Ask about this productRelated genes to: REC8 antibody
- Gene:
- REC8 NIH gene
- Name:
- REC8 meiotic recombination protein
- Previous symbol:
- REC8L1
- Synonyms:
- Rec8p, kleisin-alpha
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-29
- Date modifiied:
- 2016-01-15
Related products to: REC8 antibody
Related articles to: REC8 antibody
- During meiosis I, the cohesin Rec8 is cleaved by separase along the chromosome arms but is protected at the centromere by shugoshin (Sgo1); during meiosis II, it is not protected. In fission yeast, another meiotic regulator, meikin (Moa1), supports the protective function of Sgo1 primarily by phosphorylating Rec8 at S450. Here we show that both meiosis I-specific proteins, Sgo1 and Moa1, are degraded during anaphase I by the APC/C-Slp1 pathway. To explore the possibility of ectopic protection during meiosis II, we expressed non-degradable forms of Moa1 and Sgo1 during meiosis. Our analyses revealed that stabilization of the Sgo1 protein and phosphorylation of Rec8 at S449 and S450 are necessary and sufficient for the protection of Rec8 cohesin during meiosis II. Furthermore, our results suggest that the phosphorylation-dependent interaction between Rec8 and Sgo1 during meiosis is prominent at mono-oriented kinetochores but not at bi-oriented kinetochores. - Source: PubMed
Publication date: 2026/06/11
Liu YongxinZhang KeBai ZitengSun LiHou HaitongWatanabe Yoshinori - The Rec8 cohesin complex is required for the pairing and recombination of homologous chromosomes during meiosis, as well as for the cohesion of sister chromatids. In the fission yeast Schizosaccharomyces pombe, we previously identified a rec8-F204S mutant that lost the ability to assemble the axis-loop chromatin structure without losing sister chromatid cohesion. This mutant showed reduced meiotic recombination, indicating that pairing and recombination of homologous chromosomes require the formation of the axis-loop chromatin structure mediated by the Rec8 cohesin complex. Loading of the Rec8 cohesin complex onto chromatin is mediated by Mis4 (NIPBL in humans; Scc2 in yeast). In this study, to elucidate the functions of Mis4, we identified a mis4-LR mutant (L1150S and R1159G) that reproduced the phenotypes of the rec8-F204S mutant, which is defective in chromatin axis formation and homologous recombination while retaining sister chromatid cohesion. These mutation sites (Mis4-L1150, Mis4-R1159, and Rec8-F204) are all localized at the interaction surface between Mis4 and Rec8. Biochemical analysis revealed that the Mis4-LR mutant protein exhibited reduced Rec8-binding activity. Considering that the mis4-LR mutant phenocopied the rec8-F204S mutant, our results demonstrate that the Mis4-Rec8 interaction is required for proper formation of Rec8-dependent meiotic chromosome axis. - Source: PubMed
Sakuno TakeshiMurayama YasutoHaraguchi TokukoHiraoka Yasushi - Meiosis is a conserved yet evolutionarily varied process underpinning sexual reproduction in eukaryotes. In the malaria parasite Plasmodium, meiosis is unconventional: it occurs immediately after fertilisation (post-zygotic) and must be coordinated with the transformation of the zygote into a motile ookinete. The mechanisms synchronising these meiotic and morphogenetic programmes remain unknown. Here, we identify the Plasmodium berghei NIMA-related kinase NEK4 as a key regulator that couples meiotic initiation with zygote morphogenesis. Using ultrastructure expansion microscopy, we show that NEK4 accumulates at the microtubule-organising centre (MTOC) and the apical polar complex (APC) shortly after fertilisation, preceding the assembly of perinuclear and cortical microtubules. We reveal that Plasmodium zygotes undergo MTOC-associated nuclear migration, analogous to the meiotic nuclear movement in fission yeast. Deletion of the Pbnek4 gene results in complete developmental arrest: MTOC duplication and microtubule formation are blocked, chromatin remains uncondensed, and nuclear migration and cell polarity fail to establish. Transcriptomic and phosphoproteomic analyses reveal that absence of NEK4 causes a collapse in transcriptional and phosphoregulatory networks governing meiosis and cytoskeletal organisation, leading to reduced expression and phosphorylation of important players, including HOP1, REC8, and AP2-O. These findings establish NEK4 as a key regulator driving meiotic entry and zygote maturation. - Source: PubMed
