BioMed Central Blog
An Emirates hat-trick for BMC Biology authors
This week saw the annual BMC Research Awards presentations, in the Emirates Stadium and with a sports science theme, to acknowledge the forthcoming London Olympics. BMC Biology is very happy to be able to congratulate the authors of three BMC Biology papers that won awards reflecting the diversity of interesting topics on which we publish:-
Alexei Korennykh and colleagues won the General Biology award for their research on how ADP binding can tune the kinase in the activation of Ire, the remarkable bifunctional kinase-RNase whose activity directs the alternative splicing of a key transcription factor in the rescue program in response to the toxic accumulation of unfolded proteins in the endoplasmic reticulum.
The Molecular and Cellular Science award was taken by Judith Goodship and colleagues with an article examining the molecular details behind Ellis-van Creveld syndrome, a genetic disorder with distinctive growth defects caused by migration in the Evc protein. The authors identified a novel binding partner for Evc – Evc2 – and identify that both bind together within the basal body of the cilia, activating the hedgehog signaling pathway.
Felipe Vilas-Boas, Rita Fior, Kate Storey and colleagues were the recipients of the prize for Neuroscience, Neurology and Psychiatry for their article detailing a new reporter for detecting the activity of the Notch signaling pathway, which is involved in specification of neural cell fates. This reporter is based on a downstream promoter from a Notch target gene, Hes5-1, coupled with instability elements and a new fluorescent protein (VNP), and provides a reliable readout of Notch activity. The advantage is that the authors can now achieve single cell resolution and real time imaging, enabling more dynamic analysis of Notch activity.
Congratulations again to all our winners.
Posted by Kester Jarvis at 17:31 Comments (0)
Breaking walls and mending organs
In a recent Comment in BMC Biology, Gregory Petsko appeals to some particularly surprising patterns of comorbidity in support of the argument for breaking the traditional boundaries between disciplines in translational research. This ever-topical issue featured at a recent panel session combining two parallel Keystone conferences on Regenerative Tissue Engineering and Transplantation and Mechanisms of Whole Organ Regeneration (co-organized by Rocky S. Tuan and Alejandro Sánchez Alvarado conference), with discussion on how to overcome the main obstacles to translation of basic research into the clinic.
What enables successful translation to the clinic? Michele de Luca was highlighted as a scientist who has made this happen, with success in transplanting human cornea grown from patient’s limbal stem cells in the laboratory. Kenneth R. Chien called for a generation of “scienteers” – researchers with multi-disciplinary training in both basic research and tissue engineering. Practical needs include the establishment of appropriate manufacturing standards (GMP); use of FDA approved materials; methods to deliver technologies, for example, how to implant cells; and develop better animal models applicable to cells or drugs for therapeutic use in humans (with a move away from a focus on mice).
As a final conclusion to the panel discussions, it was agreed that funding bodies (especially the NIH) could do more to promote such interdisciplinary interactions but also that scientists need to write grants in such a way to make this happen. Leading on from this, the panel promoted publication of work in open access general journals to reach “beyond your immediate community”. With this in mind, we welcome such submissions!
J Ann Le Good, Deputy Editor, BMC Biology
Posted by Alice Plane at 17:07 Comments (0)
The future of evolutionary epidemiology
The impending age of big data has been inescapable in recent discourse, both scientific and otherwise. The prevailing metaphors cast big data as a tsunami or an avalanche, suggesting natural disaster poised to dash hapless researchers against the rocks. They are, of course, no such thing, and offer many opportunities provided that one is prepared. Some of these opportunities were on show at the Royal Society discussion meeting on “Next-generation molecular and evolutionary epidemiology of infectious disease”.
One focus, inevitably, was next-generation sequencing, with Paul Kellam speaking about its importance in tracking the spread of the three waves of the 2009 H1N1 pandemic at a population level; but also for following the rapid spread of polymorphisms though the virus population within a single patient. Bill Hanage discussed the use of whole-genome data to investigate phylogenetic relationships within highly recombinogenic bacteria like Streptococcus pneumoniae, for which traditional genetic methods simply can’t cut it.
