Serving the scientific community: FEBS Open Bio in 2024.

FEBS Open Bio is committed to not only publishing sound science but also to supporting early-career researchers and the scientific community as a whole. In this editorial, we look back at how the journal recognised and rewarded excellent research in 2023 and look forward to 2024.

FEBS fellowships: supporting excellent science for over four decades.

The Federation of European Biochemical Societies (FEBS) awarded FEBS Long-Term Fellowships from 1979 until 2020, at which time the scheme was replaced with the FEBS Excellence Award. Over four decades, FEBS awarded a huge number of Long-Term Fellowships, helping to support and promote the careers of excellent young researchers across Europe. To celebrate the exciting work performed by the FEBS Long-Term Fellows, we present here a special 'In the Limelight' issue of FEBS Open Bio, containing four Mini-reviews and four Research Protocols authored by the fellows themselves. The four Review articles provide timely updates on the respective research fields, while the Research Protocols describe how to perform challenging experimental methods in detail. We hope this issue will be a valuable resource for the community, and a celebration of the high-quality work done by young scientists.

Innovation and renovation: FEBS Open Bio in 2023.

FEBS Open Bio is constantly evolving to best suit the needs of the scientific community. In this Editorial, we review the various new initiatives introduced in 2022 and look forward to the opportunities and challenges that lie ahead in 2023.

Ensuring image integrity in the digital age.

FEBS Open Bio and our fellow FEBS Press journals have a strong commitment to maintaining the integrity of the scientific literature. The life sciences, in particular, are suffering from an ongoing reproducibility crisis, and this may in part be fuelled by mistakes, manipulation or outright fabrication of the presented data. We were recently made aware of several articles published in FEBS Open Bio that appear to contain full or partial duplications of images from other published articles in a different scientific context. In most of these cases, the duplications were taken from previously published papers. After thorough investigation and subsequent discussion within FEBS Press and with Wiley's Integrity in Publishing Group, we have retracted most of these articles.

An open chat with Laszlo Nagy.

Laszlo Nagy has been on the Editorial Board of FEBS Open Bio since the journal's inception and is a passionate supporter of FEBS Press and other society journals. Currently, he is also an editor of FEBS Letters and The Journal of Clinical Investigation (JCI). He studied medicine at the University Medical School of Debrecen in Hungary, where he graduated with an M.D. and later Ph.D., and then moved to the United States to conduct postdoctoral research at the University of Texas-Houston and subsequently the Salk Institute in San Diego. Laszlo is a Professor of Medicine and Biological Chemistry at John Hopkins School of Medicine, where he is Co-Director of the Institute for Fundamental Biomedical Research and Associate Director of the Center for Metabolic Origins of Disease, and Adjunct Professor at the University of Debrecen. Formerly, he was a Professor and Founding Director of the Genomic Control of Metabolism Program at the Sanford Burnham Prebys Medical Discovery Institute. He is also a member of the European Molecular Biology Organisation (EMBO), Academia Europaea, the Hungarian Academy of Sciences and The Henry Kunkel Society, and recipient of several awards, including the Boehringer Ingelheim Research Award, Cheryl Whitlock/Pathology Prize, a Wellcome Trust Senior Research Fellowship in Biomedical Sciences, and three Howard Hughes Medical Institute International Research Scholar Awards. In this fascinating interview, Laszlo Nagy shares the advice that changed his career trajectory, relates his views on scientific publishing, discusses new developments at The Johns Hopkins Center for Metabolic Origins of Disease, and outlines the prospects for future development of research and technology infrastructures in eastern Europe.

Entering the second decade: FEBS Open Bio in 2022.

FEBS Open Bio continues to go from strength to strength, with 2021 perhaps marking its most exciting year. In this Editorial, the Editor-in-Chief Miguel A. De la Rosa looks back at all the new developments of 2021 and forecasts the outlook for 2022.

An open chat with Takashi Gojobori.

