PLOS Data Policy: Update

Two months after the implementation of the PLOS journals’ data policy, what have we learned from our authors, reviewers, editors, correspondents, and commenters in the blogosphere?

More than 16,000 manuscripts have been submitted with a data availability statement

In order to optimise the re-use of data by readers and by data miners, authors of all new manuscripts submitted since March 3, 2014 have included a statement about where the data underlying their description of research can be found. At the time of writing, more than 16,000 sets of authors have included information about data availability with their submission. We have had fewer than 10 enquiries per week to from authors who need advice about ‘edge cases’ of data handling and availability – fewer than 1% of authors – and these cases have helped us to further update our FAQ, contributing to a decline in such enquiries over time. We would like to say a huge thankyou to all the authors and editors who have worked with us in this period to iron out wrinkles in our submission processes and helped us make it as easy as possible to capture information about data availability. Special mention is due to the pioneering subset of authors who have already published articles in PLOS journals with a Data Availability Statement, whether all data are provided within the manuscript and its supplementary files or providing links to a domain-specific repository, a non-specific repository or more diverse resources (see Image).


Screen Shot 2014-05-28 at 11 20 28


Some groups of authors still have concerns about data sharing

From our period of increasing public consultation about the PLOS data policy, we knew that at launch we would encounter authors with specific issues in two main areas: firstly, big datasets that are too large for hosting in most repositories (although some, such as the journal GigaScience target precisely this domain), and secondly around patient confidentiality and the associated need to have oversight committees for instances in which access should be restricted to appropriate individuals. Since the launch we have heard these issues raised again, but we have also heard three main arguments used by bloggers and others to justify not sharing the data underlying research articles that we find it hard to agree with. They can be summarised as follows.

It’s mine, I collected it. Most funders and institutions have moved away from this idea, but it persists in the mind of many researchers.

It’s complicated and unique: no-one else could understand it properly This “data as a unique snowflake” argument supposes that no-one other than those who collected the data can understand it enough to re-use it. Taken to an extreme, this argument would tend to suggest that there is no point in peer-reviewing or publishing research at all. We would rather work with those (e.g. BioSharing) who are working to develop standards and approaches to describing data so that it can indeed be used by others.

I’d like to share, but my lab is little and/or under-funded and/or in a lower-income country, and once I share the big guys can jump on the data and do cool things with it before I can do them myself. We of course have sympathy with this perspective, and PLOS journals work specifically with authors in less-developed countries to help them publish their work. However, as noted by panellist Joe DeRisi in a discussion of data sharing at UCSF earlier this month, it would be perverse to suggest that we delay, for example, progress in malaria research in order to allow researchers in the most-affected countries to contribute optimally.

There is one additional argument that has been made, and we acknowledge this one reflects a genuine concern, namely that it takes work to make data sharing-ready. Previously we required all PLOS authors to share data “on request”, but some bloggers have noted that no-one ever requested much of their data, or that when it was requested they in fact refused, whereas now all data should be made ready for sharing, whether ultimately needed or not. We agree that this does require work, however it takes less work to prepare the data at the same time as the publication than was previously required when trying to dig into archives to find material some time later (humorously summarised in a video cartoon). And we would note that increasingly all funders require, as a condition of a grant, that a data-management plan be included, and that this is driving researchers and their institutions to have good systems in place that will meet the criteria of the PLOS policy.

We focused on where, when and how to share, but many are still concerned about what to share

The new PLOS data policy refers to sharing the data underlying a publication, just as our previous policy did. The new part of the policy is to ask for sharing ‘up front’, at the time a manuscript is submitted, rather than subsequently and on request. But an awful lot of the responses to the policy have focussed on the issue of which datasets need to be included. It was not quite as apparent from our prior consultation as it is now: researchers in many fields don’t know which data to archive and share and which should be considered ‘disposable’ moments en route to data worth preserving. Although funders such as NIH and community organisations such as MIBBI try to outline the requirements either generally or specifically, it seems it will be a sisyphean task to provide detailed guidance for every type of experiment in every domain within science. We are therefore currently considering the extent to which we at PLOS can or should aim to provide this type of guidance, and would welcome your input on this issue.

