MOV10L1 Pre-design Chimera RNAi
- Known as:
- MOV10L1 Pre-design Chimera RNAi
- Catalog number:
- H00054456-R02
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MOV10L1 Pre-design Chimera RNAi
Related genes to: MOV10L1 Pre-design Chimera RNAi
- Gene:
- MOV10L1 NIH gene
- Name:
- Mov10 like RISC complex RNA helicase 1
- Previous symbol:
- -
- Synonyms:
- DJ402G11.8, DKFZp434B0717, CHAMP
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-31
- Date modifiied:
- 2018-06-07
Related products to: MOV10L1 Pre-design Chimera RNAi
Related articles to: MOV10L1 Pre-design Chimera RNAi
- Spermatogenesis is a complex differentiation process requiring precise spatiotemporal gene regulation, yet the functions of most testis-enriched long noncoding RNAs (lncRNAs) remain elusive. Here, we identify as a pachytene-specific lncRNA that is essential for mouse spermatogenesis. Reanalysis of single-cell RNA-seq reveals that expression is minimal in spermatogonia and preleptotene cells, sharply increases during the pachytene stage, and declines after meiosis, precisely coincides with the wave of pachytene piRNA production. In vivo knockdown of in mouse testes via AAV9-shRNA severely disrupts spermatogenesis, causing a reduction in testis size, seminiferous epithelium thickness, and epididymal sperm count, suggesting its physiological necessity. Mechanistically, we demonstrate that functions as a bona fide piRNA precursor: it harbors numerous piRNA sequences, and its overexpression in GC-2 spd(ts) cells specifically upregulates corresponding overlapping piRNAs. This processing relies on the core piRNA machinery, and co-overexpression of , together with or , promotes piRNA production. Notably, this piRNA precursor function is evolutionarily conserved, as the human homolog , which is linked to asthenozoospermia, also generates piRNAs when expressed in GC-2 spd(ts) cells. Transcriptomic analysis following overexpression in GC-2 spd(ts) cells reveals dysregulation of genes involved in metabolism and signaling, with several spermatogenesis-related genes (e.g., , ) predicted as direct targets of -derived piRNAs. Our study identifies as a pachytene-specific lncRNA essential for male fertility and demonstrates that it functions as a conserved piRNA precursor. These findings provide mechanistic insight into how an individual lncRNA contributes to the piRNA pathway and suggest that it may operate through dual mechanisms in mammalian spermatogenesis. - Source: PubMed
Publication date: 2026/05/11
Jian ShikunHan XuXie ChenyaoMa YinghaoChen PeizeLiu WeiguangXiao JunSong Xiaoyuan - Pachytene piRNAs are the least understood class of piRNAs in the mammalian male germ line. During meiosis, their biogenesis occurs near the mitochondrial outer membrane in germ granules known as intermitochondrial cement (IMC). However, how mitochondrial factors regulate the trafficking of PIWI proteins into and out of the IMC remain poorly understood. Here we show that the cytoplasmic PIWI proteins MILI and MIWI are recruited for pachytene piRNA biogenesis via distinct mitochondrial membrane proteins. Loss of the mitochondrial scaffold protein ASZ1 during meiosis in mice disrupts multiple downstream biogenesis steps, resulting in misregulation of MILI, MIWI, and MOV10L1, failure of IMC formation, and an almost complete loss of mature pachytene piRNAs. Strikingly, despite the drastic depletion of pachytene piRNAs, LINE1 transposon silencing remains unaffected. We identify three classes of pachytene piRNA pathway components that coordinate piRNA production and compartmentalization. Our findings reveal that chromatoid body precursors serve as a central hub for the accumulation of pachytene PIWI-piRNA complexes, thus establishing a connection between IMC-based biogenesis and downstream piRNA function. - Source: PubMed
Publication date: 2026/05/12
Yan XiaoyuanWei ChaoMann Jeffrey MShang GuanyiWang QianyiXie HuirongDemireva Elena YSun LiangliangDing DeqiangChen Chen - The formation of biomolecular condensates, such as Yb bodies in Drosophila ovarian somatic cells, is significantly contributed to by phase separation of scaffold proteins. Client proteins transiently accumulate via interactions with these scaffolds; however, how client flux is regulated remains unclear. Here, we investigate Shutdown, a client protein of Yb bodies-the site of Piwi-piRNA-induced silencing complex (piRISC) precursor (pre-Piwi-piRISC) formation-and show that cytosolic Shutdown connects Armitage and Piwi to promote Piwi deposition into Yb bodies before quickly returning to the cytosol. This return allows Armitage to transfer pre-Piwi-piRISC to mitochondria for maturation. Shutdown's acidic N terminus mediates self-repulsion, conferring its transient residence within Yb bodies. A point mutation in armitage, analogous to a human armitage/MOV10L1 mutation associated with azoospermia, traps Shutdown in Yb bodies, blocking Piwi-piRISC generation. This study reveals the mechanism underlying Shutdown's transient localization in Yb bodies and its essential role in Piwi-piRISC biogenesis and fertility. - Source: PubMed
