EMBO Reports最新文献

BZR1 promotes pluripotency acquisition and callus development through direct regulation of ARF7 and ARF19. BZR1通过直接调控ARF7和ARF19促进多能性获得和愈伤组织发育。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-26 DOI: 10.1038/s44319-025-00433-5

Thomas Ammitsøe, Elise Ebstrup, Noel Blanco-Touriñán, Julie Hansen, Christian S Hardtke, Morten Petersen, Eleazar Rodriguez

{"title":"BZR1 promotes pluripotency acquisition and callus development through direct regulation of ARF7 and ARF19.","authors":"Thomas Ammitsøe, Elise Ebstrup, Noel Blanco-Touriñán, Julie Hansen, Christian S Hardtke, Morten Petersen, Eleazar Rodriguez","doi":"10.1038/s44319-025-00433-5","DOIUrl":"https://doi.org/10.1038/s44319-025-00433-5","url":null,"abstract":"Plants have the remarkable ability to regenerate whole organisms through the formation of pluripotent cell masses from somatic cells. Cellular programs leading to fate change resemble lateral root (LR) formation and are chiefly regulated by auxin. Brassinosteroid signaling also plays an important role in LR formation, but little is known about the direct link between auxin and brassinosteroid components, such as BZR1 and BES1, in pluripotency acquisition. Here we show that gain-of-function mutants bzr1-D and bes1-D exhibit altered callus formation, yet disruption of these transcription factors does not cause major changes to callus formation or de novo organogenesis. Moreover, our data reveal that BZR1 displays enhanced expression in callus tissue and directly binds to the promoters of ARF7 and ARF19, two master pluripotency regulators, leading to their enhanced transcription. Remarkably, callus formation is abrogated in bzr1-D upon disruption of these ARFs, emphasizing that the callus formation via BZR1 depends on these auxin signaling components. In conclusion, we depict a link between, ARF7, ARF19, and BZR1 in promoting pluripotency acquisition, portraying BZR1 as a major supporting factor in callus formation.","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505132","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

Targeted protein degradation in Escherichia coli using CLIPPERs. 利用CLIPPERs对大肠杆菌进行靶向蛋白降解。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-25 DOI: 10.1038/s44319-025-00510-9

Matylda Anna Izert-Nowakowska, Maria Magdalena Klimecka, Anna Antosiewicz, Karol Wróblewski, Jakub Józef Kowalski, Katarzyna Justyna Bandyra, Tomasz Góral, Sebastian Kmiecik, Remigiusz Adam Serwa, Maria Wiktoria Górna

引用次数: 0

JMJD3-mediated senescence is required to overcome stress-induced hematopoietic defects. jmjd3介导的衰老是克服应激诱导的造血缺陷所必需的。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-25 DOI: 10.1038/s44319-025-00502-9

Yuichiro Nakata, Takeshi Ueda, Yasuyuki Sera, Miho Koizumi, Katsutoshi Imamura, Akinori Kanai, Ken-Ichiro Ikeda, Norimasa Yamasaki, Akiko Nagamachi, Kohei Kobatake, Masataka Taguchi, Yusuke Sotomaru, Tatsuo Ichinohe, Zen-Ichiro Honda, Takuro Nakamura, Ichiro Manabe, Toshio Suda, Keiyo Takubo, Osamu Kaminuma, Hiroaki Honda

{"title":"JMJD3-mediated senescence is required to overcome stress-induced hematopoietic defects.","authors":"Yuichiro Nakata, Takeshi Ueda, Yasuyuki Sera, Miho Koizumi, Katsutoshi Imamura, Akinori Kanai, Ken-Ichiro Ikeda, Norimasa Yamasaki, Akiko Nagamachi, Kohei Kobatake, Masataka Taguchi, Yusuke Sotomaru, Tatsuo Ichinohe, Zen-Ichiro Honda, Takuro Nakamura, Ichiro Manabe, Toshio Suda, Keiyo Takubo, Osamu Kaminuma, Hiroaki Honda","doi":"10.1038/s44319-025-00502-9","DOIUrl":"https://doi.org/10.1038/s44319-025-00502-9","url":null,"abstract":"Cellular senescence in stem cells compromises regenerative capacity, promotes chronic inflammation, and is implicated in aging. Hematopoietic stem and progenitor cells (HSPCs) are responsible for producing mature blood cells, however, how cellular senescence influences their function is largely unknown. Here, we show that JMJD3, a histone demethylase, activates cellular senescence by upregulating p16Ink4a in competition with Polycomb group proteins, and reprograms HSPC integrity to overcome hematopoietic defects induced by replicative and oncogenic stresses. Jmjd3 deficiency does not alter global H3K27me3 levels, indicating that JMJD3 epigenetically regulates specific and limited JMJD3 targets under stress. JMJD3 deficiency also impairs stem cell potential, proper cell cycle regulation, and WNT pathway activation in HSPCs under stress. These impaired phenotypes are rescued through exogenous and retroviral introduction of p16Ink4a. This JMJD3-p16INK4a axis in hematopoiesis is age-dependent and is distinct from cellular senescence. Treatment with a selective JMJD3 inhibitor attenuates leukemic potential during cellular senescence. Taken together, these results demonstrate that JMJD3-p16INK4a mediates cellular senescence and plays critical roles in the functional integrity of HSPCs under stress.","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495217","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