There can be real difficulties about ‘limited sharing’, whether during peer review or after publication. Most repositories, whether subject-specific or general, institutional or international, are set up to allow full open access. But there are two main circumstances in which more limited sharing is appropriate. The first is during peer review, when editors and reviewers need access to the data but the authors may not want it to be public; we are aware of only a few databases (e.g. Dryad) that routinely provide this facility. The second circumstance is when datasets contain sensitive information – whether about patients or, for example, endangered species’ locations -  such that it may be appropriate to share only a subset of the information more widely, and/or to share only with appropriately screened individuals. Several databases and repositories have plans to allow more limited access (e.g. Dataverse, figshare), which should help address concerns in this area, but this is a work in progress. For now, it remains a major challenge for clinical studies to both provide controlled access to the data and preserve patient confidentiality.

There is plenty still to do

The 2014 PLOS data policy deliberately set out to take just one step towards improved integration between the published literature and the data underlying it, by asking authors to say where there data can be found ( that somewhere being not on their own hard drives). We know that much more will be needed before we are dealing with data satisfactorily. For a small minority of commenters, we did not go far enough. For many more, we leave too many open questions, and we agree there are many, most of which are not unique to PLOS and need further community discussion. Among the most pressing, from our perspective:

  • When should an author choose Supplementary Files vs. a repository vs. figures and tables.
  • Should software/code be treated any differently from ‘data’? How should materials-sharing differ?
  • What does peer review of data mean, and should reviewers and editors be paying more attention to data than they did previously, now that they can do so?
  • And getting at the reason why we encourage data sharing: how much data, metadata, and explanation is necessary for replication?
  • A crucial issue that is much wider than PLOS is how to cite data and give academic credit for data reuse, to encourage researchers to make data sharing part of their everyday routine.
  • And for long-term preservation, we must ask who funds the costs of data sharing? What file formats should be acceptable and what will happen in the future with data in obsolete file formats? Is there likely to be universal agreement on how long researchers should store data, given the different current requirements of institutions and funders?

As we continue to work on these issues and others, we would once again welcome your feedback and input, here on the blog, via individual journals, or at

Theo Bloom and Jennifer Lin, for the PLOS Data Policy group.

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This week in PLOS Biology

In PLOS Biology this week you can read about metabolome evolution, protein flexibility and interactions between proteases and their inhibitors.

Image Credit: journal.pone.0041044.g001

Image Credit: journal.pone.0041044.g001

In their new research paper, Katarzyna Bozek, Philipp Khaitovich and colleagues analysed thousands of metabolites from brain, kidney and muscle tissue of humans, chimps and monkeys. They found accelerated evolution of metabolites not only in the human brain – which might be expected – but also human muscle metabolomes. The physiological impact of the surprisingly rapid evolution of human muscle remains unclear, although the authors did do a follow up study testing strength in humans and non-human primates and found human strength was barely half that of primates. Read more in the accompanying synopsis.



Image credit: pbio.1001870

Proteins often interact with other proteins and assemble into complexes.  Joseph Marsh and Sarah Teichmann computationally assessed the structural flexibility of thousands of proteins in their research article, and found that the flexibility of individual proteins aids their evolutionary recruitment into complexes with increasing numbers of distinct subunits. This flexibility becomes increasingly important as a greater number of proteins are packed together within a single complex.



Image credit: pbio.1001869

Proteases (enzymes that break down other proteins) are an important target for drug development, as deregulated protease activity is a common characteristic of many diseases. However we have incomplete understanding of their biology due in part to their complex functions: some activate other proteases whereas some inactivate inhibitors. Network modelling of interactions between proteases and their inhibitors, carried out by Nikolaus Fortelny, Christopher Overall and colleagues reveals a network of new protein connections and cascades in the protease web. They also tested some of the predicted effects in mice.

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This week in PLOS Biology

In PLOS Biology this week you can read about new ways to approach preclinical trials, signaling in the vertebrate retina, how Leishmania adapts to its environment and a protein which can stop bacterial protein synthesis when nutrients are low.

In their Perspective this week, Jonathan Kimmelman, Jeffrey Mogil and Ulrich Dirnagl discuss the recent consternation over the way in which preclinical investigations of new drugs are performed and reported. They argue that we first need to distinguish between ‘exploratory’ investigation - generating robust pathophysiological theories of disease - and ‘translational’ or ‘confirmatory’ investigation, which seeks to demonstrate reproducible effects in animal models. Kimmelman and colleagues say that each type of research requires different study designs and suffers from different validity threats, and that this should be taken into account in research policy.


