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        <title>Editor's picks</title>
        <link>http://www.biomedcentral.com/bmcbiol/</link>
        <description>The editor's pick of recent articles published by BMC Biology</description>
        <dc:date>2012-05-31T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7007/10/47" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7007/10/45" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7007/10/44" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7007/10/42" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7007/10/41" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7007/10/39" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7007/10/38" />
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/10/47">
        <title>Phylogenomics supports microsporidia as the earliest diverging clade of sequenced fungi.</title>
        <description>Background:
Microsporida is one of the taxa that have experienced the most dramatic taxonomic reclassifications. Once thought to be among the earliest diverging eukaryotes, the fungal nature of this group of intracellular pathogens is now widely accepted. However, the specific position of microsporidia within the fungal tree of life is still debated. Due to the presence of accelerated evolutionary rates, phylogenetic analyses involving microsporidia are prone to methodological artifacts such as long-branch attraction, especially when taxon sampling is limited.
Results:
Here we exploit the recent availability of six complete microsporidian genomes to re-assess the long-standing question of their phylogenetic position. We show that microsporidians have a similar low level of conservation of gene neighborhood with other groups of fungi when controlling for the confounding effects of recent segmental duplications. A combined analysis of thousands of gene trees supports a topology in which microsporidia is sister group to all other sequenced fungi. Moreover, this topology received increased support when less informative trees were discarded. This position of microsporidia was also strongly supported based on the combined analysis of 53 concatenated genes, and was robust to filters controlling for rate heterogeneity, compositional bias, long branch attraction, and heterotachy.
Conclusions:
Altogether, our data strongly support a scenario in which microsporidia is the earliest-diverging clade of sequenced fungi.</description>
        <link>http://www.biomedcentral.com/1741-7007/10/47</link>
                <dc:creator>Salvador Capella-Gutierrez</dc:creator>
                <dc:creator>Marina Marcet-Houben</dc:creator>
                <dc:creator>Toni Gabaldon</dc:creator>
                <dc:source>BMC Biology 2012, 10:47</dc:source>
        <dc:date>2012-05-31T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                            <dc:title>Establishing the phylogenetic position of Microsporidia</dc:title>
                            <dc:description>The evolutionary history of the parasitic microsporidia has always been hard to pin down, and although they are now established as fungi their precise position is still debated. A rigorous analysis of five recently-released genomes supports their positioning as a sister taxon to the rest of the fungal clade.</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>10</prism:volume>
        <prism:startingPage>47</prism:startingPage>
        <prism:publicationDate>2012-05-31T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/10/45">
        <title>Monoaminergic modulation of photoreception in ascidian:  Evidence for a proto-hypothalamo-retinal territory </title>
        <description>Background:
The retina of craniates/vertebrates has been proposed to derive from a photoreceptor prosencephalic territory in ancestral chordates, but the evolutionary origin of the different cell types making the retina is disputed. Except for photoreceptors, the existence of homologs of retinal cells remains uncertain outside vertebrates.
Results:
We show that many molecular characteristics of dopamine-synthesizing cells located in the vicinity of photoreceptors in the sensory vesicle of the ascidian Ciona intestinalis are similar to these of amacrine dopamine cells of the vertebrate retina. The ascidian dopamine cells share with vertebrate amacrine cells the expression of the key-transcription factor Ptf1a, as well as that of dopamine-synthesizing enzymes. Surprisingly, the ascidian dopamine cells accumulate serotonin via a functional serotonin transporter, as some amacrine cells also do. Moreover, dopamine cells located in the vicinity of the photoreceptors modulate the light-off induced swimming behavior of ascidian larvae by acting on alpha2-like receptors, instead of dopamine receptors, supporting a role in the modulation of the photic response. These cells are located in a territory of the ascidian sensory vesicle expressing genes found both in the retina and the hypothalamus of vertebrates (six3/6, Rx, meis, pax6, visual cycle proteins).
