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The USP12/46 deubiquitinases protect integrins from ESCRT-mediated lysosomal degradation. USP12/46 去泛素酶保护整合素免受 ESCRT 介导的溶酶体降解。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-06 DOI: 10.1038/s44319-024-00300-9
Kaikai Yu, Guan M Wang, Shiny Shengzhen Guo, Florian Bassermann, Reinhard Fässler

The functions of integrins are tightly regulated via multiple mechanisms including trafficking and degradation. Integrins are repeatedly internalized, routed into the endosomal system and either degraded by the lysosome or recycled back to the plasma membrane. The ubiquitin system dictates whether internalized proteins are degraded or recycled. Here, we use a genetic screen and proximity-dependent biotin identification to identify deubiquitinase(s) that control integrin surface levels. We find that a ternary deubiquitinating complex, comprised of USP12 (or the homologous USP46), WDR48 and WDR20, stabilizes β1 integrin (Itgb1) by preventing ESCRT-mediated lysosomal degradation. Mechanistically, the USP12/46-WDR48-WDR20 complex removes ubiquitin from the cytoplasmic tail of internalized Itgb1 in early endosomes, which in turn prevents ESCRT-mediated sorting and Itgb1 degradation.

整合素的功能通过多种机制(包括贩运和降解)受到严格调控。整合素反复被内化,进入内体系统,然后被溶酶体降解或回收到质膜。泛素系统决定了内化蛋白是被降解还是被回收。在这里,我们利用基因筛选和依赖性生物素鉴定来确定控制整合素表面水平的去泛素化酶。我们发现,由 USP12(或同源 USP46)、WDR48 和 WDR20 组成的三元去泛素复合物通过阻止 ESCRT 介导的溶酶体降解来稳定 β1 整合素(Itgb1)。从机理上讲,USP12/46-WDR48-WDR20 复合物能清除早期内体中内化的 Itgb1 胞质尾部的泛素,进而阻止 ESCRT 介导的分选和 Itgb1 降解。
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引用次数: 0
Reducing competition between msd and genomic DNA improves retron editing efficiency. 减少 msd 与基因组 DNA 之间的竞争可提高 retron 编辑效率。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-05 DOI: 10.1038/s44319-024-00311-6
Yuyang Ni, Yifei Wang, Xinyu Shi, Fan Yu, Qingmin Ruan, Na Tian, Jin He, Xun Wang

Retrons, found in bacteria and used for defense against phages, generate a unique molecule known as multicopy single-stranded DNA (msDNA). This msDNA mimics Okazaki fragments during DNA replication, making it a promising tool for targeted gene editing in prokaryotes. However, existing retron systems often exhibit suboptimal editing efficiency. Here, we identify the msd gene in Escherichia coli, which encodes the noncoding RNA template for msDNA synthesis and carries the homologous sequence of the target gene to be edited, as a critical bottleneck. Sequence homology causes the msDNA to bind to the msd gene, thereby reducing its efficiency in editing the target gene. To address this issue, we engineer a retron system that tailors msDNA to the leading strand of the plasmid containing the msd gene. This strategy minimizes msd gene editing and reduces competition with target genes, significantly increasing msDNA availability. Our optimized system achieves very high retron editing efficiency, enhancing performance and expanding the potential for in vivo techniques that rely on homologous DNA synthesis.