Image credit: pbio.1001865.

In the vertebrate retina, an interaction between the horizontal cells and photoreceptor cells allows us to remove redundant visual information in space and time, in order optimally see a scene. But how, physiologically, does this work? Rozan Vroman, Maarten Kamermans and colleagues measured current within goldfish cone-horizontal cell synapses to answer this question. They found that the horizontal cells feed back to photoreceptors via both a very fast mechanism and by a relatively slow mechanism. This slow mechanism requires ATP release from the tips of horizontal cell dendrites, followed by hydrolysis of ATP to products that acidify the synaptic cleft. Read more in the accompanying synopsis.

A research article by Jean-Michel Ubeda, Marc Ouellette and colleagues finds that the human parasite Leishmania uses gene rearrangements and repeat-mediated amplification on a genome-wide scale as a strategy to adapt to a changing environment. This means that upon selection with either drugs or culture conditions, a subpopulation can emerge where the amplicon copy number per cell increases and this clone of cells can then expand to dominate the population.


Image credit: pbio.1001866

Typical bacterial cells contain tens of thousands of ribosomes, which make the proteins needed for life. However, during hard times, when nutrients (and therefore amino acids) are low, the cell needs to slam on the brakes.  In their new paper, Boya Feng, Ning Gao and colleagues found that a protein called ObgE can bind to the large subunit of the ribosome, disrupting its association with the small subunit and stopping translation. They suggest that the presence of (p)ppGpp – a chemical made by bacteria in response to low levels of amino acids – causes ObgE to linger on the large subunit longer than it would in its normal role. Read more in the accompanying synopsis.

Category: Biology, Cell biology, Disease, Evolution, Genomics, Infectious disease, Microbiology, Molecular biology, Neuroscience, PLOS Biology, Policy, Research | Leave a comment

This week in PLOS Biology

In PLOS Biology this week you can read about the division of labour between germ cells and soma, the use of RNA interference to study morphogenesis of a giant single-celled organism and a role for RNA mimicry in the assembly of ribosomes.



Image credit: pbio.1001858

Multicellular organisms tend to have a set of cells – the germline – which are responsible for propagating the next generation, and are segregated from the somatic cells that do all the work to keep the body functioning. But what exactly drives this? Heather Goldsby, Benjamin Kerr and co-authors, in their new research article, used experimental evolution of digital organisms to show that the mutagenic side-effects of performing metabolic work can themselves trigger germ-soma differentiation in multicellular organisms. They argue that the soma can afford to perform this ‘dirty work’ while germ cells must keep their DNA pristine for future multicellular offspring. Read more in the accompanying synopsis.



Image credit: pbio.1001861

Mark Slabodnick, Wallace Marshall and colleagues showcase the use of the giant ciliate Stentor coeruleus as a model for studying morphogenesis and regeneration in single-celled organisms. This aquatic filter feeder has remarkably distinct body parts and is known for its ability to regenerate from a tiny part of itself. This study demonstrates that RNA interference can be used to study it and that a kinase regulator protein Mob1 is required for its normal development and regeneration. You can also read more in the accompanying synopsis.



Image credit: pbio.1001860

The Ribosome is a large and very complex molecular machine, found in all living cells and responsible for protein synthesis – the process by which new ribosomes are assembled is similarly complex. In their new research paper, Jérôme Loc’h, Nicolas Leulliot and colleagues determine the structure of the ribosome assembly factor Fap7 bound to a ribosomal protein, revealing that it chaperones a crucial step in the maturation of the nascent ribosome, using RNA mimicry and regulated by ATP hydrolysis.


Category: Biology, Cell biology, Computational biology, Developmental biology, Evolution, Microbiology, Molecular biology, PLOS Biology, Regeneration | Leave a comment

Why Do Scientists Ignore Female Genitalia?

Credit: Roli Roberts, with apologies to Rudolph Zallinger.

Credit: Roli Roberts, adapted from Rudolph Zallinger.

Humans have an odd attitude to genitalia. Indeed, more than 90% of you are reading this blog post merely because I put the word in the title. A new study shows that biologists, being human, also have an odd attitude to genitalia.



Sexual reproduction occurs across most of the animal kingdom, allowing us to shuffle our genes at the poker table of life. And in many cases this occurs by direct physical interaction between two sexes, usually by transfer of sperm from the male to the female via a neatly compatible USB interface known as genitalia.


