Ask about this productRelated genes to: TEX12 antibody
- Gene:
- TEX12 NIH gene
- Name:
- testis expressed 12
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-16
- Date modifiied:
- 2017-11-24
Related products to: TEX12 antibody
Related articles to: TEX12 antibody
- The synaptonemal complex (SC) is a highly ordered proteinaceous structure that assembles between homologous chromosomes during the prophase I of meiosis. Conserved as a tripartite architecture across species, the SC plays a central role in chromosome synapsis, meiotic recombination, and faithful chromosome segregation. This review marks the 70th anniversary of the discovery of the synaptonemal complex by Montrose Moses in 1956. In mammals, the SC is composed of eight core (canonical) structural proteins: SYCP1, SYCP2, SYCP3, SYCE1, SYCE2, SYCE3, SIX6OS1, and TEX12. The archetypal SC consists of two lateral elements (SYCP2 and SYCP3), a central element (SYCE1/2/3, SIX6OS1, and TEX12), and numerous transverse filaments (SYCP1). A shared structural feature of SC components is the presence of coiled-coil domains. Although the tripartite organization of the SC is evolutionarily conserved, its constituent proteins exhibit little to no sequence homology across species. In addition to these core components, a number of proteins, including HORMAD1, HORMAD2, TRIP13, SKP1, CDCA5 (Sororin), UBE2I (UBC9), SYCP2L, HSPA2, PSMA8, and FKBP6, associate with the SC. Beyond serving as a structural scaffold essential for homolog synapsis, SC proteins interact with key recombination factors such as DMC1, RAD51, and TEX11, thereby regulating recombination progression and crossover formation. Genetic, biochemical, and structural analyses of SC components have provided important mechanistic insights into SC assembly and function, as well as their clinical relevance to non-obstructive azoospermia (NOA) and premature ovarian insufficiency (POI) in humans. - Source: PubMed
Publication date: 2026/04/30
Yang FangWang P Jeremy - Synaptonemal complex (SC) is a structurally conserved, supramolecular assembly that forms at the interface of aligned chromosome axes during meiosis, where it provides a physical context for crossover recombination intermediates. In yeast, the SC is composed of Zip1 transverse filaments and central element proteins Ecm11 and Gmc2. Here, we identify a biochemically stable constitutive complex between Ecm11 and Gmc2, which is mediated by their α-helical coiled-coil regions formed of amino acids 230-302 and 59-188, respectively. We find that the Ecm11-Gmc2 is a 2 : 2 hetero-oligomer, which has an architecture and dimensions similar to the mammalian SC central element complex SYCE2-TEX12. Through targeted mutagenesis in yeast, we show that 2 : 2 Ecm11-Gmc2 complex formation is essential for SC assembly in vivo. Further, we identify key additional residues, particularly in Ecm11, that are dispensable for heterocomplex formation in vitro but critical for stability of the complex in vivo. - Source: PubMed
Ravindan Otter ChandniDavies Owen RMacQueen Amy J - Meiosis, a specialised form of cell division, is essential for sexual reproduction, which requires the proper formation of synaptonemal complex (SC) and homologous recombination (HR). However, the regulatory mechanisms underlying these processes remain incompletely understood. Here, we demonstrate that SOX30 is a key transcriptional regulator of male meiotic synapsis and recombination. In Sox30-knockout mice, zygotene spermatocytes accumulate with synapsis defects. SOX30 deficiency disrupts the SC central element components SYCE1, SYCE2, and TEX12 distribution. Furthermore, disrupted γ-H2AX distribution reveals impaired DNA double-strand break repair and the persistence of recombination proteins RAD51 and RPA2 in late spermatocytes confirms defective homologous recombination repair (HRR) which results in reduced crossover formation in Sox30-knockout mice spermatocytes. Mechanistically, SOX30 directly binds to SYCE1/SYCE2 promoters to modulate their transcription, thereby regulating SC assembly and HRR. Restoring SOX30 expression effectively rescues meiotic defects. Importantly, transcriptome co-expression analysis in non-obstructive azoospermia (NOA) testes identifies SOX30 as a central regulator of NOA transcriptional networks. Collectively, these findings underscore SOX30's crucial role in meiotic synapsis and recombination, highlighting its therapeutic potential for NOA. - Source: PubMed
Publication date: 2025/12/30
Liu KangleZhang WenfengJiang XiaoChen JianpingZhu LeiZhang ZhonghaoGu JingGuo LuluAo LinChen QingSun LeiHu YuhanWang XinLiu YaxinCao JiaHan FeiLiu Jinyi - Follicle development is a critical process in mammalian reproduction, with significant implications for ovarian reserve and fertility. is a known key factor regulating the initiation of meiosis; however, oocyte-like cells still appear in -deficient mice. Nevertheless, the underlying mechanism remains unclear and requires further investigation. Therefore, we used single-cell RNA sequencing to construct a comprehensive transcriptional atlas of ovarian cells from both wild-type and -deficient mice at embryonic stages E14.5 and E16.5. With stringent quality control, we obtained a total of 14,755 single cells of six major cell types. A further fine-scale analysis of the germ cell clusters revealed notable heterogeneity between wild-type and -deficient mice. Compared to the wild-type mice, the deficiency in led to the downregulation of meiosis-related genes (e.g., , and ), and the upregulation of apoptosis-related genes (e.g., , , and ), thereby hindering the meiotic process. Notably, we observed that, following deficiency, the expression levels of and remained elevated at this stage. Furthermore, an RNA interference analysis confirmed the potential role of these genes as regulatory factors in the formation of primordial follicle-like cells. Additionally, deficiency disrupted the signaling between germ cells and pregranulosa cells that is mediated by Mdk-Sdc1, leading to the abnormal expression of the PI3K/AKT signaling pathway. Together, these results shed light on the molecular processes governing germ cell differentiation and folliculogenesis, emphasizing the complex role of in ovarian function. - Source: PubMed
Publication date: 2025/04/15
Wang HanLiu QingchunCheng ShunfengLi LanShen WeiGe Wei - Male infertility is a growing health problem, which affects approximately 7% of the global male population. Nonobstructive azoospermia (NOA) is one of the most severe forms of male infertility caused by genetic defects, including chromosome structural abnormalities, Y chromosome microdeletions, or single-gene alterations. However, the etiology of up to 40% of NOA cases is unidentified. By whole-exome sequencing, we detected a homozygous 5-bp-deletion variant in exon 4 of the TEX12 gene (c.196-200del, p.L66fs, NM_031275.4) in two brothers with NOA of a nonconsanguineous Vietnamese family. This deletion variant of 5 nucleotides (ATTAG) results in a premature stop codon in exon 4 and truncation of the C-terminal. Segregation analysis by Sanger sequencing confirmed that the deletion variant was inherited in an autosomal recessive pattern. The 1 and 3 infertile sons were homozygous for the deletion, whereas the 2 fertile son and both parents were heterozygous. The new deletion mutation identified in TEX12 gene caused loss of function of TEX12 gene. The loss of TEX12 function has already caused infertility in male mice. Therefore, we concluded that the loss of TEX12 function may cause infertility in men. To our knowledge, this is the first case reported so far indicating disruption of human TEX12, which leads to infertility in men. - Source: PubMed
Publication date: 2023/04/03
Bui Minh DucLuong Thi Lan AnhTran Huu DinhDuong Thi Thu HaNguyen Thy NgocNguyen Dang TonNguyen Thuy DuongNong Van Hai