Some notes of restraint were sounded too. Dan Haydon told a cautionary tale about the current inability of deep sequencing to separate foot-and-mouth virus variation within an individual from technical noise, and suggested that in evolutionary studies of this virus, variation between individuals is the highest resolution at which we can currently make reliable inferences (the resulting graphs using "1 cow" as a basic unit of time amused, although we don’t imagine it shall become an SI unit any time soon). Contrary to the “sequence everything” school of thought, Sharon Peacock of the Health Protection Agency made the case for sparing use of whole-genome sequencing in clinical microbiology, where phenotypic tests still offer good effectiveness for their cost and in the majority of cases sequencing is an unnecessary expense.
Epidemiologists are perhaps uniquely interested in co-mapping phylogenetic and spatial data, given the power of explicitly tracking the recent history of disease spread, and there were a number of talks on the potential for spatial phylodynamics in modelling the spread of diseases including rabies and influenza. Perhaps the most striking example of the efficacy of this approach was given by Sharon Peacock, who showed how whole genome sequencing of MRSA allowed spatial mapping of its spread at the resolution of wards within a single hospital.
However, collecting spatial data is no straightforward task, and the future of surveillance was a popular subject. Simon Hay discussed a project to update global risk maps for disease, which are “often diabolical”, through careful curation via survey of the existing data and literature – but this is very costly in time and resources, and the future of this kind of curation might be driven by automated data-mining of resources such as PubMed and GenBank. Larry Brilliant spoke about Google.org’s Flu Trends, which tracks outbreaks through users’ flu-related search terms with surprising success – often reporting peaks in flu activity a week or two ahead of the CDC’s GP-reported data – and went on to give an overview and endorsement of the current trend for web-based crowd-sourcing of reports through sites like HealthMap and ProMED.
Readers will, of course, be wondering about the privacy issues related to these new kinds of data-collection methods, and this was on attendees’ minds too. Nowhere is the discord between the need for patient privacy and the public health benefits of data release more apparent than epidemiology, where the geographic location of a patient – a key piece of information – goes a considerable way to revealing their identity. One unsavoury possibility is the future prospect of using a combination of genetic and epidemiological data to personally identify a key patient; say, “patient zero” for a particular pandemic, or an infection-multiplying “superspreader” for HIV – although it is important to emphasise that neither of these is likely at present. The discussion of these issues was only one aspect of a lively panel discussion to close the meeting, which also took in issues of data quality and accessibility, and how encouraging data citability might be one way to solve them. (Those interested in data citation might like to read the recent blog post and associated BMC Research Notes article on the current gold standard).
For those whose interest in evolutionary epidemiology has been piqued, suggested further reading in BMC Biology comes from Trevor Bedford and colleagues’ recent research modelling the evolutionary reasons for strikingly low standing diversity in the H3N2 flu virus; and Nobel laureate Peter Doherty and colleague Paul Thomas's comment on why knowing which mutations to look for in natural H5N1 flu reservoirs is more important than the perceived dangers which lead to the redaction – now reversed – of the description of particularly virulent laboratory strains.
Posted by Kester Jarvis at 14:19 Comments (0)
Greater Depths to the Deepwater Horizon oil disaster
Two years after the Deepwater Horizon drilling disaster in the Gulf of Mexico, the extent of its ecological impact is still to be fully assessed. In field studies from coastal marsh areas four months after the spill, exposure to the oil has been linked to divergence in genomic expression and aberrant protein expression in killifish (Fundulus grandis) gills, indicative of exposure to hydrocarbon-like chemicals. Deep water coral communities are also affected: in a study by Fisher and colleagues four months following capping of the well at a site 11 km from the Macondo well, widespread signs of stress in corals (tissue loss, bleaching and covering by brown flocculent material – floc) were visible. Analyses of the floc adherent to corals show petroleum biomarkers associated with the spill.