Mental privacy: navigating risks, rights and regulation : Advances in neuroscience challenge contemporary legal frameworks to protect mental privacy. 精神隐私：驾驭风险、权利和监管：神经科学的进步挑战了当代保护精神隐私的法律框架。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-25 DOI: 10.1038/s44319-025-00505-6

Łukasz Szoszkiewicz, Rafael Yuste

引用次数: 0

LRBA deficiency impairs autophagy and contributes to enhanced antigen presentation and T-cell dysregulation. LRBA缺乏损害自噬，并有助于增强抗原呈递和t细胞失调。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-23 DOI: 10.1038/s44319-025-00504-7

Elena Sindram, Marie-Celine Deau, Laure-Anne Ligeon, Pablo Sanchez-Martin, Sigrun Nestel, Sophie Jung, Stefanie Ruf, Pankaj Mishra, Michele Proietti, Stefan Günther, Kathrin Thedieck, Eleni Roussa, Angelika Rambold, Christian Münz, Claudine Kraft, Bodo Grimbacher, Laura Gámez-Díaz

{"title":"LRBA deficiency impairs autophagy and contributes to enhanced antigen presentation and T-cell dysregulation.","authors":"Elena Sindram, Marie-Celine Deau, Laure-Anne Ligeon, Pablo Sanchez-Martin, Sigrun Nestel, Sophie Jung, Stefanie Ruf, Pankaj Mishra, Michele Proietti, Stefan Günther, Kathrin Thedieck, Eleni Roussa, Angelika Rambold, Christian Münz, Claudine Kraft, Bodo Grimbacher, Laura Gámez-Díaz","doi":"10.1038/s44319-025-00504-7","DOIUrl":"https://doi.org/10.1038/s44319-025-00504-7","url":null,"abstract":"Reduced autophagy is associated with the aberrant humoral response observed in lipopolysaccharide-responsive beige-like anchor protein (LRBA) deficiency; however, the molecular mechanisms and their impact on T-cell responses remain poorly understood. We identify two novel LRBA interactors, phosphoinositide 3-kinase regulatory subunit 4 (PIK3R4) and FYVE And Coiled-Coil Domain Autophagy Adaptor 1 (FYCO1), which each play key roles in autophagy. PIK3R4 facilitates the production of phosphatidylinositol-3 phosphate (PI(3)P) that promotes autophagosome formation and autophagosome-lysosome fusion, whereas FYCO1 supports autophagosome movement. LRBA-knockout (KO) cells show impaired PI(3)P production, reduced autophagosome-lysosome fusion, accumulation of enlarged autophagosomes, and decreased cargo degradation. In line with the role of autophagy as a major degradation system for MHC-II loading and antigen presentation, we observe increased numbers of MHC class II and LC3 vesicles, along with enhanced antigen presentation in absence of LRBA, resulting in a higher production of proinflammatory cytokines from T cells in vitro. Our work suggests a novel biological role of LRBA controlling antigen presentation and T-cell responses by positively regulating autophagy, which may contribute to T-cell immune dysregulation observed in LRBA-deficient patients.","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474323","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

X chromosome inactivation in mammals: general principles and species-specific considerations. 哺乳动物X染色体失活：一般原则和物种特异性考虑。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-19 DOI: 10.1038/s44319-025-00499-1

Charbel Alfeghaly, Claire Rougeulle

引用次数: 0

Cotyledon opening during seedling deetiolation is determined by ABA-mediated splicing regulation. 幼苗脱落过程中子叶的开放是由aba介导的剪接调控决定的。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-18 DOI: 10.1038/s44319-025-00495-5

Guiomar Martín, Ana Confraria, Irene Zapata, Alvaro Santiago Larran, Julia Irene Qüesta, Paula Duque

{"title":"Cotyledon opening during seedling deetiolation is determined by ABA-mediated splicing regulation.","authors":"Guiomar Martín, Ana Confraria, Irene Zapata, Alvaro Santiago Larran, Julia Irene Qüesta, Paula Duque","doi":"10.1038/s44319-025-00495-5","DOIUrl":"https://doi.org/10.1038/s44319-025-00495-5","url":null,"abstract":"During seedling deetiolation, plants adjust their development to expose photosynthetic tissues to sunlight, enabling the transition from heterotrophic to autotrophic growth. While various plant hormones are known to influence this process, the role of abscisic acid (ABA) remains unclear. Here, we reveal that ABA plays a major role in controlling the dynamics of cotyledon aperture during seedling deetiolation. In the dark, ABA accumulates in the cotyledons to effectively repress their opening. However, light exposure reverses this effect, allowing the cotyledons to open. Our findings indicate that ABA-mediated regulation of cotyledon dynamics is accompanied by genome-wide rearrangements in both transcriptional and splicing patterns. We demonstrate that ABA-dependent adjustments of cotyledon and splicing dynamics in response to light depend on the positive role of two splicing factors, RS40 and RS41. Moreover, we identify transcriptional and posttranscriptional mechanisms that control the activity of these proteins. Altogether, this work sheds light on the interplay between light and ABA, highlighting cotyledon opening as a new developmental outcome, and identifying alternative splicing as the underlying layer of gene regulation.","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324792","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