细菌中发现的用于抵御噬菌体的Retrons会产生一种独特的分子,即多拷贝单链DNA(msDNA)。这种 msDNA 在 DNA 复制过程中模仿冈崎片段,使其成为原核生物中一种很有前景的靶向基因编辑工具。然而,现有的 retron 系统往往表现出不理想的编辑效率。在这里,我们发现大肠杆菌中的 msd 基因是一个关键瓶颈,该基因编码用于 msDNA 合成的非编码 RNA 模板,并携带待编辑目的基因的同源序列。序列同源性会导致 msDNA 与 msd 基因结合,从而降低其编辑目的基因的效率。为了解决这个问题,我们设计了一种retron系统,将msDNA定制到含有msd基因的质粒的前导链上。这一策略最大程度地减少了msd基因的编辑,减少了与目的基因的竞争,从而大大提高了msDNA的可用性。我们的优化系统实现了极高的 retron 编辑效率,提高了性能,拓展了依赖同源 DNA 合成的体内技术的潜力。
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引用次数: 0
Making contact away from home: a bacterial secreted effector mediates inter-organelle communication. 远离家乡建立联系:细菌分泌的效应物介导细胞器间的交流。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-05 DOI: 10.1038/s44319-024-00312-5
Rachel J Ende, Isabelle Derré
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引用次数: 0
The L27 domain of MPP7 enhances TAZ-YY1 cooperation to renew muscle stem cells. MPP7的L27结构域增强了TAZ-YY1在更新肌肉干细胞方面的合作。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-04 DOI: 10.1038/s44319-024-00305-4
Anwen Shao, Joseph L Kissil, Chen-Ming Fan

Stem cells regenerate differentiated cells to maintain and repair tissues and organs. They also replenish themselves, i.e. self-renew, to support a lifetime of regenerative capacity. Here we study the renewal of skeletal muscle stem cell (MuSC) during regeneration. The transcriptional co-factors TAZ/YAP (via the TEAD transcription factors) regulate cell cycle and growth while the transcription factor YY1 regulates metabolic programs for MuSC activation. We show that MPP7 and AMOT join TAZ and YY1 to regulate a selected number of common genes that harbor TEAD and YY1 binding sites. Among these common genes, Carm1 can direct MuSC renewal. We demonstrate that the L27 domain of MPP7 enhances the interaction as well as the transcriptional activity of TAZ and YY1, while AMOT acts as an intermediate to bridge them together. Furthermore, MPP7, TAZ and YY1 co-occupy the promoters of Carm1 and other common downstream genes. Our results define a renewal program comprised of two progenitor transcriptional programs, in which selected key genes are regulated by protein-protein interactions, dependent on promoter context.

干细胞再生分化细胞,以维持和修复组织和器官。它们还能自我补充,即自我更新,以支持终生的再生能力。在这里,我们研究了骨骼肌干细胞(MuSC)在再生过程中的更新。转录辅助因子TAZ/YAP(通过TEAD转录因子)调控细胞周期和生长,而转录因子YY1则调控MuSC活化的代谢程序。我们的研究表明,MPP7和AMOT与TAZ和YY1共同调控一些带有TEAD和YY1结合位点的常见基因。在这些常见基因中,Carm1能引导MuSC的更新。我们证明,MPP7的L27结构域增强了TAZ和YY1的相互作用以及转录活性,而AMOT则作为中间体将它们连接在一起。此外,MPP7、TAZ和YY1共同占据了Carm1和其他共同下游基因的启动子。我们的研究结果定义了一个由两个祖先转录程序组成的更新程序,其中选定的关键基因受蛋白质-蛋白质相互作用的调控,并取决于启动子的上下文。
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引用次数: 0
PARP1 condensates differentially partition DNA repair proteins and enhance DNA ligation. PARP1 缩合物可对 DNA 修复蛋白进行不同的分区,并增强 DNA 连接。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-04 DOI: 10.1038/s44319-024-00285-5
Christopher Chin Sang, Gaelen Moore, Maria Tereshchenko, Hongshan Zhang, Michael L Nosella, Morgan Dasovich, T Reid Alderson, Anthony K L Leung, Ilya J Finkelstein, Julie D Forman-Kay, Hyun O Lee

