<?xml version = '1.0' encoding = 'UTF-8'?>
<?xml-stylesheet href="/rss/styledrssBMC.css" type="text/css"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns="http://purl.org/rss/1.0/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:extra="http://www.biomedcentral.com/xml/schemas/extra/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:cc="http://web.resource.org/cc/">
	<channel rdf:about="http://www.biomedcentral.com/rss">
		<extra:info rdf:parseType="Literal">
			<html:div xmlns:html="http://www.w3.org/1999/xhtml" style="font:14px Verdana, Geneva, Arial, Helvetica, sans-serif">
				<html:span style="font-weight:bold">This is an RSS newsfeed from BioMed Central</html:span>
				<html:br/>
				<html:span style="font-size: 12px;">It is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit <html:br/><html:a href="http://www.biomedcentral.com/info/about/rss/" style="color:#3333CC; font-size:12px;">http://www.biomedcentral.com/info/about/rss/</html:a><html:br/>
				</html:span>
			</html:div>
		</extra:info>
		<title>Genome Biology - Latest articles</title>
		<link>http://genomebiology.com/</link>
		<description>The latest articles from Genome Biology (ISSN 1465-6906) published by 
				
				BioMed Central
		</description>
        <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        <items>
            <rdf:Seq>
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/231"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/108"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/230"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/R133"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/R132"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/109"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/R131"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/R130"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/R129"/>			    
            
				    <rdf:li rdf:resource="http://genomebiology.com/2008/9/8/R128"/>			    
            
            </rdf:Seq>
        </items>
    </channel>  
    
		<item rdf:about="http://genomebiology.com/2008/9/8/231">
            
            <title>Reduced-representation methylation mapping</title>
			<description>The power of massively parallel sequencing has been harnessed to map cytosine methylation patterns in the mouse genome, allowing insights into the relationship of methylation with DNA sequence, histone modifications, transcriptional activity and dynamic changes in methylation status during differentiation.</description>
			<link>http://genomebiology.com/2008/9/8/231</link>
			
			 	<dc:creator>Jeffrey A Jeddeloh, John M Greally and Oliver J Rando</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:231</dc:source>
			<dc:date>2008-09-01</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-231</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>231</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-01</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/108">
            
            <title>Biodefense versus bioterrorism</title>
			<description>Genomics was essential for identifying the source of the deadly anthrax strain released after the September 11 terrorist attacks in the US. The same research that is needed to combat low-probability bioterror attacks is needed to combat high-probability natural infectious agents.</description>
			<link>http://genomebiology.com/2008/9/8/108</link>
			
			 	<dc:creator>Gregory A Petsko</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:108</dc:source>
			<dc:date>2008-09-01</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-108</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>108</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-01</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/230">
            
            <title>The phytochrome red/far-red photoreceptor superfamily</title>
			<description>Proteins of the phytochrome superfamily of red/far-red light receptors have a variety of biological roles in plants, algae, bacteria and fungi and demonstrate a diversity of spectral sensitivities and output signaling mechanisms. Over the past few years the first three-dimensional structures of phytochrome light-sensing domains from bacteria have been determined.</description>
			<link>http://genomebiology.com/2008/9/8/230</link>
			
			 	<dc:creator>Robert A Sharrock</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:230</dc:source>
			<dc:date>2008-08-28</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-230</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>230</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-28</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/R133">
            
            <title>Gene expression regulation in the context of mouse interspecific mosaic genomes</title>
			<description>Background:
There is accumulating evidence pointing to the mosaic nature of the mouse genome. However, little is known about the way the introgressed segments are regulated within the context of the recipient genetic background. To address this question we have screened the testis transcriptome of Interspecific Recombinant Congenic mouse Strains (IRCS), containing segments of Mus spretus origin at a homozygous state in a Mus musculus background. 
Results:
Most genes (75%) were not transcriptionally modified either in IRCS or in the parental spretus mice, compared to musculus. The expression level of most of the remaining transcripts were "dictated" by either musculus transcription factors ("trans-driven", 20%), or spretus cis acting elements ("cis-driven", 4%). Finally 1% of transcripts was dysregulated following a cis-trans mismatch. We observed a higher sequence divergence between M. spretus and M. musculus promoters of strongly dysregulated genes, than in promoters of similarly expressed genes. 
Conclusion:
Our study indicates that it is possible to classify the molecular events leading to expressional alterations when a homozygous graft of foreign genome segments is made in an interspecific host genome. The inadequacy of transcription factors of this host genome to recognize the foreign targets was clearly the major path leading to dysregulation.</description>
			<link>http://genomebiology.com/2008/9/8/R133</link>
			
			 	<dc:creator>David L'Hote, Catherine Serres, Reiner A Veitia, Xavier Montagutelli, Ahmad Oulmouden and Daniel Vaiman</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:R133</dc:source>
			<dc:date>2008-08-27</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-r133</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>R133</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-27</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/R132">
            