Unlike the USB, where compatibility is in everyone’s best interests, because of sex’s central role in the evolution of sexual beings, every aspect of it is subject to subversion by strong selective forces, and therefore liable to rapid and apparently capricious change – courtship behaviour, plumage, and even the molecular mechanism that determines whether you’re male or female. But what about genitalia?


Genitalia are also subject to spectacular change, and the assumption is surely that, in the case of two such intimately apposed organs, male and female genitalia should co-evolve, each driven by those motivations that tend to drive other aspects of sex – the male to sow his oats as widely as possible, and the female to be choosy as to how she apportions the costly provisioning of a future infant.


The study of the evolutionary biology of animal genitalia is indeed a vibrant field, but apparently it has a problem. A big one. A paper just published in PLOS Biology reports a survey of hundreds of recent papers and finds that the field is massively biased towards study of male genitalia – almost half of the studies only address males, with most of the remainder looking at both sexes. The bias varies according to the evolutionary model involved, with an explicitly female-driven model (cryptic female choice) being even-handed, but the others being dominated by male-only studies (red):


Sex of genitals studied, by evolutionary model. Ah-King et al.

Sex of genitals studied, by evolutionary model. Ah-King et al.


So what are the reasons for this bias? The authors look at three of the more obvious explanations:


a)      Biological: Female genitalia don’t vary enough to drive evolutionary change.

b)      Practical: They do vary, and do drive evolution, but are devilishly hard to study.

c)       Intellectual: They do vary and drive evolution, and can be studied, but the field is intellectually blinkered.


The authors use examples to argue that the first two explanations are invalid, and that the field is intellectually hobbled by a blind assumption that male genitalia indulge in all sorts of evolutionary shenanigans, but “too often the female is assumed to be an invariant container within which all this presumed scooping, hooking and plunging occurs.” Author Malin Ah-King says  “We found that the most plausible explanation for the bias is the enduring assumptions about the dominant role of males, and unimportance of variation in female genitalia.”


But where do these assumptions come from? Although the tabloid stereotype of the scientist may be of a monkish, geeky male boffin whose real-life encounters with female genitalia are tragically infrequent, clearly many scientists are women. Barron and co show that the gender of the senior author on these papers doesn’t correlate with the genital sex bias, so that simple explanation can be excluded.


The authors are studiously restrained when it comes to speculating as to what might lie behind this bias in the field. Luckily as a blogger, I’m free from academic constraints and can indulge in some cod sociology. Here are some (obvious and intertwined) suggestions:


a) Even in the 21st century there’s a bizarre societal squeamishness about female genitalia that doesn’t apply to male genitalia. This plays out in the media in odd and prurient ways, including a sex bias in the severity of taboo words and a game of “chicken” as to how much one can get away with saying. Could this background be subliminally affecting career choice, study design, funding, or publication decisions? Surely as free-thinking scientists we’re above this sort of thing?

b) It’s easy to imagine a situation, say 50+ years ago, where an influential evolutionary role for females would have been an intellectually challenging concept for a heavily male-dominated and culturally sexist academe. Could this reluctance to acknowledge evolution’s equal opportunity policy have been propagated, via the inherently conservative conduits of textbooks and undergraduate teaching, down the decades?

c) Fields can be dominated by the ideas of one or two highly persuasive individuals or schools of thought. Perhaps one or two big-shots, possibly influenced by one or both of the above cultural issues, or possibly out of a feeling of confidence in their own correctness, put forward models for genital evolution that are still able to hold sway with 21st century men and women?


The likely answer is that it’s a little of all of these – a mixture of cultural milieu and historical contingency (a bit like evolution itself). Can this field be rescued? The authors take us on a whistle-stop tour of some of the more spectacular instances of the role of female genitalia in evolution, and Ah-King hopes “that this analysis can increase the awareness of gender bias and its impeding effects on research, and thereby enable a broadened understanding of genital evolution in the future.”


Read the paper:

“Genital Evolution: Why Are Females Still Understudied?” Malin Ah-King, Andrew B. Barron, Marie E. Herberstein. PLOS Biology DOI: 10.1371/journal.pbio.1001851

Ah-King M, Barron AB, & Herberstein ME (2014). Genital evolution: why are females still understudied? PLoS biology, 12 (5) PMID: 24802812

Category: Biology, Blog, Data, Debate, Evolution, PLOS Biology, Publishing, Research | 1 Comment

This week in PLOS Biology

In PLOS Biology this week you can read research articles about dinosaurs, DNA repairTNFα and neural crest cell migration. We also have an essay on invasive species management and a perspective asking why genital evolution research shows a male bias.