Conclusion:
We propose that the dopamine cells of the ascidian larva derive from an ancestral multifunctional cell population located in the periventricular, photoreceptive field of the anterior neural tube of chordates, which also give rise to both anterior hypothalamus and retina in craniates/vertebrates. It also shows that the existence of multiple cell types associated with photic responses predates the formation of the vertebrate retina.</description>
        <link>http://www.biomedcentral.com/1741-7007/10/45</link>
                <dc:creator>Florian Razy-Krajka</dc:creator>
                <dc:creator>Euan Brown</dc:creator>
                <dc:creator>Takeo Horie</dc:creator>
                <dc:creator>Jacques Callebert</dc:creator>
                <dc:creator>Yasunori Sasakura</dc:creator>
                <dc:creator>Jean-Stephane Joly</dc:creator>
                <dc:creator>Takehiro Kusakabe</dc:creator>
                <dc:creator>Philippe Vernier</dc:creator>
                <dc:source>BMC Biology 2012, 10:45</dc:source>
        <dc:date>2012-05-29T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7007-10-45</dc:identifier>
                            <dc:title>Evolution of the vertebrate retina</dc:title>
                            <dc:description>A string of remarkable similarities between dopamine-synthesizing cells that modulate the photic responses of ascidian larvae, and amacrine cells of the vertebrate retina, suggests a common evolutionary origin from ancestral cells in the photoreceptive field of the anterior neural tube of chordates.</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>10</prism:volume>
        <prism:startingPage>45</prism:startingPage>
        <prism:publicationDate>2012-05-29T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/10/44">
        <title>MAVS ubiquitination by the E3 ligase TRIM25 and degradation by the proteasome is involved in type I Interferon production after activation of the antiviral RIG-I-Like receptors</title>
        <description>Background:
During a viral infection, the intracellular RIG-I-like receptors (RLRs) sense viral RNA and signal through the mitochondrial antiviral signaling adaptor MAVS (also known as IPS-1, Cardif and VISA) whose activation triggers a rapid production of type I interferons (IFN) and of pro-inflammatory cytokines through the transcription factors IRF3/IRF7 and NF-kappaB, respectively. While MAVS is essential for this signaling and known to operate through the scaffold protein NEMO and the protein kinase TBK1 that phosphorylates IRF3, its mechanism of action and regulation remain unclear.
Results:
We report here that RLR activation triggers MAVS ubiquitination on lysine 7 and 10 by the E3 ubiquitin ligase TRIM25 and marks it for proteasomal degradation concomitantly with downstream signaling. Inhibition of this MAVS degradation with a proteasome inhibitor does not affect NF-kappaB signaling but it hampers IRF3 activation, and NEMO and TBK1, two essential mediators in type I IFN production, are retained at the mitochondria.
Conclusions:
These results suggest that MAVS functions as a recruitment platform that assembles a signaling complex involving NEMO and TBK1, and that the proteasome-mediated MAVS degradation is required to release the signaling complex into the cytosol, allowing IRF3 phosphorylation by TBK1.</description>
        <link>http://www.biomedcentral.com/1741-7007/10/44</link>
                <dc:creator>Celine Castanier</dc:creator>
                <dc:creator>Naima Zemirli</dc:creator>
                <dc:creator>Alain Portier</dc:creator>
                <dc:creator>Dominique Garcin</dc:creator>
                <dc:creator>Nicolas Bidere</dc:creator>
                <dc:creator>Aime Vazquez</dc:creator>
                <dc:creator>Damien Arnoult</dc:creator>
                <dc:source>BMC Biology 2012, 10:44</dc:source>
        <dc:date>2012-05-24T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7007-10-44</dc:identifier>
                            <dc:title>Dynamics of intracellular antiviral responses</dc:title>
                            <dc:description>A number of proteins are now known to sense viral infection in cells and signal antiviral responses. Studies by Damien Arnoult and colleagues suggest that the interferon response involves the sequential assembly and proteasomal dissolution of a signalling complex at the mitochondrial surface.</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>10</prism:volume>
        <prism:startingPage>44</prism:startingPage>
        <prism:publicationDate>2012-05-24T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/10/42">
        <title>Q&amp;amp;A: &apos;Toxic&apos; effects of sugar: should we be afraid of fructose?</title>
        <description>No abstract. First Paragraph:Carbohydrate is an essential component of our diet. What about fructose? Can we live without any fructose intake?Glucose is unequivocally a central component of human energy metabolism. It constitutes the nearly exclusive energy fuel for the brain, since neurons lack the enzymes required for fatty acid oxidation. The only exception to this exclusive glucose metabolism in the brain is starvation, when  the expression of monocarboxylate transporters increases in brain cells, which then become able to use the ketone bodies (beta-hydroxybutyric acid and aceto-acetic acid) produced by the liver. As a consequence of this exclusive reliance on glucose for brain metabolism, intricate hormonal and neural mechanisms have evolved to maintain a constant level of glucose in the blood.</description>
        <link>http://www.biomedcentral.com/1741-7007/10/42</link>
                <dc:creator>Luc Tappy</dc:creator>
                <dc:source>BMC Biology 2012, 10:42</dc:source>
        <dc:date>2012-05-21T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7007-10-42</dc:identifier>
                            <dc:title>Fructose and metabolic disorders - is there a link?</dc:title>
                            <dc:description>Before the colonial era of sugar plantations we consumed, on average, about 15-fold less fructose than we do today. Luc Tappy explains, in question and answer format, the special features of fructose metabolism and discusses the evidence that high fructose intake has contributed to the current epidemic of obesity and metabolic disease.</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>10</prism:volume>