Takashi Gojobori was one of the original founding members of the Editorial Board of FEBS Open Bio and is easily one of our most hard-working editors, having carefully evaluated hundreds of manuscripts on bioinformatics for us over the last decade. Takashi Gojobori received his doctorate at Kyushu University, Japan, before joining the University of Texas Health Science Center as a Research Associate and then Research Assistant Professor. Takashi was formerly the Vice-Director and Professor of National Institute of Genetics (NIG), Mishima, Japan, and at present, he is Distinguished Professor of Bioscience and Bioscience Acting Director of the Computational Bioscience Research Center at King Abdullah University of Science and Technology (KAUST), Saudi Arabia. Takashi was formerly the Editor-in-Chief of the journal Gene and is also a long-term member of the Editorial Board of FEBS Letters, among other editorial appointments. In honour of his 10 years (and counting!) of service to the journal, we present here this interview with him on his research and experiences.

FEBS Open Bio: past, present and future.

In celebration of the 10th anniversary of FEBS Open Bio, we spoke to some of the key figures of the journal's genesis, development, and its future direction, and recount here their thoughts and experiences. Prof. Félix. Goñi discusses the role of the FEBS Publication Committee in the journal's beginnings, Dr Mary Purton relates her experiences as the journal's Executive Editor, Prof. László Fésüs explains how the journal developed during his tenure as Chair of the Publication Committee, and Prof. Johannes Buchner looks forward to the future of FEBS Press and academic publishing. Finally, Prof. John (Iain) Mowbray describes his "Friday afternoon thought" to start a new journal.

Ten years of FEBS Open Bio.

This month, FEBS Open Bio celebrates its 10th birthday. To celebrate the journal's first decade, we present this special anniversary issue, comprised of editorials, reviews, and research articles especially commissioned for the occasion. In this introductory editorial, we invite the reader to join us as we reminisce over the journal's past, celebrate its present, and look forward to its future.

An open chat with Stuart Ferguson.

Stuart Ferguson has been on the Editorial Board of FEBS Open Bio since its inception, and his expertise, dedication, and support have been invaluable for the journal's growth and success. Stuart Ferguson received his doctorate in biochemistry from the University of Oxford, before taking up a faculty position at the University of Birmingham and later returning to Oxford, where he is currently Emeritus Fellow at St Edmund Hall but still teaching and pursuing his research interests. Stuart is also a long-term member of the Editorial Board of our fellow FEBS Press journal, FEBS Letters. Stuart has kindly volunteered to be the second member of our Editorial Board to be interviewed, in celebration of the journal's upcoming 10th anniversary.

Insights: fear of GAD.

Welcome to Insights, a new series in which articles published in FEBS Open Bio are summarised for the wider community. We hope that this series will help make the findings we publish more accessible to the general public and encourage greater engagement. In this first article of the series, we introduce a research paper on fear in rats, authored by Professor Yuchio Yanagawa and colleagues and published in this issue. Photo: Young rat and cat in front of black background. Cynoclub/Shutterstock.com.

Multidisciplinary evidence for early banana (Musa cvs.) cultivation on Mabuyag Island, Torres Strait.

Multiproxy archaeobotanical analyses (starch granule, phytolith and microcharcoal) of an abandoned agricultural terrace at Wagadagam on Mabuyag Island, Torres Strait, Australia, document extensive, low-intensity forms of plant management from at least 2,145-1,930 cal yr BP and intensive forms of cultivation at 1,376-1,293 cal yr BP. The agricultural activities at 1,376-1,293 cal yr BP are evidenced from terrace construction, banana (Musa cultivars) cultivation and dramatic transformations to the local palaeoenvironment. The robust evidence for the antiquity of horticulture in western Torres Strait provides an historical basis for understanding the diffusion of cultivation practices and cultivars, most likely from New Guinea. This study also provides a methodological template for the investigation of plant management, potentially including forms of cultivation that were practiced in northern Australia before European colonization.