Hirakata ShigekiFukaya TakashiFujita AoiKosako HidetakaSiomi Mikiko C - Splenic nodules in dogs that were historically classified under the broad term "fibrohistiocytic nodules" are now recognised as distinct entities within likely a biological continuum. These include lymphoid hyperplasia extending to indolent lymphoma and complex hyperplasia to stromal sarcoma. However, the molecular mechanisms underpinning these proposed progressions remain largely unexplored, particularly at the genomic and transcriptomic levels. This study aimed to delineate and compare the transcriptomic landscapes of four distinct canine splenic nodules through differential gene expression profiling. RNA sequencing was performed on twelve formalin-fixed, paraffin-embedded (FFPE) splenic tissue samples obtained from dogs diagnosed with lymphoid hyperplasia, complex hyperplasia, histiocytic sarcoma, and stromal sarcoma, with normal canine spleen serving as a control tissue. Comparative transcriptomic analysis identified 47 differentially expressed genes (DEGs) between splenic nodules and normal spleen, including , , , , , , , , , , and . Furthermore, 39 DEGs were significantly altered among the four splenic lesion types, such as , , , , , , , , , , , , , and . Many of these genes have previously been implicated in tumorigenesis and metastasis in other malignancies. These findings suggest that dysregulated gene expression may contribute to the activation of stromal cells and macrophages within the spleen, facilitating malignant transformation. Overall, these findings deliver novel transcriptomic insights into canine splenic tumorigenesis that may improve diagnostic precision, inform prognostic assessment, and support the development of targeted therapeutic strategies in veterinary oncology. - Source: PubMed
Publication date: 2026/01/29
Spröhnle-Barrera CleideAllavena RachelPalmieri Chiara - Male infertility, accounting for approximately 50% of global infertility cases, is a growing concern in reproductive medicine. A fundamental cause lies in disrupted spermatogenesis-a complex, highly regulated process involving mitotic proliferation, meiotic division, and spermiogenic remodeling. Among the key regulatory pathways, PIWI-interacting RNAs (piRNAs) and their associated PIWI proteins have emerged as essential players in maintaining germline genome integrity and ensuring successful sperm development. However, their clinical relevance remain underexplored. This review provides a comprehensive synthesis of the piRNA pathway's multifaceted roles across the full spectrum of spermatogenesis. We describe how piRNAs, together with PIWI proteins, silence transposable elements (TEs), guide chromatin remodeling, regulate mRNA translation, and protect sperm from environmental insults. We detail the stage-specific functions of piRNA machinery during spermatocytogenesis, spermatidogenesis, and spermiogenesis, supported by evidence from gene knockout models and cross-species studies. Particular emphasis is placed on piRNA biogenesis, including the primary processing pathway, the ping-pong amplification cycle, and terminal modifications mediated by enzymes such as PNLDC1 and TDRKH. Genetic disruptions in key piRNA pathway genes-including , , , and -have been linked to clinical phenotypes such as non-obstructive azoospermia and severe oligozoospermia. We explore how these mutations impair piRNA maturation, compromise TE silencing, and trigger germ cell arrest, highlighting their diagnostic and therapeutic relevance. In addition, we discuss emerging applications of piRNAs as non-invasive biomarkers in seminal plasma, with altered piRNA profiles correlating with reduced sperm count and motility. Beyond pathogenesis, the piRNA pathway presents a promising frontier for reproductive interventions. We examine translational strategies targeting piRNA-associated proteins (e.g., RNF8-MIWI interaction modulators) and the potential for piRNA-guided gene silencing in germ cells. Moreover, we consider the impact of environmental toxins and epigenetic stressors on piRNA dynamics, suggesting new angles for fertility preservation. In summary, this review positions the piRNA pathway as a central regulator of male reproductive health. By integrating molecular biology with clinical genetics, we provide a roadmap for leveraging piRNA biology in the diagnosis, management, and treatment of male infertility. - Source: PubMed
Publication date: 2025/09/22
Hong ZhidanHuang SihanLi LiGao YingMa BinyuFan QigangZhang YuanzhenWang Mei