Poly(ADP-ribose) polymerase 1 (PARP1) is one of the first responders to DNA damage and plays crucial roles in recruiting DNA repair proteins through its activity - poly(ADP-ribosyl)ation (PARylation). The enrichment of DNA repair proteins at sites of DNA damage has been described as the formation of a biomolecular condensate. However, it remains unclear how exactly PARP1 and PARylation contribute to the formation and organization of DNA repair condensates. Using recombinant human single-strand repair proteins in vitro, we find that PARP1 readily forms viscous biomolecular condensates in a DNA-dependent manner and that this depends on its three zinc finger (ZnF) domains. PARylation enhances PARP1 condensation in a PAR chain length-dependent manner and increases the internal dynamics of PARP1 condensates. DNA and single-strand break repair proteins XRCC1, LigIII, Polβ, and FUS partition in PARP1 condensates, although in different patterns. While Polβ and FUS are both homogeneously mixed within PARP1 condensates, FUS enrichment is greatly enhanced upon PARylation whereas Polβ partitioning is not. XRCC1 and LigIII display an inhomogeneous organization within PARP1 condensates; their enrichment in these multiphase condensates is enhanced by PARylation. Functionally, PARP1 condensates concentrate short DNA fragments, which correlates with PARP1 clusters compacting long DNA and bridging DNA ends. Furthermore, the presence of PARP1 condensates significantly promotes DNA ligation upon PARylation. These findings provide insight into how PARP1 condensation and PARylation regulate the assembly and biochemical activities of DNA repair factors, which may inform on how PARPs function in DNA repair foci and other PAR-driven condensates in cells.

聚(ADP-核糖)聚合酶 1(PARP1)是 DNA 损伤的第一反应器之一,通过其聚(ADP-核糖)化(PARylation)活动在招募 DNA 修复蛋白方面发挥着至关重要的作用。DNA 修复蛋白在 DNA 损伤部位的富集被描述为生物分子凝聚物的形成。然而,PARP1 和 PARylation 究竟如何促进 DNA 修复凝聚物的形成和组织,目前仍不清楚。利用体外重组人类单链修复蛋白,我们发现PARP1很容易以DNA依赖的方式形成粘性生物分子凝聚物,而这取决于它的三个锌指(ZnF)结构域。PARylation 能以 PAR 链长度依赖性的方式增强 PARP1 凝聚,并增加 PARP1 凝聚物的内部动态。DNA和单链断裂修复蛋白XRCC1、LigIII、Polβ和FUS在PARP1凝聚体中分化,但模式不同。虽然 Polβ 和 FUS 都均匀地混合在 PARP1 凝聚物中,但在 PARylation 作用下,FUS 的富集作用大大增强,而 Polβ 的分区作用则没有增强。XRCC1 和 LigIII 在 PARP1 凝聚物中显示出不均匀的组织结构;它们在这些多相凝聚物中的富集在 PARylation 作用下会增强。在功能上,PARP1凝聚体集中了短DNA片段,这与PARP1簇压缩长DNA并连接DNA末端有关。此外,PARP1凝聚体的存在能显著促进PAR化后的DNA连接。这些发现深入揭示了 PARP1 聚合和 PARylation 如何调控 DNA 修复因子的组装和生化活动,这可能有助于了解 PARPs 如何在细胞中的 DNA 修复灶和其他 PAR 驱动的聚合体中发挥作用。
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引用次数: 0
Severe fever with thrombocytopenia syndrome virus induces lactylation of m6A reader protein YTHDF1 to facilitate viral replication. 严重发热伴血小板减少综合征病毒诱导 m6A 读取蛋白 YTHDF1 乳化,以促进病毒复制。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-04 DOI: 10.1038/s44319-024-00310-7
Bingxin Liu, Xiaoyan Tian, Linrun Li, Rui Zhang, Jing Wu, Na Jiang, Meng Yuan, Deyan Chen, Airong Su, Shijie Xu, Zhiwei Wu

