http://jbiol.com/ The most accessed research articles published by Journal of Biology 2010-02-24T00:00:00Z Journal of Biology launches a re-review opt-out experiment in response to widespread dissatisfaction with peer review, and publishes the first of two new regular features - a full review on the ribosome and a question-and-answer feature on systems biology. http://jbiol.com/content/8/1/1 Journal of Biology 2009, null:1 2009-01-27T00:00:00Z doi:10.1186/jbiol111 Ending the peer review 'nightmare' Journal of Biology launches a re-review opt-out experiment in response to widespread dissatisfaction with peer review, and publishes the first of two new regular features - a full review on the ribosome and a question-and-answer feature on systems biology. /content/figures/jbiol111-toc.gif Journal of Biology 1475-4924 ${item.volume} 1 2009-01-27T00:00:00Z XML Good early training of graduate students and postdocs is needed to prevent them turning into future generations of manuscript-savaging reviewers. How can we intercalate typical papers into our training? http://jbiol.com/content/8/3/24 Journal of Biology 2009, null:24 2009-03-09T00:00:00Z doi:10.1186/jbiol125 With or without lipstick Virginia Walbot accepts some of the blame for remorselessly negative reviewers, and suggests a training program for graduate students and post docs that will deliver a fairer assessment of manuscripts. /content/figures/jbiol125-toc.gif Journal of Biology 1475-4924 ${item.volume} 24 2009-03-09T00:00:00Z XML Because emotions enhance memory processes and music evokes strong emotions, music could be involved in forming memories, either about pieces of music or about episodes and information associated with particular music. A recent study in BMC Neuroscience has given new insights into the role of emotion in musical memory. http://jbiol.com/content/7/6/21 Journal of Biology 2008, null:21 2008-08-08T00:00:00Z doi:10.1186/jbiol82 /content/figures/jbiol82-toc.gif Journal of Biology 1475-4924 ${item.volume} 21 2008-08-08T00:00:00Z XML Background: Forkhead transcription factors belonging to the FOXO subfamily are negatively regulated by protein kinase B (PKB) in response to signaling by insulin and insulin-like growth factor in Caenorhabditis elegans and mammals. In Drosophila, the insulin-signaling pathway regulates the size of cells, organs, and the entire body in response to nutrient availability, by controlling both cell size and cell number. In this study, we present a genetic characterization of dFOXO, the only Drosophila FOXO ortholog. Results: Ectopic expression of dFOXO and human FOXO3a induced organ-size reduction and cell death in a manner dependent on phosphoinositide (PI) 3-kinase and nutrient levels. Surprisingly, flies homozygous for dFOXO null alleles are viable and of normal size. They are, however, more sensitive to oxidative stress. Furthermore, dFOXO function is required for growth inhibition associated with reduced insulin signaling. Loss of dFOXO suppresses the reduction in cell number but not the cell-size reduction elicited by mutations in the insulin-signaling pathway. By microarray analysis and subsequent genetic validation, we have identified d4E-BP, which encodes a translation inhibitor, as a relevant dFOXO target gene. Conclusion: Our results show that dFOXO is a crucial mediator of insulin signaling in Drosophila, mediating the reduction in cell number in insulin-signaling mutants. We propose that in response to cellular stresses, such as nutrient deprivation or increased levels of reactive oxygen species, dFOXO is activated and inhibits growth through the action of target genes such as d4E-BP. http://jbiol.com/content/2/3/20 Martin Jünger Felix Rintelen Hugo Stocker Jonathan Wasserman Mátyás Végh Thomas Radimerski Michael Greenberg Ernst Hafen Journal of Biology 2003, null:20 2003-08-07T00:00:00Z doi:10.1186/1475-4924-2-20 /content/figures/1475-4924-2-20-toc.gif Journal of Biology 1475-4924 ${item.volume} 20 2003-08-07T00:00:00Z XML None of the advantages of traditional scientific journals need be sacrificed in order to provide free online access to scientific journal articles. Objections that open access to scientific journal literature requires the sacrifice of peer-review, revenue, copyright protection, or other strengths of traditional journals, are based on misunderstandings. http://jbiol.com/content/1/1/3 Peter Suber Journal of Biology 2002, null:3 2002-06-18T00:00:00Z doi:10.1186/1475-4924-1-3 /content/figures/1475-4924-1-3-toc.gif Journal of Biology 1475-4924 ${item.volume} 3 2002-06-18T00:00:00Z XML Background: Vertebrates share the same general body plan and organs, possess related sets of genes, and rely on similar physiological mechanisms, yet show great diversity in morphology, habitat and behavior. Alteration of gene regulation is thought to be a major mechanism