FEBS Journal最新文献

{"title":"Proteasome inhibition alters mitotic progression through the upregulation of centromeric α-Satellite RNAs.","authors":"Rodrigo E Cáceres-Gutiérrez,&nbsp;Marco A Andonegui,&nbsp;Diego A Oliva-Rico,&nbsp;Rodrigo González-Barrios,&nbsp;Fernando Luna,&nbsp;Cristian Arriaga-Canon,&nbsp;Alejandro López-Saavedra,&nbsp;Diddier Prada,&nbsp;Clementina Castro,&nbsp;Laurent Parmentier,&nbsp;José Díaz-Chávez,&nbsp;Yair Alfaro-Mora,&nbsp;Erick I Navarro-Delgado,&nbsp;Eunice Fabian-Morales,&nbsp;Bao Tran,&nbsp;Jyoti Shetty,&nbsp;Yongmei Zhao,&nbsp;Nicolas Alcaraz,&nbsp;Carlos De la Rosa,&nbsp;José L Reyes,&nbsp;Sabrine Hédouin,&nbsp;Florent Hubé,&nbsp;Claire Francastel,&nbsp;Luis A Herrera","doi":"10.1111/febs.16261","DOIUrl":"https://doi.org/10.1111/febs.16261","url":null,"abstract":"<p><p>Cell cycle progression requires control of the abundance of several proteins and RNAs over space and time to properly transit from one phase to the next and to ensure faithful genomic inheritance in daughter cells. The proteasome, the main protein degradation system of the cell, facilitates the establishment of a proteome specific to each phase of the cell cycle. Its activity also strongly influences transcription. Here, we detected the upregulation of repetitive RNAs upon proteasome inhibition in human cancer cells using RNA-seq. The effect of proteasome inhibition on centromeres was remarkable, especially on α-Satellite RNAs. We showed that α-Satellite RNAs fluctuate along the cell cycle and interact with members of the cohesin ring, suggesting that these transcripts may take part in the regulation of mitotic progression. Next, we forced exogenous overexpression and used gapmer oligonucleotide targeting to demonstrate that α-Sat RNAs have regulatory roles in mitosis. Finally, we explored the transcriptional regulation of α-Satellite DNA. Through in silico analyses, we detected the presence of CCAAT transcription factor-binding motifs within α-Satellite centromeric arrays. Using high-resolution three-dimensional immuno-FISH and ChIP-qPCR, we showed an association between the α-Satellite upregulation and the recruitment of the transcription factor NFY-A to the centromere upon MG132-induced proteasome inhibition. Together, our results show that the proteasome controls α-Satellite RNAs associated with the regulation of mitosis.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":"289 7","pages":"1858-1875"},"PeriodicalIF":5.4,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f7/7a/FEBS-289-1858.PMC9299679.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39846324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structure of Pseudomonas aeruginosa spermidine dehydrogenase: a polyamine oxidase with a novel heme-binding fold.","authors":"Shiyou Che, Yakun Liang, Yujing Chen, Wenyue Wu, Ruihua Liu, Qionglin Zhang, Mark Bartlam","doi":"10.1111/febs.16264","DOIUrl":"10.1111/febs.16264","url":null,"abstract":"<p><p>The opportunistic pathogen Pseudomonas aeruginosa can utilize polyamines (including putrescine, cadaverine, 4-aminobutyrate, spermidine, and spermine) as its sole source of carbon and nitrogen. Spermidine dehydrogenase (SpdH) is a component of one of the two polyamine utilization pathways identified in P. aeruginosa, but little is known about its structure and function. Here, we report the first crystal structure of SpdH from P. aeruginosa to 1.85 Å resolution. The resulting core structure confirms that SpdH belongs to the polyamine oxidase (PAO) family with flavin-binding and substrate-binding domains. A unique N-terminal extension wraps around the flavin-binding domain of SpdH and is required for heme binding, placing a heme cofactor in close proximity to the FAD cofactor. Structural and mutational analysis reveals that residues in the putative active site at the re side of the FAD isoalloxazine ring form part of the catalytic machinery. PaSpdH features an unusual active site and lacks the conserved lysine that forms part of a lysine-water-flavin N5 atom interaction in other PAO enzymes characterized to date. Mutational analysis further confirms that heme is required for catalytic activity. This work provides an important starting point for understanding the role of SpdH, which occurs universally in P. aeruginosa strains, in polyamine metabolism.