Ask about this productRelated genes to: SYCP1 antibody
- Gene:
- SYCP1 NIH gene
- Name:
- synaptonemal complex protein 1
- Previous symbol:
- -
- Synonyms:
- HOM-TES-14, SCP1, CT8
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-14
- Date modifiied:
- 2016-10-05
Related products to: SYCP1 antibody
Related articles to: SYCP1 antibody
- Meiotic recombination plays a crucial role in the correct separation of homologous chromosomes. The DNA mismatch repair protein Msh4 is a meiosis specific protein and msh4 defects were reported to associate with azoospermia and ovarian dysfunction in mammal. However, its role has not been elucidated in an important model animal, zebrafish. Here, we examined the role of Msh4 in meiosis and gametogenesis by knocking out msh4 using CRISPR/Cas9 technology. The resultant msh4 mutants showed male predominance (98.5%) and brought asynaptic meiosis to form unpaired univalents evidenced by the immunofluorescence detection of the synaptonemal complex protein Sycp3 and Sycp1, and the recombination protein Rad51. Such unusual meiotic configurations led to meiotic arrest and subsequent abortive spermatogenesis. In contrast, msh4 deficiency induced infrequent msh4 female (1.5%) that laid eggs which developed to normal (40-80%) or abnormal (20-60%) progeny by fertilizing with sperm of wild type. Thus, Msh4 is essential for the meiosis in males, but is not strictly required in females. - Source: PubMed
Publication date: 2026/02/26
Guo YankunZhang YunbangMei YihuiHuang YuweiZheng YuxuanZhang NanJiang YuxinJiang HanjunZhang ZijieLi AngxiaoFan JinchangArai KatsutoshiGao JianCao Xiaojuan - Human germline gene expression is normally constrained to the germ cells, responsible for the production of sperm and oocytes. Cancer-germline (CG) genes, a subset of germline genes involved in testis development, are frequently aberrantly activated in cancer cells. The present study investigates the broader hypothesis that epigenetic modifications, specifically DNA methylation, can modulate the expression profiles of several CG genes in cancer and germ cells. Breast cancer (BC), normal breast (NB), and chronic myelogenous leukemia (CML) cell lines were treated with the DNA methyltransferase inhibitor (DNMTi) 5-aza-2'-deoxycytidine for three days. The effects of this treatment on the transcriptional activation of CG genes (SYCP1, ADAD1, SYCE1, PRSS54, DMRTC2, and TEX101) were then evaluated. We comprehensively analyzed differential methylation, survival analysis (Kaplan-Meier), correlation (Spearman's), and pathway enrichment analysis (GO/KEGG) of CG genes (SYCP1, ADAD1, SYCE1, PRSS54, DMRTC2, and TEX101) in BC and leukemia. Treatment with 5-aza-2'-deoxycytidine upregulated CG genes in BC cells but downregulated them in leukemia cells, highlighting tissue-specific epigenetic responses. Differential methylation analysis revealed cancer-specific patterns: ADAD1 was hypermethylated in both malignancies, while PRSS54 was hypomethylated in leukemia. Survival analysis linked SYCE1 and PRSS54 to prolonged survival in BC, whereas TEX101 and SYCP1 correlated with poorer outcomes. Functional enrichment identified ADAD1 and SYCP1 as key players in BC and leukemia pathways, respectively. Meta-analysis validated SYCP1 as a robust biomarker with consistent effect sizes across datasets. Methylation-expression correlations were stronger in tumors, with SYCE1 and DMRTC2 showing inverse relationships in leukemia. These findings demonstrate that the expression of a subset of CG genes is responsive to modulation by hypomethylating drugs in a tissue-specific manner, highlighting their promise as candidates for future investigation in cancer immunotherapy. - Source: PubMed
Publication date: 2025/12/18