Severe fever with thrombocytopenia syndrome virus (SFTSV), an emerging infectious pathogen with a high fatality rate, is an enveloped tripartite segmented single-stranded negative-sense RNA virus. SFTSV infection is characterized by suppressed host innate immunity, proinflammatory cytokine storm, failure of B-cell immunity, and robust viral replication. m6A modification has been shown to play a role in viral infections. However, interactions between m6A modification and SFTSV infection remain poorly understood. Through MeRIP-seq, we identify m6A modifications on SFTSV RNA. We show that YTHDF1 can bind to m6A modification sites on SFTSV, decreasing the stability of SFTSV RNA and reducing the translation efficiency of SFTSV proteins. The SFTSV virulence factor NSs increases lactylation of YTHDF1 and YTHDF1 degradation, thus facilitating SFTSV replication. Our findings indicate that the SFTSV protein NSs induce lactylation to inhibit YTHDF1 as a countermeasure to host's YTHDF1-mediated degradation of m6A-marked viral mRNAs.

严重发热伴血小板减少综合征病毒(SFTSV)是一种致死率很高的新出现的传染性病原体,它是一种有包膜的三方分段单链负义 RNA 病毒。SFTSV 感染的特点是宿主先天性免疫受到抑制、促炎细胞因子风暴、B 细胞免疫失败以及病毒复制旺盛。然而,人们对 m6A 修饰与 SFTSV 感染之间的相互作用仍然知之甚少。我们通过 MeRIP-seq 鉴定了 SFTSV RNA 上的 m6A 修饰。我们发现YTHDF1能与SFTSV上的m6A修饰位点结合,从而降低SFTSV RNA的稳定性并降低SFTSV蛋白的翻译效率。SFTSV毒力因子NSs可增加YTHDF1的乳化和YTHDF1的降解,从而促进SFTSV的复制。我们的研究结果表明,SFTSV蛋白NSs诱导乳酰化以抑制YTHDF1,作为宿主YTHDF1介导的m6A标记病毒mRNA降解的对策。
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引用次数: 0
Genetic linkage disequilibrium of deleterious mutations in threatened mammals. 受威胁哺乳动物中有害突变的遗传连锁不平衡。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 DOI: 10.1038/s44319-024-00307-2
Chunyan Hu, Gaoming Liu, Zhan Zhang, Qi Pan, Xiaoxiao Zhang, Weiqiang Liu, Zihao Li, Meng Li, Pingfen Zhu, Ting Ji, Paul A Garber, Xuming Zhou

The impact of negative selection against deleterious mutations in endangered species remains underexplored. Recent studies have measured mutation load by comparing the accumulation of deleterious mutations, however, this method is most effective when comparing within and between populations of phylogenetically closely related species. Here, we introduced new statistics, LDcor, and its standardized form nLDcor, which allows us to detect and compare global linkage disequilibrium of deleterious mutations across species using unphased genotypes. These statistics measure averaged pairwise standardized covariance and standardize mutation differences based on the standard deviation of alleles to reflect selection intensity. We then examined selection strength in the genomes of seven mammals. Tigers exhibited an over-dispersion of deleterious mutations, while gorillas, giant pandas, and golden snub-nosed monkeys displayed negative linkage disequilibrium. Furthermore, the distribution of deleterious mutations in threatened mammals did not reveal consistent trends. Our results indicate that these newly developed statistics could help us understand the genetic burden of threatened species.

在濒危物种中,针对有害突变的负选择所产生的影响仍未得到充分探索。最近的研究通过比较有害突变的积累来衡量突变负荷,然而,这种方法在比较系统发育上密切相关的物种种群内部和种群之间时最为有效。在这里,我们引入了新的统计量 LDcor 及其标准化形式 nLDcor,它允许我们使用无相位基因型检测和比较不同物种间有害突变的全球连锁不平衡。这些统计量测量平均的成对标准化协方差,并根据等位基因的标准差对突变差异进行标准化,以反映选择强度。我们随后研究了七种哺乳动物基因组的选择强度。老虎表现出有害突变的过度分散,而大猩猩、大熊猫和金丝猴则表现出负的连锁不平衡。此外,受威胁哺乳动物中有害突变的分布也没有显示出一致的趋势。我们的研究结果表明,这些新开发的统计数据可以帮助我们了解濒危物种的遗传负担。
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引用次数: 0
STAG2 loss in Ewing sarcoma alters enhancer-promoter contacts dependent and independent of EWS::FLI1. 尤文肉瘤中 STAG2 的缺失会改变增强子-启动子接触,这种改变既依赖于 EWS::FLI1 也独立于 EWS::FLI1。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 DOI: 10.1038/s44319-024-00303-6
Daniel Giménez-Llorente, Ana Cuadrado, María José Andreu, Inmaculada Sanclemente-Alamán, Maria Solé-Ferran, Miriam Rodríguez-Corsino, Ana Losada