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":"289 7","pages":"1911-1928"},"PeriodicalIF":5.4,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39848261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"More important than ever: understanding how plants cope with stress","authors":"P. Macheroux","doi":"10.1111/febs.16434","DOIUrl":"https://doi.org/10.1111/febs.16434","url":null,"abstract":"In view of the unprecedented rate of current climate change, plants are exposed to an avalanche of adverse environmental conditions that will challenge their ability to cope with abiotic and biotic stresses. These changes are bound to affect crop plants as well, and thus, have the potential to jeopardize food security on a global scale. Hence, it will be critical to understand the molecular defence and adaptation mechanisms that enable plants to thrive in an increasingly hostile environment. In this Subject Collection, The FEBS Journal presents a collection of reviews and original articles dealing with aspects of plant defence systems and mechanisms of pathogenicity.","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45194294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploiting formyl peptide receptor 2 to promote microglial resolution: a new approach to Alzheimer's disease treatment.","authors":"Edward S Wickstead,&nbsp;Murray A Irving,&nbsp;Stephen J Getting,&nbsp;Simon McArthur","doi":"10.1111/febs.15861","DOIUrl":"https://doi.org/10.1111/febs.15861","url":null,"abstract":"<p><p>Alzheimer's disease and dementia are among the most significant current healthcare challenges given the rapidly growing elderly population, and the almost total lack of effective therapeutic interventions. Alzheimer's disease pathology has long been considered in terms of accumulation of amyloid beta and hyperphosphorylated tau, but the importance of neuroinflammation in driving disease has taken greater precedence over the last 15-20 years. Inflammatory activation of the primary brain immune cells, the microglia, has been implicated in Alzheimer's pathogenesis through genetic, preclinical, imaging and postmortem human studies, and strategies to regulate microglial activity may hold great promise for disease modification. Neuroinflammation is necessary for defence of the brain against pathogen invasion or damage but is normally self-limiting due to the engagement of endogenous pro-resolving circuitry that terminates inflammatory activity, a process that appears to fail in Alzheimer's disease. Here, we discuss the potential for a major regulator and promoter of resolution, the receptor FPR2, to restrain pro-inflammatory microglial activity, and propose that it may serve as a valuable target for therapeutic investigation in Alzheimer's disease.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":"289 7","pages":"1801-1822"},"PeriodicalIF":5.4,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/febs.15861","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25554994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plant programmed cell death meets auxin signalling.","authors":"Joanna Kacprzyk,&nbsp;Rory Burke,&nbsp;Johanna Schwarze,&nbsp;Paul F McCabe","doi":"10.1111/febs.16210","DOIUrl":"https://doi.org/10.1111/febs.16210","url":null,"abstract":"<p><p>Both auxin signalling and programmed cell death (PCD) are essential components of a normally functioning plant. Auxin underpins plant growth and development, as well as regulating plant defences against environmental stresses. PCD, a genetically controlled pathway for selective elimination of redundant, damaged or infected cells, is also a key element of many developmental processes and stress response mechanisms in plants. An increasing body of evidence suggests that auxin signalling and PCD regulation are often connected. While generally auxin appears to suppress cell death, it has also been shown to promote PCD events, most likely via stimulation of ethylene biosynthesis. Intriguingly, certain cells undergoing PCD have also been suggested to control the distribution of auxin in plant tissues, by either releasing a burst of auxin or creating an anatomical barrier to auxin transport and distribution. These recent findings indicate novel roles of localized PCD events in the context of plant development such as control of root architecture, or tissue regeneration following injury, and suggest exciting possibilities for incorporation of this knowledge into crop improvement strategies.