MSH4 (internal)
- Known as:
- MSH4 (middlesequence)
- Catalog number:
- Y213805
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MSH4 (internal)
Related genes to: MSH4 (internal)
- Gene:
- MSH4 NIH gene
- Name:
- mutS homolog 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: MSH4 (internal)
(I) LightCycler 1. 0; (Internal Control can't be used for this system) ; (II) LightCycler2. 0; (III) PE5700, MJ_Opticon etc. single color systems; (IV) ABI7000, ABI7300, ABI7500, ABI7900, ABI StepO1.0ml Self-Standing Cryovial Internal Thread w/ O-Ring Seal1.2ml Cryogenic Vial,Self-Standing, Internal Thread1.2ml Self-Standing Cryovial Internal Thread w per O-Ring Seal1.2ml Self-Standing Cryovial Internal Thread w per Silicone Wa1.2ml Self-Standing Cryovial Internal Thread w per Washer Seal1.2ml Self-Standing Cryovial Internal Thread w/ O-Ring Seal1.2ml Self-Standing Cryovial Internal Thread w/ O-Ring Seal1.2ml Self-Standing Cryovial Internal Thread w/ Silicone Wa1.2ml Self-Standing Cryovial Internal Thread w/ Silicone Wa1.2ml Self-Standing Cryovial Internal Thread w/Washer Seal1.2ml Self-Standing Cryovial Internal Thread w/Washer Seal1.2ml Self-Standing Cryovial Internal Thread w_ O-Ring Seal1.2ml Self-Standing Cryovial Internal Thread w_ Silicone Wa1.5-times expansion model of ear dissection, external, middle & internal ear, 4 parts Related articles to: MSH4 (internal)
- Meiotic crossovers are generated from the repair of programmed DNA double-strand breaks (DSBs). In the budding yeast Saccharomyces cerevisiae and mammals, most crossovers are generated through the Class I pathway, involving the mismatch-repair related complex Msh4-Msh5, while a smaller fraction is produced by the Mms4-Mus81 endonuclease (Class II pathway). We present the first report on the genome-wide localization of the Mms4 protein during meiosis in S. cerevisiae. Surprisingly, Mms4 localization showed a trend towards weak DSB sites, unlike the localization of the Class I crossover protein -Msh5, which is biased towards strong DSB sites. This preference for weaker DSB hotspots was retained in a msh5∆ mutant, arguing against competitive models of Mms4 and Msh5 association on meiotic chromosomes. The chromosomal association of Mms4 does not require the formation of meiotic DNA breaks but is facilitated by chromosome axis assembly. These results suggest Mms4 is primarily associated with chromosomal axis regions positioned near recombination intermediates. Mms4 binding is also largely insensitive to heterozygosity, unlike Msh5, consistent with its independence from recombination for localization. Together, these findings support a model in which Mms4-Mus81 enhances the robustness of meiotic recombination with a trend towards binding DSB hotspots that are weaker or are located in regions with sequence divergence that may be processed less efficiently by the Class I pathway. - Source: PubMed
Publication date: 2026/03/30
Farnaz Amamah FarzlinJoshi SameerSarath PraseethaJogwar GirijaNishant Koodali T - 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 - Meiotic recombination generates crossovers (COs), reciprocal exchanges between homologous chromosomes critical for accurate chromosome segregation. Inappropriate CO frequency and distribution drive aneuploidy in human oocytes, with error rates up to 10-fold higher than in sperm despite females exhibiting higher CO frequencies. COs form in the context of the proteinaceous synaptonemal complex (SC) that tethers homologs during prophase I. SC length strongly correlates with CO number, and sexual dimorphism in recombination has long been attributed to longer SCs in females. However, this model is challenged by wild-derived PWD mice in which males consistently generate more COs despite having shorter SCs. Here, we exploit natural genetic variation among inbred mouse strains to dissect the structural and regulatory basis of sexually dimorphic CO regulation. Using cytological markers of SC assembly (SYCP3), recombination progression (RAD51, MSH4), class I CO designation (HEI10, MLH1/MLH3), and chiasmata, we show that SC length is not the sole predictor of CO number. PWD males exhibit stronger CO interference and higher CO number than females, despite reduced SC length. Notably, females show reduced efficiency in designating recombination intermediate to become COs, whereas PWD males display exceptional proficiency. Unexpectedly, although class II COs are rare, they play a disproportionate role in ensuring that every chromosome pair receives at least one CO, thereby safeguarding against aneuploidy. Together, these findings challenge the prevailing view that SC length is the primary determinant of sexually dimorphic CO rates and instead highlight sex-specific regulation of CO designation and pathway usage as key drivers of recombination outcomes. - Source: PubMed
Publication date: 2025/12/22
Horan Tegan SWood AnnaTanis StephanieGabarrell Carme PeirauCohen Paula E - Despite being essential for fertility, many proteins involved in meiotic homologous recombination have diverged rapidly. The evolutionary forces driving this divergence remain mostly unknown, in part because of challenges in accounting for the interplay of sequence changes with constraints imposed by proteins' structures and physiological roles. Here, we explore strategies to more sensitively detect signatures of positive or relaxed selection by integrating evolutionary analyses with structural and functional information, using meiotic recombination proteins in four taxa-primates, rodents, birds and budding yeasts. By mapping selection rate estimates onto predicted protein structures, we characterized protein regions likely to have experienced positive selection. We further identified subtle sequence variation within protein domains that are well conserved generally because of structural constraints. To detect sequence variation masked by these constraints, we analyzed selection at structurally matched residues, comparing homologs across different lineages as well as between meiosis-specific and generalist paralogs. These approaches identified lineage- and paralog-restricted enrichment of non-synonymous substitutions that may indicate loss of functional constraints and/or adaptive innovation. Finally, we used cross-species complementation experiments in to show that sequence variation in the pro-crossover factor MSH4 modulates recombination proficiency. We suggest that evolutionary plasticity per se is a key conserved characteristic of the meiotic recombination machinery. More generally, our approach provides a mechanistic framework to analyze protein evolution. - Source: PubMed
Publication date: 2025/11/10
Arter MeretVedanayagam JeffreyLu MinDiop MomarLiu KaixianLai Eric CKeeney Scott - Recent research in male infertility genetics has identified numerous candidate genes, some of which were also involved in DNA repair. Mismatch repair (MMR) genes, such as MSH4 and MSH5, have been linked to male infertility due to their role in meiosis, suggesting that other MMR genes may also contribute to impaired spermatogenesis. To investigate the role of MMR genes in male infertility, we first conducted a systematic review focusing on their involvement in impaired spermatogenesis, which was followed by a multicenter cohort study assessing the occurrence of rare deleterious variants in MMR genes among men with severely impaired fertility. The present study aimed to assess the contribution of MMR genes to male infertility and to evaluate their potential clinical utility in the diagnostic workup of men with severely impaired fertility. - Source: PubMed
Publication date: 2025/11/19
Podgrajsek RebekaHodzic AlenkaMaver AlesStimpfel MartinAndjelic AleksanderMiljanovic OliveraRistanovic MomciloNovakovic IvanaPlaseska-Karanfilska DijanaNoveski PredragOstojic SasaBuretic-Tomljanovic AlenaPeterlin Borut