Image credit: pbio.1001854

Most of the dinosaurs went extinct 65 million years ago. However one exceptionally successful lineage is still around today – the birds. Roger Benson, David Evans and colleagues have put forward a possible explanation for their success. The adaptive radiation hypothesis predicts that organisms will diversify into a multitude of new forms, to fill available niches and maintain their evolutionary potential. By estimating the body mass of 426 dinosaur species, Benson and colleagues showed that rapid changes in body size, including dramatic reduction, took place soon after the bird lineage appeared, and that this high potential for diversification has been sustained ever since, allowing them to survive where other dinosaurs failed. Read more about adaptive radiation in the accompanying primer.


Tim Blackburn and colleagues, in their essay this week, call for a more unified approach to classifying alien species. They present a classification system which allows each species to be assigned an impact level – from Minimal to Massive. Currently the management of alien species does not usually take into account the variation of impacts between species and ecosystems, and even cases where there are net benefits to their presence. Limited resources can be better allocated if a more integrated approach is taken.


The neural crest is an important population of migratory cells which in the developing vertebrate give rise to a diverse range of cell types such as bone and smooth muscle. Adam Tuttle, Thomas Schilling and colleagues found, using a zebrafish model, a role for the endosomal protein Rabconnectin-3a in Wnt signalling during neural crest migration, suggesting a role for endosomes in this process.



Image credit: pbio.1001856

Damage to DNA can result in mutations leading to cell death or cancer. Therefore the cell’s mechanisms for repairing DNA are vital. In a new research article this week, Fabio Pessina & Noel Lowndes show the importance of the RSF1 chromatin remodeling protein in facilitating repairs. This protein coordinates the process, so that damaged DNA becomes more accessible to other repair proteins. People with mutations that affect these proteins can have an increased risk of cancer and shortened life span.


A perspective this week by Malin Ah-King, Andrew Barron & Marie Herbertstein asks why the focus of research into the evolution of animal genitalia shows such a strong male bias. They argue that our understanding of genital evolution is hampered by an outdated single-sex bias. Read more in a blog post by PLOS Biology editor Roli Roberts.



Image credit: pbio1001855

Overexpression of tumor necrosis factor alpha (TNFα) is implicated in autoimmune and inflammatory diseases such as inflammatory bowel disease. Therefore anti-TNFα therapies are used in their treatment. However side effects can include the onset of skin diseases psoriasis and lichen planus. Sergio Candel, Victoriano Mulero & colleagues used a zebrafish model to explain the mechanism by which TNFα depletion causes skin inflammation. Some of the players in this feedback loop could potentially be useful in treatment of these skin disorders.



Category: Biology, Cancer, Cell biology, Climate, Debate, Developmental biology, Disease, Ecology, Environment, Evolution, Molecular biology, PLOS Biology | Leave a comment

Cold Spring Harbor Asia Conference on Epigenetics, Chromatin & Transcription: Jin-Qiu Zhou

As part of its mission to encourage engagement within the genetics community, PLOS Genetics is sponsoring a number of conferences and meetings this year. In order to raise awareness about these conferences and the researchers who attend them we are featuring a number of these conferences on Biologue, with posts written by the organizers or PLOS Genetics editors who are involved.

The second of these conferences is the third Cold Spring Harbor Asia Conference on Epigenetics, Chromatin & Transcription, which takes place in Suzhou between the 5th and 9th of May. We hear from Jin-Qiu Zhou, PLOS Genetics Associate Editor and Principal Investigator of the Institute of Biochemistry and Cell Biology, about why he is attending the conference, and the aspects of epigenetics that he finds exciting.