In a recent paper published in BMC Biology, Michael Barresi and colleagues report the results of an investigation of the possible lasting damage to marine life using the well characterized laboratory zebrafish as a powerful model for assessing the effects of toxicants from oil samples on embryonic development. They found that water-soluble components of crude oil samples from the Deepwater Horizon disaster containing polycyclic aromatic hydrocarbons cause defects in embryonic zebrafish development, leading to circulatory, locomotor and brain defects.They were also able to identify some of the molecular pathways activated by the oil.
Following the second anniversary of the Deepwater Horizon oil spill (on April 20), a panel of experts funded by the National Center for Ecological Analysis and Synthesis have recommended that strategies to deal with such deep water spills may need to change in future to meet the special ecological challenge of oil retained at depth in the ocean. In light of the research by Barresi and colleagues on zebrafish, it seems that profound effects of the oil spill may continue to surface and the committee’s concerns on the ecological risk are well founded.
J. Ann Le Good, Deputy Editor, BMC Biology
Posted by Kester Jarvis at 16:16 Comments (0)
Painless publishing and the roots of the re-review revolt
Over the past few weeks, eLife has posted a manifesto, and EMBOencounters and Journal of Cell Biology have published editorials, all promising strategies to avoid the iniquities of iterative reviewing, recently also the focus of invective from Hidde Ploegh and Gregory Petsko. We have addressed the problem with a policy we call re-review opt-out.
Clearly the movement to refocus journals on promoting the publication of papers, rather than assiduously filtering them, is gaining ground.
Lest it be overlooked in the more recent coverage, I should like to take the opportunity to assign credit to a rather earlier attempt to draw attention to the plight of postdocs and untenured academics whose careers are imperilled by publication delays due to obstructive referees and unduly compliant editors.
Some years before Ploegh inveighed in Nature against the tyranny (sic) of ‘reviewer experiments’, or the manifesto of eLife inspired an enthusiastic endorsement from Petsko in Genome Biology, Raff, Johnson and Walter made precisely the same points in a succinct and eloquent letter to Science entitled ‘Painful Publishing’.
They were a large part of the inspiration for our own re-review opt-out policy, now in its fourth year of operation, and this is a good time to acknowledge the debt.
Miranda Robertson
Editor, BMC Biology
Posted by Alice Plane at 18:17 Comments (2)
Topographic modelling and the global search for ring species
‘Ring species’ or ‘circular overlaps’ present a unique opportunity to reconstruct the history of speciation. They occur when a chain of gradually diverging populations encircles a geographic barrier. Interbreeding occurs between neighbouring populations, but the two ends of the chain eventually meet as reproductively isolated species. They thus allow us to follow the process of geographic speciation step by step, and also demonstrate that speciation may occur even in the presence of gene flow. Yet despite their significance, very few genuine examples of ring species have been documented to date.
In a new study published in BMC Biology William Monahan and colleagues suggest a way to discover new examples of ring species, through a global topographic model that utilises information on the geographic barriers involved in the formation of known ring species to predict where other candidate barriers might be found.
Darren Irwin, in an accompanying commentary for BMC Biology, discusses how the model could be extended to incorporate geographic and environmental features not included in the current model, and examines their relative importance in known examples of ring speciation.
Heidi Seears, Assistant Editor, BMC Biology
Posted by Alice Plane at 10:57 Comments (0)
The concept of the stem cell niche – as a microenvironment for pluripotent stem cells – is an old one but one that evolves with advances in the tools to identify stem cells and visualize the niche. In a new Forum article for BMC Biology eight experts in different fields discuss the definition of a stem cell niche and what is important about the niche they are studying. The niches discussed include the well-established nematode germline cell niche (by Judith Kimble), the more “classical” niches of the skin (by Elaine Fuchs) and gut (by Hans Clevers), niches of the muscle (by Didier Montarras and Margaret Buckingham), neuron (by Anne Calof) and bone marrow (by Andreas Trumpp), and the more recently described niche for metastatic/cancer stem cells (by Thordur Oskarsson). Our experts describe how each niche forms and highlight its unique characteristics, for example, what triggers a stem cell to leave its quiescent state (ranging from injury to activation by various signaling pathways) and how the extracellular matrix influences the niche.
