EMBO JOURNALEMBO杂志
EMBO JOURNAL(英文缩写 EMBO J),ISSN 0261-4189,eISSN 1460-2075,中文译名:EMBO杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 13.783 | Q1 |
| 2022 | 11.400 | Q1 |
| 2023 | 9.400 | Q1 |
| 2024 | 8.300 | Q1 |
| 2025 | 8.400 | Q1 |
EMBO JOURNAL 最新收录文献
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1. Whole genome duplication through mitotic slippage causes nuclear instability.
PMID:日期:2026-09-19Whole-genome duplication (WGD), leading to polyploidy can arise in physiological and pathological contexts. WGD can occur via non-canonical cell cycles such as mitotic slippage, cytokinesis failure or endoreplication. Whether the routes to WGD influence the behaviour of the resulting polyploid cells remains unclear. Here, we compared these routes under both physiological and non-physiological conditions. Remarkably, only mitotic slippage led to widespread nuclear abnormalities defined by highly variable nuclear deformations that we termed nuclear instability. Mechanistically, we found that these nuclei were softer and thus more vulnerable to microtubule-driven deformations. The resulting nuclear instability leads to local nuclear reorganisation and changes in 3D genome organisation. Importantly, we observed similar nuclear instability in megakaryocytes, which are physiological polyploid cells generated by mitotic slippage, providing a molecular mechanism for their atypical nuclear architecture. In striking contrast, nuclear shape was stable in different physiological polyploid cells generated by cytokinesis failure and endoreplication. Overall, our findings highlight that the route towards WGD matters and that mitotic slippage uniquely destabilizes nuclear architecture, with implications for both physiology and disease.
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2. The BRCA1 coiled-coil domain is dispensable for suppression of tandem duplications and tolerance of FANCM loss.
PMID:日期:2026-09-18BRCA1-linked cancers contain abundant ~10 kb 'Group 1' tandem duplications (TDs). Group 1 TDs form at a Tus/Ter replication-fork barrier in DNA-end resection-defective mouse embryonic stem (mES) cells lacking Brca1 exon 11. To elucidate how BRCA1 suppresses Group 1 TDs, we analyzed Brca1 coiled-coil (CC)-domain mutants-separation-of-function alleles impaired for homologous recombination (HR) through loss of PALB2-binding and RAD51-loading functions but competent for DNA-end resection. Notably, Brca1 CC mutants retain the ability to suppress Group 1 TDs in the Tus/Ter system and in a mouse model of Brca1-linked mammary tumorigenesis. These data suggest that Brca1 CC domain-mutant cancers follow a path of tumorigenesis distinct from that of other Brca1-linked cancers. FANCM is a TD co-suppressor, loss of which is synthetic lethal/sick in Brca1 exon 11-deleted cells. In contrast, Fancm deletion unexpectedly improves the growth of Brca1 CC mutant and Brca2 mutant mES cells. Thus, Group 1 tandem duplication formation and Fancm synthetic lethality are linked phenotypes, potentially related to defective BRCA1-mediated DNA end resection but genetically separable from BRCA1/PALB2-mediated RAD51 loading.
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3. Transgenerational inheritance of altered H3K27me3 in wild-type Caenorhabditis elegans.
PMID:日期:2026-09-18Epigenetic inheritance provides mutation-free mechanisms for phenotypic adaptation, including modifications to DNA or DNA-associated proteins that create patterns of heritable gene regulation. However, the limits and regulation of this inheritance remain incompletely understood. Here, we developed a C. elegans system to study the transgenerational epigenetic inheritance of H3K27me3, a conserved histone posttranslational modification associated with gene repression. We find that transiently induced alterations of the genome-wide H3K27me3 landscape and the associated fertility defects persist for many generations in genetically wildtype descendants under selective pressure. We uncover that the inheritance of the altered H3K27me3 landscape involves an initiation phase that relies on SET-32/H3K23me3 and a maintenance phase that requires MES-4/H3K36me3. Our results indicate that epigenetic inheritance can act as a mutation-independent, heritable mechanism of adaptation.
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4. ZEP1 orchestrates template choice and crossover pathways to ensure meiotic genome integrity in rice.