Insights from human NF-κB knockouts. 来自人类NF-κB基因敲除的见解。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-18 DOI: 10.1038/s44319-025-00500-x

Maximilian Pfisterer, Jan Dreute, M Lienhard Schmitz

{"title":"Insights from human NF-κB knockouts.","authors":"Maximilian Pfisterer, Jan Dreute, M Lienhard Schmitz","doi":"10.1038/s44319-025-00500-x","DOIUrl":"https://doi.org/10.1038/s44319-025-00500-x","url":null,"abstract":"The well-studied NF-κB signaling system is a key mediator of the inflammatory response. Large-scale sequencing studies in humans now allow initial insights into non-essential human genes in which both alleles carry mutations that prevent protein expression or function. Here, we compiled the non-essential genes identified in various sequencing studies and analyzed the occurrence of knockouts in the human NF-κB signaling system. This revealed a lower knockout frequency in the NF-κB system compared to the entire genome. Since drugs inhibiting NF-κB pathway components were unsuccessful in clinical trials so far, the naturally occurring knockouts of NF-κB and its upstream regulators could provide new candidates for therapeutic intervention. To investigate the potential functional importance of posttranslational modifications (PTMs) occurring on NF-κB components, we analyzed not only their evolutionary conservation but also, as a second criterion, their genetic constraint in the sequenced individuals. This approach revealed the absence of missense mutations at key modification sites involved in NF-κB activation and identified additional candidate sites for future studies.","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324796","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

GPNMB marks a quiescent cell population in melanoma and promotes metastasis formation. GPNMB标志着黑色素瘤中的静止细胞群并促进转移形成。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-17 DOI: 10.1038/s44319-025-00501-w

Fiorenza Lotti, Marine Melixetian, Thalia Vlachou, Marco S Nobile, Leone Bacciu, Marco Malferrari, Nicolò Quaresima, Stefania Rapino, Federica Marocchi, Massimo Barberis, Chiara Soriani, Barbara Gallo, Velia Mollo, Ilaria Ferrarotto, Daniela Bossi, Pier Francesco Ferrucci, Pier Giuseppe Pelicci, Lucilla Luzi, Luisa Lanfrancone

{"title":"GPNMB marks a quiescent cell population in melanoma and promotes metastasis formation.","authors":"Fiorenza Lotti, Marine Melixetian, Thalia Vlachou, Marco S Nobile, Leone Bacciu, Marco Malferrari, Nicolò Quaresima, Stefania Rapino, Federica Marocchi, Massimo Barberis, Chiara Soriani, Barbara Gallo, Velia Mollo, Ilaria Ferrarotto, Daniela Bossi, Pier Francesco Ferrucci, Pier Giuseppe Pelicci, Lucilla Luzi, Luisa Lanfrancone","doi":"10.1038/s44319-025-00501-w","DOIUrl":"https://doi.org/10.1038/s44319-025-00501-w","url":null,"abstract":"Melanoma exhibits high intratumoral heterogeneity, characterized by a diverse population of cells undergoing dynamic transitions between cellular states. These adaptive changes enable melanoma cells to survive in the harsh tumor microenvironment, acquire drug resistance, and metastasize. One such state, quiescence, has been linked to both relapse and drug resistance, but its underlying biology and molecular mechanisms remain poorly understood. Our study challenges the conventional understanding of melanoma quiescence. Contrary to the notion of a rare, unique subpopulation, we demonstrate that quiescence is a highly dynamic state accessible to most, if not all, melanoma cells. This state is exquisitely sensitive to microenvironmental cues. We identify GPNMB as a marker of quiescence, that is expressed in both primary and metastatic tumors. GPNMB-positive cells exhibit a pro-metastatic phenotype and are enriched in metastatic sites, suggesting a potential role for quiescence in tumor dissemination. Our findings position GPNMB as a valuable marker for isolating quiescent melanoma cells and as a potential therapeutic target to tackle metastasis.","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316204","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

Author Correction: Biometrics' new identity-measuring more physical and biological traits. 作者更正：生物识别技术的新身份——测量更多的生理和生物特征。

IF 6.5 1区生物学

EMBO Reports Pub Date : 2025-06-16 DOI: 10.1038/s44319-025-00506-5

Andrea Rinaldi

引用次数: 0