With this topical discussion, BMC Biology launches its Forum articles, in which the perspectives of several experts are brought together in one article to answer the same question.
The Forum on stem cell niches is part of the cross-journal stem cell collection, comprising articles on many aspects of stem cell research, and is introduced by Arthur Lander, Consulting Editor for BMC Biology on the series, and who speculates that the niche may act as “a hub of inter-lineage coordination”, commenting that with emerging novel in vivo imaging techniques and methods to identify the niche and stem cells within that environment, we can hope to see the answers to the many open questions that he and our experts delineate.
Ann Le Good, Deputy Editor, BMC Biology
Posted by Alice Plane at 14:55 Comments (0)
Wasps, aphids and endosymbiotic bacteria: who wins the arms race?
There is a nursery rhyme that goes:
“Big fleas have little fleas
Upon their backs to bite 'em,
And little fleas have lesser fleas,
And so ad infinitum.”
A fine natural illustration of this principle can be found in the pea aphid Acyrthosiphon pisum, which is infected by a bacterial endosymbiont Hamiltonella defensa, which is in turn infected by the bacteriophage APSE. Only there’s no ad infinitum here – instead, there’s an evolutionary arms race the latest twist in whose story has just been published by Kerry Oliver and colleagues in BMC Biology.
A. pisum, as well as being host to endosymbiotic H. defensa, is also parasitized by the wasp Aphidius ervi, which engages in the gruesome practice of laying eggs in living hosts. This is, as one might imagine, usually terminal for the host, but it’s also where the symbionts come in. When aphids contain symbiotic H. defensa, and those H. defensa contain APSE, the developing wasps are killed and the aphids are saved from an awful fate. This latest study shows that the wasps can fight back: the authors investigated the effects of wasps’ laying multiple eggs in the same aphid (known as “superparasitism”) and found that it’s an effective way to overcome the protection which symbionts confer – probably due to the extra dose of virulence factors which accompany each egg. The more interesting result, however, was that wasps are capable of detecting which aphids have endosymbionts and altering their parasitism strategy accordingly: they’ll tend to lay only a single egg in unprotected aphids, but multiple eggs in those protected by H. defensa. Quite how wasps determine the difference between the two isn’t clear. The authors suggest that they may literally “sniff out” protected aphids, which produce less of a certain alarm pheromone than do unprotected aphids, but whether this is actually the case remains to be seen.
The co-evolutionary “arms race” between hosts and parasites is oft-discussed: indeed, artificial laboratory co-evolution of these very species has been shown to result in increased wasp virulence. This study serves as a reminder that behavioral and biochemical adaptations are all part of the same conflict – and that behavior allows on-the-fly (as it were) adjustments that biochemistry might not.
Posted by Kester Jarvis at 14:30 Comments (0)
Transmissible H5N1 – if they publish, will we perish?
Two influenza research papers remain suspended in press since the US government’s request for their redaction, made on the recommendation of the National Science Advisory Board for Biosecurity (NSABB) late last year. Were this to be upheld, it would be an unprecedented example of censorship of the scientific literature, justified as a necessary measure to protect against bioterror. A comment published in BMC Biology by Peter Doherty and Paul Thomas counters this justification, arguing that although the work raises legitimate safety concerns, full publication of these studies would not add significantly to the vanishingly small risk that influenza might be effectively harnessed to nefarious ends. By contrast, Doherty and Thomas see it as imperative that the research community continue to investigate, without undue impediment, how highly pathogenic avian influenza might adapt to become transmissible in mammals, so that we are better able to monitor and counter the significant risk that this might happen naturally, without any human design or intent.