Almutairi Mikhlid HAlrubie Turki M - Non-obstructive azoospermia (NOA) is one of the most severe manifestations of male infertility, accounting for up to 70% of azoospermic cases and affecting approximately 1% of the male population. Advances in genomics and epigenetics have transformed our understanding of NOA from a primarily idiopathic condition into a biologically heterogeneous disorder driven by diverse molecular mechanisms. This review synthesizes the current knowledge of the genetic and epigenetic landscape of NOA, integrating chromosomal abnormalities, single-gene mutations, and non-coding RNA (ncRNA) dysregulation. First, we systematically examine classical and emerging chromosomal defects-including karyotype anomalies, Y-chromosome microdeletions, and structural rearrangements-that disrupt meiotic pairing and chromatin organization. Next, we explore syndromic and non-syndromic monogenic mutations affecting meiotic regulators, DNA repair factors, transcription regulators, and chromatin remodelers. Particular emphasis is placed on recently identified genes such as SYCP1, SYCE1 and HORMAD1, whose pathogenic variants are frequently linked to spermatogenic arrest. We then discuss the expanding role of ncRNAs-including microRNAs, PIWI-interacting RNAs, long non-coding RNAs, and circular RNAs-in regulating germ cell apoptosis, transposon silencing, and epigenetic reprogramming. Furthermore, we highlight the translational potential of these molecular insights (including gene variants, ncRNAs and protein) in clinical applications. Genotype-guided sperm retrieval, non-invasive biomarkers, and multi-omic approaches are discussed as promising tools to improve diagnosis and treatment. Moreover, we summarize current and emerging strategies for the treatment and fertility preservation of NOA. Finally, we identify persisting challenges, such as genotypic heterogeneity and incomplete functional validation, and emphasize the need to elucidate interactions between ncRNA and classical genetic pathways to uncover regulatory hierarchies underlying NOA. By integrating molecular genetics with testicular histopathology and clinical phenotypes, this review highlights emerging genetic and ncRNA biomarkers and underscores their potential applications in the clinical management of NOA. Ultimately, a comprehensive understanding of the genetic and epigenetic underpinnings of NOA will be essential for advancing precision diagnostics and improving reproductive outcomes in affected men. - Source: PubMed
Publication date: 2025/12/03
Wang XiaojieNie LinhangHong ZhidanLi LiFan QigangMa BinyuLi ZihangGao YingZhang MingZhang YuanzhenWang Mei - Homologous synapsis and recombination are the central events that take place in the prophase I of meiosis. Signaling that promotes the germ cell differentiation and prophase I remains elusive. Here we show a key Kitl/Kit signaling between somatic cells and germ cells in regulating meiotic prophase I in the mouse fetal gonad. Disruption of Kitl/Kit signaling, both in vivo and in vitro, impairs meiosis initiation, disrupts homologous synapsis and recombination. Moreover, mTOR/p-S6 signaling induced by Kitl/Kit elevates the levels of critical proteins such as Stra8, Sycp1 and Sycp3 for meiosis entry and homologous synapsis. Blocking Kitl/Kit signaling suppresses the mTOR and decreases the protein levels of Stra8, Sycp1, Sycp3 and Vasa, impairing the prophase I. In contrast, activating mTOR can rescue the meiotic defects caused by somatic Kitl deficiency. The activated p-AKT links Kitl/Kit to promoting mTOR/p-S6 signaling in the fetal germ cells. These findings reveal the critical functions and mechanisms of somatic Kitl in meiosis entry and homologous synapsis and recombination during the prophase I. - Source: PubMed
Publication date: 2025/11/17
Liu ChangJin ZiyiChen JiyuLi JieFeng GuofengYin GuoxingYu YongqinYe XiaoyingSun HaoweiZhang HuaGao FeiLiu Lin - Epidemiological studies have shown a small but significantly increased risk of leukemia in children conceived by in vitro fertilization. Atypical DNA methylation patterns observed in pediatric cancers are suspected to occur in utero, and it is known that periconceptional conditions linked to assisted reproductive technologies (ART) are responsible for DNA methylation modifications. - Source: PubMed
Publication date: 2025/10/21
Ducreux BastienFirmin JulieFerreux LucilePatrat CatherineClavel JacquelineGhantous AkramHerceg ZdenkoCallanan MaryFauque Patricia