PMID:日期:2026-09-17Meiotic crossovers (COs) are tightly regulated to ensure chromosome segregation while limiting aberrant recombination. Transverse filament (TF) proteins of the synaptonemal complex (SC) regulate class I crossoverts, yet how the SC coordinates homologous recombination (HR) to maintain faithful recombination remains unclear. Here, we show that loss of rice TF protein ZEP1 does not uniformly enhance HEI10-marked class I COs; instead, ZEP1 null mutants display asynapsis, multivalent formation, and chromosome fragmentation. These defects depend on double-strand breaks (DSBs) and genetically place ZEP1 function after strand invasion. ZEP1 interacts with anti-crossover factors MEICA1, FIGNL1, and RMI1, and is required for their enrichment at the synaptonemal complex; its loss causes persistent DMC1/RAD51 signals, indicating dysregulated strand invasion. Genetic interactions further support impaired recombination intermediate homeostasis, with ZMM removal partially alleviating chromosome abnormalities, while MUS81 becomes increasingly essential. We propose that the synaptonemal complex functions as a structural hub, where ZEP1 concentrates anti-crossover modules that restrain invasion and coordinate recombination intermediate processing to promote HR repair. Furthermore, ZEP1 dosage may provide a constrained lever to tune CO outcomes in a background-dependent manner.
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5. Hox/Meis-dependent gene-regulatory transition underlies cardiopharyngeal neural crest diversification.
PMID:日期:2026-09-15Neural crest cells (NCCs) are multipotent migratory cells essential for cardiac development, yet the lineage trajectories and gene regulatory networks underlying their differentiation in the cardiopharyngeal region remain unclear. Here, we integrate single-cell RNA-seq, spatial transcriptomics, and multiomic analyses to construct a comprehensive map of NCC lineages in developing mouse cardiopharyngeal tissues. We identify a transition from Hox-positive pharyngeal NCCs to Hox-negative intracardiac populations associated with the outflow tract cushion, accompanied by a shift in Meis transcription factor binding and gene-regulatory network architecture. By contrast, NCCs forming the aorticopulmonary septum and great vessel smooth muscle retain distinct Hox-codes. A Meis2-Sox9-Scx gene-regulatory network defines a skeletogenic progenitor-like intermediate state that gives rise to coronary artery smooth muscle and semilunar valves. Our findings suggest that the loss of Hox-dependent regional identity enables pharyngeal NCCs to acquire new fates upon entering the cardiac cushion, providing insight into the developmental origins of coronary and valvular calcification.
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6. Microtubule posttranslational modifications provide unique recognition patterns for associated proteins.
PMID:日期:2026-09-12Microtubules are key components of the eukaryotic cytoskeleton involved in vital functions in virtually every cell. Among the emerging molecular mechanisms to adapt microtubules to their diverse functions is the biochemical diversification of tubulin molecules by posttranslational modifications (PTMs) and differential gene expression, a concept known as the 'tubulin code'. A key question remains whether the tubulin code has the potential to selectively control microtubule interactions of different microtubule-associated proteins (MAPs) to act as a specific signalling system. To answer this question, we used a medium-throughput in vitro approach to screen 46 proteins for their binding preferences to microtubules with altered PTM or isotype composition. We demonstrate that subsets of these MAPs have unique sensitivities to PTMs, while other proteins are not affected. As a result, PTMs, or combinations of them, differentially attract or repulse individual MAPs to microtubules. Our findings offer mechanistic proof for a key hypothesis of the tubulin code-the capacity to selectively and differentially regulate MAP-microtubule interactions.
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7. KDM6A loss enhances oxidative phosphorylation uncovering tissue-level convergent evolution.