Cohesin complexes carrying STAG1 or STAG2 organize the genome into chromatin loops. STAG2 loss-of-function mutations promote metastasis in Ewing sarcoma, a pediatric cancer driven by the fusion transcription factor EWS::FLI1. We integrated transcriptomic data from patients and cellular models to identify a STAG2-dependent gene signature associated with worse prognosis. Subsequent genomic profiling and high-resolution chromatin interaction data from Capture Hi-C indicated that cohesin-STAG2 facilitates communication between EWS::FLI1-bound long GGAA repeats, presumably acting as neoenhancers, and their target promoters. Changes in CTCF-dependent chromatin contacts involving signature genes, unrelated to EWS::FLI1 binding, were also identified. STAG1 is unable to compensate for STAG2 loss and chromatin-bound cohesin is severely decreased, while levels of the processivity factor NIPBL remain unchanged, likely affecting DNA looping dynamics. These results illuminate how STAG2 loss modifies the chromatin interactome of Ewing sarcoma cells and provide a list of potential biomarkers and therapeutic targets.

携带 STAG1 或 STAG2 的凝聚素复合物将基因组组织成染色质环。STAG2功能缺失突变可促进尤文肉瘤的转移,尤文肉瘤是一种由融合转录因子EWS::FLI1驱动的小儿癌症。我们整合了患者和细胞模型的转录组数据,确定了与预后恶化相关的 STAG2 依赖性基因特征。随后的基因组图谱分析和来自 Capture Hi-C 的高分辨率染色质相互作用数据表明,粘合素-STAG2 促进了 EWS::FLI1 结合的长 GGAA 重复序列(可能充当新增强子)与其目标启动子之间的交流。还发现了与 EWS::FLI1 结合无关的 CTCF 依赖性染色质接触的变化。STAG1 无法弥补 STAG2 的缺失,染色质结合的凝聚素严重减少,而加工因子 NIPBL 的水平保持不变,这可能会影响 DNA 循环动力学。这些结果阐明了STAG2缺失如何改变尤文肉瘤细胞的染色质相互作用组,并提供了潜在的生物标记物和治疗靶点列表。
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引用次数: 0
Dinoflagellate mRNA is pervasively modified with m1A. 甲藻 mRNA 普遍被 m1A 修饰。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-09-20 DOI: 10.1038/s44319-024-00263-x
Jianheng Fox Liu, Samie R Jaffrey
{"title":"Dinoflagellate mRNA is pervasively modified with m<sup>1</sup>A.","authors":"Jianheng Fox Liu, Samie R Jaffrey","doi":"10.1038/s44319-024-00263-x","DOIUrl":"10.1038/s44319-024-00263-x","url":null,"abstract":"","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":null,"pages":null},"PeriodicalIF":6.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142282177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CHK1 controls zygote pronuclear envelope breakdown by regulating F-actin through interacting with MICAL3. CHK1 通过与 MICAL3 相互作用来调节 F-肌动蛋白,从而控制子代原核包膜的破裂。
IF 6.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-10-02 DOI: 10.1038/s44319-024-00267-7
Honghui Zhang, Ying Cui, Bohan Yang, Zhenzhen Hou, Mengge Zhang, Wei Su, Tailai Chen, Yuehong Bian, Mei Li, Zi-Jiang Chen, Han Zhao, Shigang Zhao, Keliang Wu