The arguments against censorship would seem to be gaining momentum. Last week the World Health Organization convened a meeting which brought together a group of influenza researchers and global public health experts with key players: the lead authors of the two papers, representatives of those who funded the work, editors from the journals concerned (Science and Nature), and Paul Keim, chairman of the NSABB. Keim stood by the original recommendation for redaction and the balance of reasoning behind it, but the workability of making the full data available on a “need to know” basis was questioned, and a consensus reached that it would be better to delay publication of the papers until safety concerns were addressed and they could be published in full.
A second outcome of last week’s meeting is an extension of the voluntary moratorium on research to create and study transmissible strains of avian influenza, pending the further discussion of how safety issues should be dealt with. The virus already created in Ron Fouchier’s laboratory was obtained by serial passage in ferrets, is transmitted through the air between their cages, and is highly pathogenic so biosafety issues are an obvious concern; the study demonstrates that such adaptation can occur, could thus occur in nature, and identifies a specific pathway of mutation by which it can occur. The virus created by Yoshihiro Kawaoka is no more pathogenic in ferrets than the H1N1 2009 pandemic virus from which it was derived, but instead of H1, it bears the H5 haemagglutinin molecule of avian H5NA. Both studies show that H5-bearing viruses can be transmissible in mammals and therefore pose a risk to be monitored, and against which we should prepare.
Penelope Austin
Posted by Alice Plane at 11:51 Comments (0)
Post-genomic outlooks on neuropsychiatric disease
Two forward-looking views of research into
neuropsychiatric disease and its treatment are published today in BMC Biology. Aiden Corvin predicts how the identification of susceptibility
genes may transform the diagnosis and treatment of patients who are today
classified as suffering from schizophrenia on the basis of purely clinical
criteria. Kevin Mitchell, Josh Huang, Bita Moghaddam and Akira Sawa assert that it is time to discard behavioral approaches to
modeling psychiatric disorders in animals, and lay out a framework for using
causal genetic variants, together with the latest neurogenetic tools, instead.
Both articles consider recent genetic
advances, and how the identification of rare structural variants that have a
large effect in predisposing people to one or more of these disorders has
challenged previous thinking. Disorders such as schizophrenia, bipolar
disorder and autism are common, and for much of the last 60 years a consensus
has held sway that common diseases, unlike rare Mendelian diseases, are caused
not by mutations of large effect, but by the combined effect of numerous common
variants. Corvin explains how, in the case of schizophrenia, this model was
first assailed by two rare cytogenetic mutations found in the pre-genome era,
followed, in the post-genomic era, by rare copy number variants (short
deletions or duplications) that together account for about 5% of schizophrenia
cases. Both he and Mitchell and colleagues also predict that sequencing
studies are likely to uncover many more rare variants associated with
disease. The two articles take a different view, however, on whether
previous thinking has been completely overturned. Corvin summarizes the recent
findings from genome-wide association studies reflecting the ongoing debate in the
field.
Penelope Austin
Posted by Tara Cronin at 16:20 Comments (1)
'Feed a cold, starve a tumor' – glucose deprivation as a therapy for TSC-related tumors
Tuberous
Sclerosis Complex (TSC) is an autosomal dominant disorder, caused by mutation
in one of the tumor-suppressor genes, TSC1 or TSC2. The condition is characterized by the
formation of multiple non-malignant tumours throughout the brain and other
vital organs of the body, and is prevalent in nearly one million
people worldwide, with symptoms ranging from mild skin abnormalities to
uncontrollable seizures and kidney failure.
In the latest research published in Cell & Bioscience, Jiang et al. demonstrate that the growth and cell proliferation of TSC-related tumors can be inhibited by 2-deoxyglucose (2-DG), which restricts glucose metabolism. In stark contrast, a “carb-free” diet fails to prove effective in reducing tumor growth and leads to increased tumor size.