Work in Jin-Qiu Zhou’s Lab

The long-term goal of my lab is to understand the processes by which eukaryotic cells faithfully maintain their chromosomes to avoid chromosomal instability. Currently, most of our work has been focused on the structure, function and replication of telomeres, mainly using baker’s yeast as a model. We use a combination of genetic, biochemical and cell biological approaches to address:


Schematic diagram of dynamic chromatin at telomere and subtelomere. The telomere heterochromatin is defined by Rap1p-dependent Sir complex recruitment. Subtelomeric euchromatin uses multiple strategies to antagonize heterochromatin spreading, including histone H4 acetylation or deactylation, mediated by NuA4 or Rpd3L complex respectively. Chromatin boundaries separate silent and active chromatin. To solve the end replication problem, the telomerase machinery is recruited onto the chromatin end to extend the short telomeres. Image credit: Zhou lab

(1) how telomere length and structure are maintained, and the biological relevance of telomere regulation to genome stability and cellular aging;

(2) how a cell establishes the boundary between the telomere silent chromatin and adjacent active chromatin to prevent the telomeric heterochromatin spreading;

(3) the epigenetic codes and information that are employed when telomere replication or DNA double-strand break occurs;

(4) the molecular basis for telomere-length-dependent or -independent cellular aging.

The CSHA Conference

Epigenetics is the study of heritable changes in gene activity that are not caused by changes in the DNA sequence. It also can be used to describe the study of stable, long-term alterations in the transcriptional potential of a cell that are not necessarily heritable. Unlike simple genetics based on changes to the DNA sequence (the genotype), the changes in gene expression or cellular phenotype of epigenetics have other causes. Examples of mechanisms that produce such changes are DNA methylation and histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. These epigenetic changes may last through cell divisions for the duration of the organism’s life, and may even last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism; instead, non-genetic factors cause the organism’s genes to behave, or “express themselves”, differently (Bird A. 2007 Nature 447: 396).

James Watson Auditorium

The James Watson auditorium. The Suzhou Dushu Lake Conference Center, located by Dushu Lake, is situated in the southeast of SIP Suzhou, 90 km away from Shanghai. The meeting will be held in the James Watson auditorium. Image credit: Biobay

Inaugurated in 2010, Cold Spring Harbor Asia (CSHA) is the Asia-Pacific subsidiary of the New York based Cold Spring Harbor Laboratory (CSHL). As one of CSHL’s world strategies, CSHA’s principal aim is to develop and operate an annual program of scientific conferences in Asia modeled on the Cold Spring Harbor meeting format and style. This program includes large conferences, training workshops and Banbury-style meetings, covering a broad spectrum of biomedical research topics, including molecular biology, molecular genetics, neuroscience, cancer, developmental and cell biology, and plant biology.

The 3rd Cold Spring Harbor Asia Conference on Epigenetics, Chromatin & Transcription, which I will attend, will take place in Suzhou from May 5th to 9th. More than 30 top biologists in epigenetics and transcription have been invited to give talks during the conference, and some interesting works are also selected to be presented as short talks. The conference will include eight oral sessions and two poster sessions covering the latest findings across many topics in epigenetic biology. I hope that every attendee will get inspiration from discussions with new friends and establish collaborations with different labs in the future.

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Detecting cancer-causing genes, computing how to beat jetlag and a review of research into decision-making: The PLOS Comp Biol April issue

Here is our selection of PLOS Computational Biology highlights for April.

Computer-based multi-client game for investigating human group movement. Image credit: Johannes Pritz, Courant Research Centre Evolution of Social Behavior, University of Gõttingen, Germany.

Computer-based multi-client game for investigating human group movement. Image credit: Johannes Pritz, Courant Research Centre Evolution of Social Behavior, University of Gõttingen, Germany.

Computational prediction of cancer-associated single nucleotide polymorphisms (SNPs) from SNP datasets can now be used as a tool for detecting probable cancer-causing genes. This work, by Rituraj Purohit et al., applies computational tools to prioritize the most harmful disease associated mutation in Aurora kinases. Sequence and structural based approaches were used to refine cancer associated mutation, and a long-term simulation (MDS) was applied in order to understand the changes in structural conformation and function of the aurora kinases upon mutation. Out of 60 SNPs, 24 were calculated to be deleterious as well as damaging.

Two papers we published in April received widespread attention in the media. The first paper, by Daniel Forger et al., presents a mathematical model for dealing with the effects of jet lag. By calculating thousands of schedules, the authors show how the human circadian pacemaker is capable of shifting much more rapidly than previously thought, simply by adjusting the timing of the beginning and end of each day. You can read the New Scientist article here.