        <prism:startingPage>42</prism:startingPage>
        <prism:publicationDate>2012-05-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/10/41">
        <title>Mending walls</title>
        <description>First paragraph (this article has no abstract)Before I built a wall I&apos;d ask to knowWhat I was walling in or walling out-	Robert Frost, &apos;Mending Wall&apos;In rural New England, as in much of the rest of the world, people mark their territory, like some race of architecturally-adept spaniels, by building a wall around its borders. In some cases this is done for defensive purposes. In others, it is meant to keep in something that should not be allowed to roam freely (spaniels again, perhaps). But much of the time it is simply there to say, &apos;this is mine, not yours.&apos;</description>
        <link>http://www.biomedcentral.com/1741-7007/10/41</link>
                <dc:creator>Gregory A Petsko</dc:creator>
                <dc:source>BMC Biology 2012, 10:41</dc:source>
        <dc:date>2012-05-11T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7007-10-41</dc:identifier>
                            <dc:title>Mending walls (not)</dc:title>
                            <dc:description>The real topic of Gregory Petsko&apos;s Comment in our Metabolism diet and disease series is not, despite its title, mending walls, but patterns of comorbidity that argue for cross-disciplinary research: obesity and cancer are linked, for example, but apparently not if you are also schizophrenic.</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>10</prism:volume>
        <prism:startingPage>41</prism:startingPage>
        <prism:publicationDate>2012-05-11T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/10/39">
        <title>A never ending race for new and improved fluorescent proteins</title>
        <description>Bioluminescent and fluorescent proteins are now used as tools for research in all organisms. There has been massive progress over the past 15 years in creating a palette of fluorescent proteins with a wide spectrum of specific properties. One of the big challenges is to decide which variant may be best for a certain application. A recent article by Mann et al. in BMC Biotechnology describes a new orange fluorescent protein in plants.See research article http://www.biomedcentral.com/1472-6750/12/17</description>
        <link>http://www.biomedcentral.com/1741-7007/10/39</link>
                <dc:creator>Alexander M Jones</dc:creator>
                <dc:creator>David W Ehrhardt</dc:creator>
                <dc:creator>Wolf B Frommer</dc:creator>
                <dc:source>BMC Biology 2012, 10:39</dc:source>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7007-10-39</dc:identifier>
                            <dc:title>Visualizing proteins in plants</dc:title>
                            <dc:description>Visualizing proteins in plants requires stable expression of fluorescent proteins, with brightness able to overcome the autofluorescence of chlorophyll.  Wolf Frommer and colleagues provide a broad overview of what makes an optimal fluorophore and evaluate the virtues of a novel orange fluorescent protein described recently in BMC Biotechnology.</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>10</prism:volume>
        <prism:startingPage>39</prism:startingPage>
        <prism:publicationDate>2012-05-03T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/10/38">
        <title>Canalization of the evolutionary trajectory of the human influenza virus</title>
        <description>Background:
Since its emergence in 1968, influenza A (H3N2) has evolved extensively in genotype and antigenic phenotype.  However, despite strong pressure to evolve away from human immunity and to diversify in antigenic phenotype, H3N2 influenza shows paradoxically limited genetic and antigenic diversity present at any one time.  Here, we propose a simple model of antigenic evolution in the influenza virus that accounts for this apparent discrepancy.
Results:
This model displays rapid evolution but low standing diversity and simultaneously accounts for the epidemiological, genetic, antigenic and geographical patterns displayed by the virus.  In this model, antigenic phenotype is represented by a N-dimensional vector and virus mutations perturb phenotype within this continuous Euclidean space.  We implement this model in a large-scale individual-based simulation, and in doing so, find a remarkable correspondence between model behavior and observed influenza dynamics.  We find that evolution away from existing human immunity results in rapid population turnover in the influenza virus and that this population turnover occurs primarily along a single antigenic axis.
Conclusions:
Selective dynamics induce a canalized evolutionary trajectory, in which the evolutionary fate of the influenza population is surprisingly repeatable.  In the model, the influenza population shows a 1-2 year timescale of repeatability, suggesting a window in which evolutionary dynamics could be, in theory, predictable.</description>
        <link>http://www.biomedcentral.com/1741-7007/10/38</link>
                <dc:creator>Trevor Bedford</dc:creator>
                <dc:creator>Andrew Rambaut</dc:creator>
                <dc:creator>Mercedes Pascual</dc:creator>
                <dc:source>BMC Biology 2012, 10:38</dc:source>
        <dc:date>2012-04-30T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7007-10-38</dc:identifier>
                            <dc:title>&quot;Short sighted&quot; influenza lacks diversity</dc:title>
                            <dc:description>The influenza virus evolves rapidly, but this doesn&apos;t usually lead to a genetically diverse population as one might expect. A new model suggests how short-term selection to avoid human immune responses could cause this long-term lack of diversity.</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>10</prism:volume>
        <prism:startingPage>38</prism:startingPage>
        <prism:publicationDate>2012-04-30T00:00:00Z</prism:publicationDate>
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