in phenotypic variation and evolution, but relatively little is known about the broad patterns of conservation in gene expression in non-mammalian vertebrates. Results: We measured expression of all known and predicted genes across twenty tissues in chicken, frog and pufferfish. By combining the results with human and mouse data and considering only ten common tissues, we have found evidence of conserved expression for more than a third of unique orthologous genes. We find that, on average, transcription factor gene expression is neither more nor less conserved than that of other genes. Strikingly, conservation of expression correlates poorly with the amount of conserved nonexonic sequence, even using a sequence alignment technique that accounts for non-collinearity in conserved elements. Many genes show conserved human/fish expression despite having almost no nonexonic conserved primary sequence. Conclusions: There are clearly strong evolutionary constraints on tissue-specific gene expression. A major challenge will be to understand the precise mechanisms by which many gene expression patterns remain similar despite extensive cis-regulatory restructuring. http://jbiol.com/content/8/3/33 Esther Chan Gerald Quon Gordon Chua Tomas Babak Miles Trochesset Ralph Zirngibl Jane Aubin Michael Ratcliffe Andrew Wilde Michael Brudno Quaid Morris Timothy Hughes Journal of Biology 2009, null:33 2009-04-16T00:00:00Z doi:10.1186/jbiol130 Gene expression enigma High conservation of tissue-specific expression is found across vertebrates yet there is a lack of conservation in common regulatory sequences/signatures. /content/figures/jbiol130-toc.gif Journal of Biology 1475-4924 ${item.volume} 33 2009-04-16T00:00:00Z XML A phylogeographic analysis of gene sequences important in determining body size in dogs, recently published in BMC Biology, traces the appearance of small body size to the Neolithic Middle East. This finding strengthens the association of this event with the development of sedentary societies, and perhaps even has implications for the inception of human social inequality.See research article http://www.biomedcentral.com/1741-7007/8/16/ http://jbiol.com/content/9/2/10 Journal of Biology 2010, null:10 2010-02-24T00:00:00Z doi:10.1186/jbiol226 Levantine taming of the wolves Commenting on a phylogeographic analysis in BMC Biology that supports a Middle Eastern origin of small dogs, Driscoll and Macdonald speculate on the implications of wolf domestication and size reduction occurring at a time of transition between hunter-gatherer and sedentary societies. /content/figures/jbiol226-toc.gif Journal of Biology 1475-4924 ${item.volume} 10 2010-02-24T00:00:00Z XML Background: Chemotherapy in cancer patients can be associated with serious short- and long-term adverse neurological effects, such as leukoencephalopathy and cognitive impairment, even when therapy is delivered systemically. The underlying cellular basis for these adverse effects is poorly understood. Results: We found that three mainstream chemotherapeutic agents – carmustine (BCNU), cisplatin, and cytosine arabinoside (cytarabine), representing two DNA cross-linking agents and an antimetabolite, respectively – applied at clinically relevant exposure levels to cultured cells are more toxic for the progenitor cells of the CNS and for nondividing oligodendrocytes than they are for multiple cancer cell lines. Enhancement of cell death and suppression of cell division were seen in vitro and in vivo. When administered systemically in mice, these chemotherapeutic agents were associated with increased cell death and decreased cell division in the subventricular zone, in the dentate gyrus of the hippocampus and in the corpus callosum of the CNS. In some cases, cell division was reduced, and cell death increased, for weeks after drug administration ended. Conclusion: Identifying neural populations at risk during any cancer treatment is of great importance in developing means of reducing neurotoxicity and preserving quality of life in long-term survivors. Thus, as well as providing possible explanations for the adverse neurological effects of systemic chemotherapy, the strong correlations between our in vitro and in vivo analyses indicate that the same approaches we used to identify the reported toxicities can also provide rapid in vitro screens for analyzing new therapies and discovering means of achieving selective protection or targeted killing. http://jbiol.com/content/5/7/22 Joerg Dietrich Ruolan Han Miranda Yang Margot Mayer-Proschel Mark Noble Journal of Biology 2006, null:22 2006-11-30T00:00:00Z doi:10.1186/jbiol50 Chemotherapy affects neural cells Chemotherapeutic agents are more toxic to cells of the central nervous system than to cancer cells when administered to mice and cultured cells, providing an explanation for adverse