Ask about this productRelated genes to: PIWIL4 antibody
- Gene:
- PIWIL4 NIH gene
- Name:
- piwi like RNA-mediated gene silencing 4
- Previous symbol:
- -
- Synonyms:
- FLJ36156, HIWI2, Miwi2
- Chromosome:
- 11q21
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-26
- Date modifiied:
- 2016-04-19
Related products to: PIWIL4 antibody
Related articles to: PIWIL4 antibody
- BOLL, a highly conserved gene crucial for meiosis in spermatogenesis, is epigenetically regulated through DNA methylation in various species. This study aimed to determine whether BOLL promoter methylation contributes to its downregulation in azoospermic men with hypospermatogenesis (HS) and to explore its potential regulatory association with human spermiogenesis. - Source: PubMed
Publication date: 2026/03/07
Lin Tsung-YenChen Hsing-YiCheng Yung-HsuanLu Chun-WunMa Hsiu-YenHou Hsiu-ChiungLin Yung-MingLin Shih-ChiehCheng Yu-Sheng - Spermatogonial stem cells (SSCs) are essential for long-term spermatogenesis and hold therapeutic potential for treating male infertility. While rodent SSCs are well characterized, human SSCs remain poorly understood. Here, we screen antibodies against proteins encoded by genes enriched in specific subsets of human undifferentiated spermatogonia (uSPG) identified by single-cell RNA sequencing. We characterize four markers labeling distinct uSPG subsets: PIWIL4 marks primitive, quiescent uSPG; EGR4 marks uSPG at a proliferative crossroads; and PPP1R36 and NANOS3 label distinct proliferative subsets poised for differentiation. The most and least advanced subsets-PIWIL4+ and NANOS3+ cells-do not overlap. Comparative transcriptomics uncover candidate pathways involved in uSPG fate transitions, including RAS signaling. Using FSD1, a pan-uSPG cell-surface marker identified here, we purify the entire uSPG population and demonstrate that RAS signaling maintains the primitive uSPG state. These findings provide a framework for human uSPG identity, with broad implications for reproductive biology and regenerative medicine. - Source: PubMed
Publication date: 2026/01/23
Capponi ChiaraSmith ChristopherMedica AlexaHsieh Tung-ChinOrwig Kyle ETan Kun - Respiratory syncytial virus (RSV) is a leading cause of acute lower respiratory tract infections with significant morbidity and mortality in young children, the elderly and immunocompromised hosts. Despite its clinical burden, no effective RSV vaccine or therapy exists for infants, only prophylactic treatment. Small non-coding RNAs have emerged as important regulators of host-pathogen interactions. PIWI-interacting RNAs (piRNAs) are a distinct class of small non-coding RNAs known for maintaining the genome complexity and integrity in gonadal cells. However, there is growing evidence of their role in controlling gene expression in somatic cells. The biogenesis and function of piRNAs is associated with P-element Induced Wimpy testis (Piwi) proteins, whose function in the respiratory epithelium in response to infections remains largely unexplored. Here, we characterize the expression and function of the Piwi-like protein PIWIL4 in the context of RSV infection. We found that PIWIL4 is expressed in both primary and immortalized small airway epithelial cells and is significantly induced at the mRNA and protein levels following RSV infection or poly I:C stimulation, a proxy of viral infection. Immunofluorescence microscopy revealed that PIWIL4 was primarily nuclear in uninfected cells but translocated to the cytoplasm upon RSV exposure. While siRNA-mediated knockdown of PIWIL4 did not significantly affect RSV replication, it led to decreased secretion of several cytokines, chemokines and growth factors, indicating a role in modulating host innate immune responses. Transcriptomic analysis of PIWIL4-silenced iSAE cells showed significant changes in gene expression both in basal conditions and upon RSV infection. Ingenuity Pathway analysis of differentially expressed genes underscored the role of PIWIL4 in modulation of interferon signaling, cytokine production, stress and metabolic responses, as well as airway remodeling pathways. Silencing of PIWIL4 also resulted in global alteration of piRNA expression both in uninfected and infected cells. However, the predicted targets of the differentially expressed piRNAs had limited overlap with the differentially expressed genes identified by transcriptomics, suggesting a function of PIWIL4 in regulating airway epithelial cell responses at least in part independent of piRNAs. Taken together, our study uncovers an important role for PIWIL4 in somatic cells and position it as a key regulator of airway epithelial innate immunity. A better understanding of the mechanisms by which PIWIL4 affects host cells responses following a pathogen exposure may identify novel therapeutic strategies for RSV, as well as other viral respiratory infections. - Source: PubMed