Publication date: 2026/05/12
Yanase RyujiHair MollyZeeshan MohammadFerguson David J PBrady DeclanPasquarello CarlaBottrill AndrewBhanvadia SuhaniNeal ArmundTromer Eelco CLe Roch Karine GHainard AlexandreHolder Anthony AVaughan SueGuttery David STewari Rita - Non-homologous end joining (NHEJ) is an error-prone but efficient primary repair pathway for DNA double-strand breaks (DSBs) during mitosis. A critical unresolved question is whether NHEJ acts as a backup when homologous recombination (HR) is impaired during meiosis. Here, we integrated biochemical, cytological, and genetic approaches to dissect the biological role of KU70/KU80, the core component of the NHEJ machinery, in both mitotic and meiotic DSB repair in rice (Oryza sativa). Biochemical analysis confirmed that KU70 and KU80 form a stable heterodimer. KU deficiency caused hypersensitivity to bleomycin in somatic cells, underscoring its essential function in mitotic DSB repair. KU70 localized to meiotic telomeres but was dispensable for normal meiotic progression and DSB repair efficiency. Moreover, KU deficiency neither altered the aberrant chromosome associations in HR-defective mutants (com1, rec8, meica1, hus1, and rad1) nor genetically interacted with key HR factors (ZIP4 and MER3). Taken together, our findings establish rice meiosis operates under an HR-dominant DSB repair regime independent of KU-mediated NHEJ. This stands in striking contrast to the critical role of NHEJ in mitotic DSB repair and clearly demonstrates that KU-mediated NHEJ does not serve as a backup repair pathway for impaired HR during plant meiosis. - Source: PubMed
Publication date: 2026/05/03
Zhao YangziWang BingxinPang YunfeiYou HanliCao LeiZhong WeijieWang YuhaoZhang JiaruiChen YangGong ZhiyunLi YafeiCheng Zhukuan - Cohesin is a ring-shaped protein complex that mediates sister-chromatid cohesion (SCC) to ensure accurate chromosome segregation during mitosis and meiosis. In Saccharomyces cerevisiae, cohesin consists of four core subunits-Smc1, Smc3, Scc1/Mcd1, and Scc3. During meiosis, the mitotic α-kleisin Scc1/Mcd1 is replaced by the meiosis-specific α-kleisin Rec8. Rec8-containing cohesin is essential for multiple meiotic processes, including chromosome morphogenesis, homologous recombination, axis and synaptonemal complex formation, SCC, and transcriptional regulation. While stable association of Rec8-cohesin with chromatin is required to maintain SCC from premeiotic S phase through anaphase II, dynamic chromatin association is thought to underlie its roles in recombination, chromosome architecture, and transcription via loop extrusion. Whether distinct stable and dynamic pools of Rec8-cohesin coexist during meiosis and how their functions are partitioned remained unclear. Here, we employed an anchor-away strategy to conditionally deplete only the dynamic pool of Rec8-cohesin from the nucleus while preserving the stable pool. Selective depletion reduced sporulation efficiency and spore viability without compromising SCC. Calibrated ChIP-seq revealed a genome-wide reduction in Rec8-cohesin levels rather than locus-specific loss. Functional analyses demonstrated that the dynamic pool of Rec8-cohesin is required for efficient meiotic recombination, establishment of meiosis-specific chromosome architecture and synaptonemal complex formation, and proper transcriptional regulation of key meiotic regulators. In contrast, the stable pool alone was sufficient to maintain spindle pole body cohesion. Together, our findings demonstrate the existence of two functionally distinct pools of Rec8-cohesin during yeast meiosis. - Source: PubMed
Publication date: 2026/04/24
Paliwal SheetalDey ParthaKumari AkritiSadasivam KirithikaJoshi SameerRaghuvanshi RitikaGoyal RohitSanyal KaustuvNishant K TShinohara AkiraMehta Gunjan