neurological effects of systemic chemotherapy. /content/figures/jbiol50-toc.gif Journal of Biology 1475-4924 ${item.volume} 22 2006-11-30T00:00:00Z XML Background: Cell growth underlies many key cellular and developmental processes, yet a limited number of studies have been carried out on cell-growth regulation. Comprehensive studies at the transcriptional, proteomic and metabolic levels under defined controlled conditions are currently lacking. Results: Metabolic control analysis is being exploited in a systems biology study of the eukaryotic cell. Using chemostat culture, we have measured the impact of changes in flux (growth rate) on the transcriptome, proteome, endometabolome and exometabolome of the yeast Saccharomyces cerevisiae. Each functional genomic level shows clear growth-rate-associated trends and discriminates between carbon-sufficient and carbon-limited conditions. Genes consistently and significantly upregulated with increasing growth rate are frequently essential and encode evolutionarily conserved proteins of known function that participate in many protein-protein interactions. In contrast, more unknown, and fewer essential, genes are downregulated with increasing growth rate; their protein products rarely interact with one another. A large proportion of yeast genes under positive growth-rate control share orthologs with other eukaryotes, including humans. Significantly, transcription of genes encoding components of the TOR complex (a major controller of eukaryotic cell growth) is not subject to growth-rate regulation. Moreover, integrative studies reveal the extent and importance of post-transcriptional control, patterns of control of metabolic fluxes at the level of enzyme synthesis, and the relevance of specific enzymatic reactions in the control of metabolic fluxes during cell growth. Conclusion: This work constitutes a first comprehensive systems biology study on growth-rate control in the eukaryotic cell. The results have direct implications for advanced studies on cell growth, in vivo regulation of metabolic fluxes for comprehensive metabolic engineering, and for the design of genome-scale systems biology models of the eukaryotic cell. http://jbiol.com/content/6/2/4 Juan Castrillo Leo Zeef David Hoyle Nianshu Zhang Andrew Hayes David Gardner Michael Cornell June Petty Luke Hakes Leanne Wardleworth Bharat Rash Marie Brown Warwick Dunn David Broadhurst Kerry O'Donoghue Svenja Hester Tom Dunkley Sarah Hart Neil Swainston Peter Li Simon Gaskell Norman Paton Kathryn Lilley Douglas Kell Stephen Oliver Journal of Biology 2007, null:4 2007-04-30T00:00:00Z doi:10.1186/jbiol54 Systems biology of cell growth The first comprehensive systems biology study on growth rate control in yeast integrates information from the transcriptome, proteome and metabolome to reveal how cell growth underlies key cellular and development processes. /content/figures/jbiol54-toc.gif Journal of Biology 1475-4924 ${item.volume} 4 2007-04-30T00:00:00Z XML Background: Eukaryotic cells have evolved various response mechanisms to counteract the deleterious consequences of oxidative stress. Among these processes, metabolic alterations seem to play an important role. Results: We recently discovered that yeast cells with reduced activity of the key glycolytic enzyme triosephosphate isomerase exhibit an increased resistance to the thiol-oxidizing reagent diamide. Here we show that this phenotype is conserved in Caenorhabditis elegans and that the underlying mechanism is based on a redirection of the metabolic flux from glycolysis to the pentose phosphate pathway, altering the redox equilibrium of the cytoplasmic NADP(H) pool. Remarkably, another key glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), is known to be inactivated in response to various oxidant treatments, and we show that this provokes a similar redirection of the metabolic flux. Conclusion: The naturally occurring inactivation of GAPDH functions as a metabolic switch for rerouting the carbohydrate flux to counteract oxidative stress. As a consequence, altering the homoeostasis of cytoplasmic metabolites is a fundamental mechanism for balancing the redox state of eukaryotic cells under stress conditions. http://jbiol.com/content/6/4/10 Markus Ralser Mirjam Wamelink Axel Kowald Birgit Gerisch Gino Heeren Eduard Struys Edda Klipp Cornelis Jakobs Michael Breitenbach Hans Lehrach Sylvia Krobitsch Journal of Biology 2007, null:10 2007-12-21T00:00:00Z doi:10.1186/jbiol61 Eukaryotes counteracting oxidative stress Yeast and C. elegans share a conserved cellular mechanism that counteracts the fatal consequences of oxidative stress by enabling the redirection of metabolic flux from glycolysis to the pentose phosphate pathway. /content/figures/jbiol61-toc.gif Journal of Biology 1475-4924 ${item.volume} 10 2007-12-21T00:00:00Z XML