Publication date: 2025/12/06
Corsello TizianaLiu TianshuangKudlicki Andrzej SZhang YuanyiDillman NicholasFazal SeharGarofalo Roberto PCasola Antonella - The maintenance of mammalian spermatogenesis depends on the intricate molecular and cellular interactions between spermatogonial stem cells and their cognate niche in the seminiferous epithelium of the testis. To sustain the continuous production of sperm, spermatogonia proliferate and differentiate under the control of various niche factors, promoting either self-renewal or commitment to spermatogonial differentiation. Single-cell RNA sequencing analyses have identified different subpopulations of spermatogonia in primates based on the expression of specific marker genes (PIWIL4, GFRA1, NANOS3, and KIT). However, the spatial distribution of the different spermatogonial subpopulations and their relationship with the niche has not been described yet. Here, we investigate the topological localization of spermatogonia in primates. To this end, immunohistochemical stainings for PIWIL4, GFRA1, NANOS3 and KIT were performed on Bouin fixed samples of Macaca fascicularis and quantitatively analyzed. Strauss linear selectivity index (Linear Index, Li) was employed to assess the regional distribution of spermatogonial subpopulations in the basal compartment of seminiferous tubules. Remarkably, PIWIL4+ spermatogonia showed a random distribution along the basal compartment across all the stages of the seminiferous epithelium cycle. In contrast, GFRA1+, NANOS3+, and KIT+ spermatogonia displayed stage-dependent localization patterns. The spatial organization of different spermatogonial subpopulations, appeared coordinated with the cycle of the seminiferous epithelium, suggesting a dynamic regulation of spermatogonial behavior throughout the process of sperm production. Our study contributes to the growing body of literature aimed at deciphering the complexities of SSC biology and the regulation of spermatogenesis in mammalian species, with implications for understanding male fertility. - Source: PubMed
Palazzoli MartinaCapponi ChiaraDi Persio SaraFera StefaniaFilippini AntonioSchlatt StefanNeuhaus NinaVicini Elena - The mouse PIWI-interacting RNA (piRNA) pathway provides sustained anti-transposon immunity to the developing male germline by directing transposon DNA methylation. The first step in this process is the recruitment of SPOCD1 to young LINE1 loci. Thereafter, piRNA-mediated tethering of the PIWI protein MIWI2 (also known as PIWIL4) to the nascent transposon transcript recruits the DNA methylation machinery. The piRNA pathway needs to methylate all active transposon copies but how this is achieved remains unknown. Here we show that nuclear piRNA and de novo methylation factors are all euchromatic, exposing constitutive heterochromatin as a genomic blind spot for the piRNA pathway. We discover a 'nowhere-to-hide' mechanism that enables piRNA pathway-mediated LINE1 surveillance of the entire genome. We find that SPOCD1 directly interacts with the nuclear pore component TPR, which forms heterochromatin exclusion zones adjacent to nuclear pores. In fetal gonocytes undergoing piRNA-directed DNA methylation, TPR is found both at the nuclear periphery and throughout the nucleoplasm. We find that the SPOCD1-TPR interaction is required for complete non-stochastic piRNA-directed LINE1 methylation. The loss of the SPOCD1-TPR interaction results in a fraction of SPOCD1 and other chromatin-bound piRNA factors relocalizing to constitutive heterochromatin where they are no longer accessible to MIWI2 and the de novo methylation machinery. In summary, the piRNA pathway has co-opted TPR to guarantee that LINE1s are accessible to the piRNA and de novo methylation machineries. - Source: PubMed
Publication date: 2026/01/14
Chowdhury TamoghnaBoyle ShelaghZoch AnsgarXiang XinyuMirandela Madeleine DiasFieler HannaSpanos ChristosZou JuanKelly DavidBickmore Wendy ACook Atlanta GO'Carroll Dónal