(Ubi)quitin' the h2bit: recent insights into the roles of H2B ubiquitylation in DNA replication and transcription.

The reversible ubiquitylation of histone H2B has long been known to regulate gene transcription, and is now understood to modulate DNA replication as well. In this review, we describe how recent, genome-wide analyses have demonstrated that this histone mark has further reaching effects on transcription and replication than once thought. We also consider the ongoing efforts to elucidate the molecular mechanisms by which H2B ubiquitylation affects processes on the DNA template, and outline the various hypothetical scenarios.

H2B mono-ubiquitylation facilitates fork stalling and recovery during replication stress by coordinating Rad53 activation and chromatin assembly.

The influence of mono-ubiquitylation of histone H2B (H2Bub) on transcription via nucleosome reassembly has been widely documented. Recently, it has also been shown that H2Bub promotes recovery from replication stress; however, the underling molecular mechanism remains unclear. Here, we show that H2B ubiquitylation coordinates activation of the intra-S replication checkpoint and chromatin re-assembly, in order to limit fork progression and DNA damage in the presence of replication stress. In particular, we show that the absence of H2Bub affects replication dynamics (enhanced fork progression and reduced origin firing), leading to γH2A accumulation and increased hydroxyurea sensitivity. Further genetic analysis indicates a role for H2Bub in transducing Rad53 phosphorylation. Concomitantly, we found that a change in replication dynamics is not due to a change in dNTP level, but is mediated by reduced Rad53 activation and destabilization of the RecQ helicase Sgs1 at the fork. Furthermore, we demonstrate that H2Bub facilitates the dissociation of the histone chaperone Asf1 from Rad53, and nucleosome reassembly behind the fork is compromised in cells lacking H2Bub. Taken together, these results indicate that the regulation of H2B ubiquitylation is a key event in the maintenance of genome stability, through coordination of intra-S checkpoint activation, chromatin assembly and replication fork progression.

More equal societies have less mental illness: what should therapists do on Monday morning?

BACKGROUND: Therapists seeing poor clients may ask if countries with greater income equality have less mental illness. If so, how should therapists respond? MATERIAL: A review of epidemiological studies, theories of inequality and democratic reform movements in psychiatry and psychology leads to four arguments. DISCUSSION: (1) Increasing income equality improves the health of societies. (2) An elite opposes greater equality, partly by persuading the majority to consent to the existing order. (3) Therapists may inadvertently help in this persuasive effort. (4) However, therapists in democratic traditions create systems of care that support movements for greater income equality.

Histone ubiquitylation and chromatin dynamics.

Histones are subject to several post-translational modifications, which act to regulate gene expression and other processes on the DNA template. One such modification is the addition of a single ubiquitin moiety, which has been reported to influence chromatin dynamics and exhibit cross-talk with other histone modifications. Mono-ubiquitylation of H2B has been reported in eukaryotes as divergent as budding yeast, flies and humans, and is linked to transcriptional activation and gene silencing. Furthermore, ubiquitylation of H2A is also important for transcriptional repression in higher eukaryotes, and both histones play key roles in DNA repair. In this review, we will give an overview of the enzymes important for ubiquitylation and deubiquitylation of the various histone species, before examining the role of ubiquitylated histones in shaping the chromatin landscape and thus controlling the accessibility of DNA to effector proteins, through putative roles in promoting histone-histone interactions and stabilizing the structure of nucleosomes. We will finally discuss other processes reported to involve ubiquitylation of histones, including DNA repair, recombination and mRNA processing, underlining the diverse actions of these modifications.

Flickin' the ubiquitin switch: the role of H2B ubiquitylation in development.