CHK1 mutations could cause human zygote arrest at the pronuclei stage, a phenomenon that is not well understood at the molecular level. In this study, we conducted experiments where pre-pronuclei from zygotes with CHK1 mutation were transferred into the cytoplasm of normal enucleated fertilized eggs. This approach rescued the zygote arrest caused by the mutation, resulting in the production of a high-quality blastocyst. This suggests that CHK1 dysfunction primarily disrupts crucial biological processes occurring in the cytoplasm. Further investigation reveals that CHK1 mutants have an impact on the F-actin meshwork, leading to disturbances in pronuclear envelope breakdown. Through co-immunoprecipitation and mass spectrometry analysis of around 6000 mouse zygotes, we identified an interaction between CHK1 and MICAL3, a key regulator of F-actin disassembly. The gain-of-function mutants of CHK1 enhance their interaction with MICAL3 and increase MICAL3 enzymatic activity, resulting in excessive depolymerization of F-actin. These findings shed light on the regulatory mechanism behind pronuclear envelope breakdown during the transition from meiosis to the first mitosis in mammals.

CHK1突变可导致人类子代在前核阶段停滞,但这一现象在分子水平上还不甚明了。在这项研究中,我们进行了实验,将来自CHK1突变子代的前单核转移到正常有核受精卵的细胞质中。这种方法挽救了突变导致的子代停滞,从而产生了高质量的囊胚。这表明,CHK1 功能障碍主要破坏了发生在细胞质中的关键生物过程。进一步的研究发现,CHK1 突变体对 F-肌动蛋白网状结构有影响,导致原核包膜破裂紊乱。通过对大约 6000 个小鼠胚胎进行共免疫沉淀和质谱分析,我们确定了 CHK1 与 F-肌动蛋白分解的关键调控因子 MICAL3 之间的相互作用。CHK1的功能增益突变体增强了与MICAL3的相互作用,提高了MICAL3的酶活性,导致F-肌动蛋白过度解聚。这些发现揭示了哺乳动物从减数分裂过渡到第一次有丝分裂期间代核包膜破裂背后的调控机制。
{"title":"CHK1 controls zygote pronuclear envelope breakdown by regulating F-actin through interacting with MICAL3.","authors":"Honghui Zhang, Ying Cui, Bohan Yang, Zhenzhen Hou, Mengge Zhang, Wei Su, Tailai Chen, Yuehong Bian, Mei Li, Zi-Jiang Chen, Han Zhao, Shigang Zhao, Keliang Wu","doi":"10.1038/s44319-024-00267-7","DOIUrl":"10.1038/s44319-024-00267-7","url":null,"abstract":"<p><p>CHK1 mutations could cause human zygote arrest at the pronuclei stage, a phenomenon that is not well understood at the molecular level. In this study, we conducted experiments where pre-pronuclei from zygotes with CHK1 mutation were transferred into the cytoplasm of normal enucleated fertilized eggs. This approach rescued the zygote arrest caused by the mutation, resulting in the production of a high-quality blastocyst. This suggests that CHK1 dysfunction primarily disrupts crucial biological processes occurring in the cytoplasm. Further investigation reveals that CHK1 mutants have an impact on the F-actin meshwork, leading to disturbances in pronuclear envelope breakdown. Through co-immunoprecipitation and mass spectrometry analysis of around 6000 mouse zygotes, we identified an interaction between CHK1 and MICAL3, a key regulator of F-actin disassembly. The gain-of-function mutants of CHK1 enhance their interaction with MICAL3 and increase MICAL3 enzymatic activity, resulting in excessive depolymerization of F-actin. These findings shed light on the regulatory mechanism behind pronuclear envelope breakdown during the transition from meiosis to the first mitosis in mammals.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":null,"pages":null},"PeriodicalIF":6.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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