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":"289 7","pages":"1731-1745"},"PeriodicalIF":5.4,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39434154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of MerTK in promoting cell migration is enhanced by the oncogenic Ras/IL-33 signaling axis.","authors":"Satoshi Ohta,&nbsp;Kenji Tago,&nbsp;Takahiro Kuchimaru,&nbsp;Megumi Funakoshi-Tago,&nbsp;Hisanaga Horie,&nbsp;Chihiro Aoki-Ohmura,&nbsp;Jitsuhiro Matsugi,&nbsp;Ken Yanagisawa","doi":"10.1111/febs.16271","DOIUrl":"https://doi.org/10.1111/febs.16271","url":null,"abstract":"<p><p>Ras genes are frequently mutated in many cancer types; however, there are currently no conclusively effective anticancer drugs against Ras-induced cancer. Therefore, the downstream effectors of Ras signaling need to be identified for the development of promising novel therapeutic approaches. We previously reported that oncogenic Ras induced the expression of NF-HEV/IL-33, a member of the interleukin-1 family, and showed that intracellular IL-33 was required for oncogenic Ras-induced cellular transformation. In the present study, we demonstrated that the c-Mer proto-oncogene tyrosine kinase (MerTK), a receptor tyrosine kinase, played essential roles in oncogenic Ras/IL-33 signaling. The expression of MerTK was enhanced in transformed NIH-3T3 cells by the expression of oncogenic Ras, H-Ras (G12V), in an IL-33-dependent manner. In human colorectal cancer tissues, MerTK expression also correlated with IL-33 expression. The knockdown of IL-33 or MerTK effectively attenuated the migration of NIH-3T3 cells transformed by H-Ras (G12V) and A549, LoVo, and HCT116 cells harboring an oncogenic K-Ras mutation. Furthermore, the suppression of Ras-induced cell migration by the knockdown of IL-33 was rescued by the enforced expression of MerTK. The present results also revealed that MerTK was effectively phosphorylated in NIH-3T3 cells transformed by Ras (G12V). Ras signaling was essential for the tyrosine phosphorylation of MerTK, and the kinase activity of MerTK was indispensable for accelerating cell migration. Collectively, the present results reveal a novel role for MerTK in cancer malignancy, which may be utilized to develop novel therapeutic strategies that target Ras-transformed cells.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":"289 7","pages":"1950-1967"},"PeriodicalIF":5.4,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39596339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Issue Information","authors":"","doi":"10.1111/febs.15971","DOIUrl":"https://doi.org/10.1111/febs.15971","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49348865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Issue Information","authors":"","doi":"10.1111/febs.15416","DOIUrl":"https://doi.org/10.1111/febs.15416","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44196912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Table of Contents.","authors":"","doi":"10.1111/febs.15417","DOIUrl":"https://doi.org/10.1111/febs.15417","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":"288 21 1","pages":"6304"},"PeriodicalIF":5.4,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41815978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ever-expanding landscape of cancer therapeutic approaches.","authors":"Christine J Watson","doi":"10.1111/febs.16228","DOIUrl":"https://doi.org/10.1111/febs.16228","url":null,"abstract":"<p><p>Cancer is a leading cause of death and a major health problem worldwide, particularly in more developed countries. There is, therefore, an urgent clinical need to develop more effective therapies to treat cancer and metastatic disease. In this Editorial, the content of The FEBS Journal's Special Issue on Cancer Therapeutics is outlined. The interesting collection of recent articles in this issue covers a wide repertoire of cancer therapeutic approaches. While some of the articles discuss broad-spectrum applications such as immunotherapy and oncolytic virus therapy, others focus on a particular type of cancer or a signalling pathway that has gone awry such as aberrant Ca²⁺ signalling, glycosylation or pre-mRNA processing. Finally, an article featured in this issue reviews our current understanding of how cancer cells can become dormant, often for decades, and which pathways reactivate these cells to cause relapse. I am sure there is something for everyone in this issue.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":"288 21","pages":"6082-6086"},"PeriodicalIF":5.4,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9459306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}