The reversible ubiquitylation of histone H2B has long been implicated in transcriptional activation and gene silencing. However, many questions regarding its regulation and effects on chromatin structure remain unanswered. In addition, while several studies have uncovered an involvement of this modification in the control of certain developmental processes, a more general understanding of its requirement is lacking. Herein, we present a broad overview of the pathways known to be regulated by H2B ubiquitylation, while drawing parallels between findings in disparate organisms, in order to facilitate continued delineation of its spatiotemporal role in development. Finally, we integrate the findings of recent studies into how H2B ubiquitylation affects chromatin, and cast an eye over emerging areas for future research.

The C-terminus of histone H2B is involved in chromatin compaction specifically at telomeres, independently of its monoubiquitylation at lysine 123.

Telomeric heterochromatin assembly in budding yeast propagates through the association of Silent Information Regulator (SIR) proteins with nucleosomes, and the nucleosome array has been assumed to fold into a compacted structure. It is believed that the level of compaction and gene repression within heterochromatic regions can be modulated by histone modifications, such as acetylation of H3 lysine 56 and H4 lysine 16, and monoubiquitylation of H2B lysine 123. However, it remains unclear as to whether or not gene silencing is a direct consequence of the compaction of chromatin. Here, by investigating the role of the carboxy-terminus of histone H2B in heterochromatin formation, we identify that the disorderly compaction of chromatin induced by a mutation at H2B T122 specifically hinders telomeric heterochromatin formation. H2B T122 is positioned within the highly conserved AVTKY motif of the αC helix of H2B. Heterochromatin containing the T122E substitution in H2B remains inaccessible to ectopic dam methylase with dramatically increased mobility in sucrose gradients, indicating a compacted chromatin structure. Genetic studies indicate that this unique phenotype is independent of H2B K123 ubiquitylation and Sir4. In addition, using ChIP analysis, we demonstrate that telomere structure in the mutant is further disrupted by a defect in Sir2/Sir3 binding and the resulting invasion of euchromatic histone marks. Thus, we have revealed that the compaction of chromatin per se is not sufficient for heterochromatin formation. Instead, these results suggest that an appropriately arrayed chromatin mediated by H2B C-terminus is required for SIR binding and the subsequent formation of telomeric chromatin in yeast, thereby identifying an intrinsic property of the nucleosome that is required for the establishment of telomeric heterochromatin. This requirement is also likely to exist in higher eukaryotes, as the AVTKY motif of H2B is evolutionarily conserved.

Alternative splicing in the voltage-gated sodium channel DmNav regulates activation, inactivation, and persistent current.

Diversity in neuronal signaling is a product not only of differential gene expression, but also of alternative splicing. However, although recognized, the precise contribution of alternative splicing in ion channel transcripts to channel kinetics remains poorly understood. Invertebrates, with their smaller genomes, offer attractive models to examine the contribution of splicing to neuronal function. In this study we report the sequencing and biophysical characterization of alternative splice variants of the sole voltage-gated Na+ gene (DmNav, paralytic), in late-stage embryos of Drosophila melanogaster. We identify 27 unique splice variants, based on the presence of 15 alternative exons. Heterologous expression, in Xenopus oocytes, shows that alternative exons j, e, and f primarily influence activation kinetics: when present, exon f confers a hyperpolarizing shift in half-activation voltage (V1/2), whereas j and e result in a depolarizing shift. The presence of exon h is sufficient to produce a depolarizing shift in the V1/2 of steady-state inactivation. The magnitude of the persistent Na+ current, but not the fast-inactivating current, in both oocytes and Drosophila motoneurons in vivo is directly influenced by the presence of either one of a pair of mutually exclusive, membrane-spanning exons, termed k and L. Transcripts containing k have significantly smaller persistent currents compared with those containing L. Finally, we show that transcripts lacking all cytoplasmic alternatively spliced exons still produce functional channels, indicating that splicing may influence channel kinetics not only through change to protein structure, but also by allowing differential modification (i.e., phosphorylation, binding of cofactors, etc.). Our results provide a functional basis for understanding how alternative splicing of a voltage-gated Na+ channel results in diversity in neuronal signaling.