-like (Tdrd5l)在果蝇卵发生过程中识别一种新的种系体并调控母体rna。

IF 3.3 3区 生物学 Q2 GENETICS & HEREDITY
Genetics Pub Date : 2025-04-17 DOI:10.1093/genetics/iyaf024
Caitlin Pozmanter, Leif Benner, Sydney E Kelly, Harrison Curnutte, Laura Emilfork, Mark Van Doren
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引用次数: 0

摘要

都铎结构域蛋白因其在种系发育和生育中的功能而在动物王国中被保守。之前,我们证明了Tudor结构域蛋白5-like (Tdrd5l)在生殖系中发挥重要作用,它促进了男性身份。然而,在生殖系发育的后期阶段,Tdrd5l也在卵巢和睾丸中表达,这表明它在两性的生殖系分化中都起作用。我们发现Tdrd5l定位于一种潜在的新型种系体,并在转录后基因调控中发挥作用。此外,由tdrd5l突变雌性产下的胚胎存活率降低,并显示出背附件缺陷,这表明正常的背-腹(D/V)模式失败。由于D/V模式依赖于gurken (grk),我们检测了grk在卵子发生过程中的表达。我们观察到Grk蛋白在护理细胞中的过早积累,表明mRNA转运到卵母细胞的过程中,翻译不再被适当地抑制。我们还观察到护理细胞中细胞质聚腺苷化元件结合蛋白Oo18 rna结合蛋白(Orb或CPEB)的积累增加,这是一种grk的翻译激活剂。orb功能的降低能够部分挽救Tdrd5l突变体的表型,因此orb缺陷可能是Tdrd5l突变体缺陷的主要原因。我们的数据表明,Tdrd5l在母系mrna(如orb)在哺乳细胞合成并运输到卵母细胞过程中,对其翻译抑制很重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tudor domain containing protein 5-like identifies a novel germline body and regulates maternal RNAs during oogenesis in Drosophila.

Tudor domain-containing proteins are conserved across the animal kingdom for their function in germline development and fertility. Previously, we demonstrated that Tudor domain-containing protein 5-like plays an important role in the germline where it promotes male identity. However, Tudor domain-containing protein 5-like is also expressed in both the ovary and testis during later stages of germline development, suggesting that it plays a role in germline differentiation in both sexes. We found that Tudor domain-containing protein 5-like localizes to a potentially novel germline body and plays a role in posttranscriptional gene regulation. Additionally, embryos laid by Tdrd5l-mutant females exhibited reduced viability and displayed dorsal appendage defects suggesting a failure of proper dorsal-ventral patterning. As dorsal-ventral patterning is dependent on gurken (grk), we examined Gurken expression during oogenesis. We observed premature accumulation of Gurken protein in nurse cells indicating that translation is no longer properly repressed during mRNA transport to the oocyte. We also observed increased nurse cell accumulation of the cytoplasmic polyadenylation element binding protein Oo18 RNA-binding protein, a translational activator of grk. Decreasing orb function was able to partially rescue the Tdrd5l-mutant phenotype, and so defects in Orb expression are likely a primary cause of the defects in Tdrd5l mutants. Our data indicate that Tdrd5l is important for translational repression of maternal mRNAs such as orb, and possibly others, following their synthesis in the nurse cells and during their transport to the oocyte.

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来源期刊
Genetics
Genetics GENETICS & HEREDITY-
CiteScore
6.90
自引率
6.10%
发文量
177
审稿时长
1.5 months
期刊介绍: GENETICS is published by the Genetics Society of America, a scholarly society that seeks to deepen our understanding of the living world by advancing our understanding of genetics. Since 1916, GENETICS has published high-quality, original research presenting novel findings bearing on genetics and genomics. The journal publishes empirical studies of organisms ranging from microbes to humans, as well as theoretical work. While it has an illustrious history, GENETICS has changed along with the communities it serves: it is not your mentor''s journal. The editors make decisions quickly – in around 30 days – without sacrificing the excellence and scholarship for which the journal has long been known. GENETICS is a peer reviewed, peer-edited journal, with an international reach and increasing visibility and impact. All editorial decisions are made through collaboration of at least two editors who are practicing scientists. GENETICS is constantly innovating: expanded types of content include Reviews, Commentary (current issues of interest to geneticists), Perspectives (historical), Primers (to introduce primary literature into the classroom), Toolbox Reviews, plus YeastBook, FlyBook, and WormBook (coming spring 2016). For particularly time-sensitive results, we publish Communications. As part of our mission to serve our communities, we''ve published thematic collections, including Genomic Selection, Multiparental Populations, Mouse Collaborative Cross, and the Genetics of Sex.
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