PMID:日期:2026-09-04The tumor suppressor KDM6A/UTX, a histone demethylase and a 2-oxoglutarate-dependent dioxygenase, is frequently lost in many cancer types. We show that KDM6A loss pervasively activates oxidative phosphorylation in several solid tumors, generating a pseudo-hyperoxic environment, opposite from the pseudo-hypoxia observed in VHL-mutated renal carcinomas. Mechanistically, KDM6A sustains the expression of the coil-coil domain gene CCDC3, which inhibits CREB1-driven transcription of the mitochondrial regulator PPARGC1A. In the hematological cancer multiple myeloma where KDM6A is frequently deleted, its loss similarly promotes oxidative phosphorylation, but via an alternative mechanism: the increased transfer of mitochondria from stromal to myeloma cells via tunneling nanotubes, triggered by the loss of the mTORC1 inhibitor TRAF3IP3. Beyond cancer, KDM6A regulates oxidative phosphorylation also during development and in adult tissues, engaging either the CCDC3-CREB1 or the TRAF3IP3-mTORC1 pathways. These mutually exclusive associations suggest a tissue-level convergent evolution, positioning KDM6A as a central modulator of mitochondrial activity through context-specific partners.
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8. Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer's disease.
PMID:日期:2026-09-01The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease. Brain recordings have revealed synaptic hyperexcitation during asymptomatic and early stages of AD, reverting to overinhibition as dementia progresses. Here, we show that endogenous APP and its proteolytic C-terminal fragments (APP-CTFs), the precursors of amyloid-β (Aβ), are enriched at excitatory synapses. Pharmacological modulation of endogenous APP metabolite levels suggests a role for APP-CTFs, in particular APP-CTFβ, in regulating glutamatergic synaptic transmission. Presynaptic accumulation of APP-CTFβ promotes its oligomerization, increases synaptic vesicle docking, and causes vesicle release defects, accompanied by enhanced neuronal network activity. Examination of post-mortem AD patient brains yields consistent results, namely, elevated APP-CTFβ levels at synaptic compartments and enlarged excitatory presynaptic boutons. Strikingly, acute application of Aβ preparations enriched in monomeric species counteracts APP-CTFβ-induced hyperexcitability. Our findings indicate a role for presynaptic APP-CTFβ in modulating excitatory synaptic function and network activity, suggesting that amyloidogenic APP processing intermediates may contribute to early synaptic alterations in Alzheimer's disease.
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9. From water to land: evolution of tRNA gene repertoires in photosynthetic organisms.
PMID:日期:2026-09-01Photosynthetic eukaryotes have undergone evolutionary shifts from aquatic to terrestrial habitats, accompanied by changes in genome organization and gene regulation. Yet, the evolution of transfer RNA (tRNA) gene repertoires has received limited attention despite their central role in translation. Here, we review how tRNA gene content, structure, and genomic organization diversified across photosynthetic lineages, mainly Archaeplastida, and how changes relate to evolutionary transitions. We show that tRNA gene repertoires are shaped by ecological transitions, genome architecture, and translational demands. We highlight terrestrialization as a shift in tRNA evolution, marked by loss of selenocysteine and its dedicated tRNA, and changes in intron prevalence and structure. Copy number variation correlates with codon usage and amino acid composition, and in angiosperms, nuclear tRNA genes display reinforced cis-regulatory elements consistent with increased translational demands. We show that plant tRNA genes exhibit evenly dispersed arrangements, except in some algae enriched in clustered configurations. Together, these observations support a model in which tRNA gene repertoires are drivers of genome evolution, integrating translational demand, genomic organization, and ecological adaptation across photosynthetic lineages.
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10. FAF1 and FAF2 enhance unfolding by p97-UFD1-NPL4 complex enabling rational design of p97 activators.
PMID:日期:2026-09-01VCP/p97 is an AAA+ ATPase that, together with its cofactors UFD1-NPL4 (p97-UN), unfolds ubiquitylated substrates to maintain cellular homeostasis. The human p97-UN complex associates with additional cofactors, but how these cofactors modulate p97-UN activity is not fully understood. Here, we screen cofactors and identify FAF2 to potently enhance substrate unfolding by p97-UN. Using biochemical and structural approaches, we show how FAF2 engages p97-UN and polyubiquitin to promote unfolding. We define a conserved activation motif in FAF2 that contacts both UFD1 and the ubiquitin proximal to the initiator, thereby stabilizing and supporting the unfolding of the initiator ubiquitin in a UFD1-dependent manner. We leverage the features of the FAF2 activation motif to engineer de novo proteins that potently enhance unfolding, providing a rational strategy to boost p97 activity. Our findings reveal how cofactors can provide additional adaptive control, fine-tuning human p97 activity to unfold challenging substrates and those modified with short ubiquitin chains.