The second paper to gain attention, by David J. McIver and John S. Brownstein, estimated levels of influenza in America by monitoring Internet traffic on specific Wikipedia articles. The developed model can accurately estimate the percentage of Americans with influenza-like illnesses in real-time. You can read more about it in this article by the Huffington Post

Despite the research that has gone into the workings of decision-making, the neural mechanisms underlying these processes are not fully understood. This Review article by Ranulfo Romo et al. looks at the recent progress made in this field of study and performs a critical evaluation of the available results from a computational perspective. The study was guided by a central question, which was “how does the spatiotemporal structure of sensory stimuli affect the perceptual decision-making process?

Category: Bioinformatics, Biology, Computational biology, News, PLOS Computational Biology, Review, Uncategorized | Tagged | Leave a comment

This week in PLOS Biology

In PLOS Biology this week you can read about a new protein used by the parasite Toxoplasma and how rhodopsin is recycled in the eye.



Image credit: doi: pbio.1001845

Lena Pernas, John C. Boothroyd & colleagues shed new light on the host-pathogen interactions of a globally prevalent and often chronic disease – toxoplasmosis, caused by the parasitic protozoan Toxoplasma gondii. The parasite lives in vacuoles within human cells, and recruits mitochondria to the membranes of the vacuole (the benefit to the parasite is presumed to be a metabolic one). Pernas and colleagues showed that a parasite protein ‘MAF1’ is needed to recruit the mitochondria. MAF1 is only present in two of the toxoplasma strains tested, suggesting that evolutionary niches exist where association with mitochondria is either advantageous or disadvantageous. Also read more in the accompanying synopsis.



Image credit: doi: pbio.1001847

Rhodopsin is a photoresponsive protein found in the cells of the retina which is vital for our perception of light. After it is activated by light it must then be degraded or recycled, but some aspects of the recycling pathway are unclear. In new research published this week, Shiuan Wang, Hugo Bellen & colleagues found that in flies, an evolutionarily conserved protein complex called the retromer is required for the recycling of rhodopsins. Interestingly, when retromer subunits were up-regulated, degeneration of photoreceptor cells could be alleviated in some contexts. This could have potential therapeutic uses if it also works in humans.


Category: Biology, Cell biology, Cell signalling, Disease, Infectious disease, Molecular biology, PLOS Biology, Research | Leave a comment

This week in PLOS Biology

In PLOS Biology this week you can read about a new General Ecosystem Model for predicting the effects of human activities, a global attempt to characterise a protein superfamily and new information about how a vital human transcription factor folds.



Image credit: doi:10.1371/journal.pbio.1001841.g007

Human activities (such as climate change) are causing degradation of ecosystems at an unprecedented rate worldwide. One approach now commonly taken by scientists trying to understand these impacts is to model them mathematically. This week in PLOS Biology, Michael Harfoot, Drew Purves and colleagues make what is really the first attempt at modelling whole ecosystems mechanistically on a global scale – using their ‘General Ecosystem Model’ (GEM). It covers organisms of all sizes and can be simulated at any spatial scale from local to global. By using fundamental ecological processes experienced by all species (e.g. reproducing or being eaten), encoding them mathematically and then simulating the impacts of future scenarios, this GEM has the potential to help us manage key environmental issues better. The model is being released as open source code to allow it to be used and improved upon.


New research by Susan Mashiyama, Patricia Babbitt and colleagues sets out to revolutionise our knowledge of one of the great protein superfamilies: the cytosolic glutathione S-transferases (cytGSTs), whose main role involves making lipophilic (‘fat loving’) toxins soluble, so they can be attacked by other enzymes in the body. The authors made a systematic survey of the current knowledge of more than 13,000 cytGSTs, and then attempted to fill in the gaps regarding their structure and function. The resulting picture is dizzyingly complex, but represents an important first step for the work that lies ahead. Read more in the accompanying synopsis.



Image credit: Kasembeli et al.

Stat3 is a transcription factor that is upregulated in some pathological conditions, including inflammatory diseases and cancer. Moses Kasembeli, David Tweardy and colleagues found that the folding and function of Stat3 are regulated by its interaction with TRiC – a type of protein called a chaperonin, which assist in the folding of other proteins. Manipulation of Stat3′s interaction with TRiC could be explored for therapeutic purposes.


Category: Bioinformatics, Biology, Cancer, Climate, Computational biology, Disease, Ecology, Environment, Evolution, Molecular biology, PLOS Biology, Resources | Leave a comment