Csibi and Blenis, in a commentary published in BMC Biology, discuss these new findings and their therapeutic potential:
“Cancer therapy is increasingly shifting toward individualized therapeutic approaches based on the genetic abnormalities exhibited by transformed cells. Jiang et al. demonstrate that targeting glucose addiction is an effective approach for decreasing the growth of tumors driven by TSC mutations. Thus glucose addiction may prove to be the ‘Achilles’ heel’ for the treatment of TSC.”
This research raises questions as to the potential use of 2-DG in treating TSC-tumors, in light of whether the toxic effects of 2-DG can be minimised, and moreover whether this will translate into a therapeutic approach for other tumor types.
Posted by Elizabeth Bal at 15:21 Comments (0)
New evidence for active DNA transposons in somatic cells
Mobile DNA, or transposable elements, constitutes much
of the genome in all organisms. Some elements, retrotransposons, copy themselves
in a two-stage process, first from DNA to RNA by transcription, then from RNA
back to DNA by reverse transcription. By contrast, DNA transposons move via a
simple ‘cut-and-paste’ mechanism, without involving an RNA intermediate.
A major question within the field of mobile DNA is when does most transposition take place? Contrary to the long-standing assumption that all transposition occurs during germ-cell development as opposed to somatic-cell development, a growing body of evidence is emerging for the insertion of mobile elements in somatic cells.
In a recent article published in Mobile DNA, Eickbush and Eickbush report the somatic retrotransposition of R2 elements in the early development of Drosophila. They highlight that transposition events early in development can give rise to both somatic and germline mosaicism, often misinterpreted as germline events in the next generation. This adds to previous findings of the L1 insertions transposition, which has been shown to occur in human and mouse somatic cells.
From an evolutionary perspective, somatic insertion events are ‘dead ends’, in that they are not inherited from one generation to the next, providing no apparent benefit to the re-arrangement of genetic material in this way.
Haig Kazazian, in a commentary published in BMC Biology, discusses this recent evidence for somatic retrotransposition, and the important questions it raises:
“Transposition of mobile DNA can be destructive to gene function and host organisms possess mechanisms for suppressing transposition, especially in the germline. So why does somatic retrotransposition occur? Why don't host controls on retrotransposition block it in early embryogenesis?”
To answer these questions, Kazazian comments that future work will be needed to ascertain the frequency of somatic retrotransposition events in different organisms and tissue types, as well as the stages in which most somatic insertions occur during embryonic development, and their potential role in oncogenesis.
To keep up-to-date with further research and developments in Mobile DNA, please do visit the journal website and sign up for article alerts.
Posted by Elizabeth Bal at 09:29 Comments (0)
Neural Stem Cell focus in Cambridge
BioMed Central attended the Cambridge Neural Stem Cell Symposium last week. The meeting was co-hosted by the Cambridge Stem Cell Initiative to bring together a focus upon the recent advances the of field of neural stem cell biology and to encourage further collaboration and interaction between nearly 300 delegates. This gathering exposed the accelerating pace of discovery in the field of neurogenesis, especially in normal adults, and the role of defects in growth and differentiation in disease. There was much interest amongst the attendees in the recent Stem Cell thematic series published by BioMed Central's flagship journals, BMC Biology, BMC Medicine and Genome Medicine.
An energetic kick-off was delivered in the opening talk by Gerd Kemperman, who reviewed convincing evidence to support the impact of 
exercise on the growth of hippocampal neurons. Several high profile Editorial Board Members of the journal Neural Development were amongst the strong line-up of speakers, including Jonas Frisen, Arturo Alvarez-Buylla, Andrea Brand and Francois Guillemot, as well as the meeting co-organizer, Bill Harris (Editor-in-Chief). The Plenary sessions were also delivered by Neural Development board members Fiona Doetsch (Stem Cell Biology, Cell Specification & Differentiation) and Fred ‘Rusty’ Gage. During the latter session, Fred presented exciting new work showing that LINE-1 retrotransposon “jumping gene” insertion into the adult brain leads to the enrichment of neuronal differentiation.
The event also brought together many students and young scientists in the area, who contributed to workshop presentations and posters. The Editorial Board of Neural Development presented an award for the best poster to Eva Porlan (University of Valencia) for her presentation of N-cadherin-mediated quiescence of subependymal neural stem cells in adult mouse brain. We wish Eva many congratulations on the impressive results of her hard work.
Posted by Helen Whitaker at 13:50 Comments (0)
In an editorial on the debate surrounding the role and abundance of “dark matter” RNA, BMC Biology concluded that we need to know more about the function of specific non-coding RNAs before we can make more general judgments about their role.
So what do we know about ncRNA function so far? Quite a lot – but only about a few of them. Known functional ncRNAs, and the diversity of methods by which they might act, are well-covered by Chris Ponting in a 2009 review. But those dark matter RNAs for which we have a known function and mechanism are hugely outnumbered by those for which we don’t, with less than 100 being well-characterized so far. There are significantly more for which intriguing correlations have been seen – between long ncRNAs and certain cancers, for example (collated in a recent Molecular Cancer review) – but correlation does not equal causation, of course, and for many of these a definitive function or proposed mechanism are missing.
A recent study in malaria discussed this month in BMC Biology provides a tantalizing example. The authors detected long ncRNAs which are present in the pathogenic human blood stage, and further investigation showed that these have some sequence similarity to promoters of the var genes – these encode a family of virulence factors which regularly switch expression to avoid the human immune response, and whose regulation is currently mysterious. But while this is a suggestive and interesting observation, we don’t know anything about the mechanism by which these ncRNAs might act – although this has not inhibited speculation in the article itself and the accompanying BMC Biology commentary. The challenge now will be to turn genomic observations into biochemical insights.
Posted by Kester Jarvis at 15:53 Comments (0)
Genome Medicine’s 250th article: Stuart Orkin launches the stem cell series
The latest editorial in Genome Medicine, written by Guest Editor Stuart Orkin (Dana-Farber Cancer Institute), is the 250th article published in the journal since its launch in 2009. This editorial, published in the June issue, sets the scene for a new thematic series of articles on stem cell genomics. The series aims to highlight key advances in basic and translational research in this evolving field with specially commissioned review and comment articles.
Stuart Orkin introduces the series by discussing recent developments in stem cell genomics and cellular reprogramming, predicting what new insights and therapeutic strategies might emerge in the future.
Kicking off the series, Joanna Wysocka (Stanford University) reviews technological advances that have enabled epigenomic profiling of human pluripotent stem cells, and discusses how the findings could improve our understanding of complex diseases. Mary Majumder (Baylor College of Medicine) muses on the converging themes and areas of concern in shaping policies for research in the stem cell and genomics fields. Genome Medicine’s June issue also features a Research Highlight by George Daley (Children’s Hospital Boston) on the topic of microRNA-based cellular reprogramming. Soon to follow is a Review by Lawrence Goldstein (University of California, San Diego) on the ability of induced pluripotent stem cells to model Alzheimer’s disease and another by Gordon Weir (Harvard Stem Cell Institute) on stem cell approaches for understanding and treating diabetes. William Lensch, who is also affiliated with Harvard Stem Cell Institute, reflects on public perceptions and engagement in stem cell genomics research in an upcoming Musings. All series articles are freely available online.
The series is also featured on a special webpage as part of a cross-journal “Focus on stem cells” alongside related commissioned content from two of our sister journals, BMC Medicine and BMC Biology. The initial contributions to the thematic series have been brought together in a special print collection, which is available at the BioMed Central Booth #908 at the ISSCR meeting happening next week in Toronto – do pick up a copy if you are attending the meeting.
Genome Medicine is now accepting submissions of Research manuscripts offering original translational and clinical insights gained from genome-scale analyses of stem cells, which will be published as part of this ongoing series. Please contact the editors for further details or to submit a presubmission enquiry.
We hope that these articles and future additions to the series will continue to fuel interest in stem cell genomics research and illustrate its importance for translational research and personalized medicine.
Posted by Paraminder Dhillon at 15:44 Comments (0)