            <title>Preferential regulation of duplicated genes by microRNAs in mammals</title>
			<description>Background:
Although recent advances have been made in identifying and analyzing instances of microRNA-mediated gene regulation, it remains unclear by what mechanisms attenuation of transcript expression through microRNAs becomes an integral part of post-transcriptional modification, and it is even less clear to what extent this process occurs for mammalian gene duplicates (paralogs). Specifically, while mammalian paralogs are known to overcome their initial complete functional redundancy through variation in regulation and expression, the potential involvement of microRNAs in this process has not been investigated.
Results:
We comprehensively investigated the impact of microRNA-mediated posttranscriptional regulation on duplicated genes in human and mouse. Using predicted targets derived from several analysis methods, we report the following observations. (i) microRNA targets are significantly enriched for duplicate genes, implying their roles in the differential regulation of paralogs. (ii) On average duplicate microRNA target genes have longer 3'UTRs than singleton targets, and are regulated by more microRNA species, suggesting a more sophisticated mode of regulation. (iii) Ancient duplicates were more likely to be regulated by microRNAs and on average have greater expression divergence than recent duplicates. (iv) Ancient duplicate genes share fewer ancestral microRNA regulators, and recent duplicate genes share more common regulating microRNAs.   
Conclusions:
Collectively these results demonstrate that microRNAs comprise an important element in evolving the regulatory patterns of mammalian paralogs. We further present an evolutionary model in which microRNAs not only adjust imbalanced dosage effects created by gene duplication, but also help maintain long-term buffering of the phenotypic consequences of gene deletion or ablation.</description>
			<link>http://genomebiology.com/2008/9/8/R132</link>
			
			 	<dc:creator>Jingjing Li, Gabriel Musso and Zhaolei Zhang</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:R132</dc:source>
			<dc:date>2008-08-26</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-r132</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>R132</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/109">
            
            <title>Isolated populations and complex disease gene identification</title>
			<description>The utility of genetically isolated populations (population isolates) in the mapping and identification of genes is not only limited to the study of rare diseases; isolated populations also provide a useful resource for studies aimed at improved understanding of the biology underlying common diseases and their component traits. Well characterized human populations provide excellent study samples for many different genetic investigations, ranging from genome-wide association studies to the characterization of interactions between genes and the environment.</description>
			<link>http://genomebiology.com/2008/9/8/109</link>
			
			 	<dc:creator>Kati Kristiansson, Jussi Naukkarinen and Leena Peltonen</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:109</dc:source>
			<dc:date>2008-08-26</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-109</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>109</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/R131">
            
            <title>Molecular evolution of neuropeptides in the genus Drosophila</title>
			<description>Background:
Neuropeptides are the most diverse group of neuronal signaling molecules. They often occur as multiple sequence-related copies within single precursors (the prepropeptides). These multiple sequence-related copies have not arisen by gene duplication, and it is debated whether they are mutually redundant or serve specific functions. The fully sequenced genomes of 12 Drosophila species provide a unique opportunity to study the molecular evolution of neuropeptides. 
Results:
We data-mined the 12 Drosophila genomes for homologs of neuropeptide genes identified in D. melanogaster. We then predicted peptide precursors and the neuropeptidome, and biochemically identified about half of the predicted peptides by direct mass spectrometric profiling of neuroendocrine tissue in four species covering main phylogenetic lines of Drosophila. We found that all species have an identical neuropeptidome and peptide hormone complement. Calculation of amino acid distances showed that ortholog peptide copies are highly sequence-conserved between species, whereas the observed sequence variability between peptide copies within single precursors must have occurred prior to the divergence of the Drosophila species.
Conclusions:
We provide a first genomic and chemical characterization of fruit fly neuropeptides outside D. melanogaster. Our results suggest that neuropeptides including multiple peptide copies are under stabilizing selection, which suggests that multiple peptide copies are functionally important and not dispensable. The last common ancestor of Drosophila obviously had a set of neuropeptides and peptide hormones identical to that of modern fruit flies. This is remarkable, since drosophilid flies have adapted to very different environments.</description>
			<link>http://genomebiology.com/2008/9/8/R131</link>
			
			 	<dc:creator>Christian Wegener and Anton Gorbashov</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:R131</dc:source>
			<dc:date>2008-08-21</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-r131</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>R131</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-21</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/R130">
            
            <title>Global transcriptome analysis reveals circadian regulation of key pathways in plant growth and development</title>
			<description>Background:
As non-motile organisms, plants must rapidly adapt to ever-changing environmental conditions, including those caused by daily light/dark cycles.  One important mechanism for anticipating and preparing for such predictable changes is the circadian clock.  Nearly all organisms have circadian oscillators that, when they are in phase with the Earth's rotation, provide a competitive advantage.  In order to understand how circadian clocks benefit plants, it is necessary to identify the pathways and processes that are clock-controlled.
Results:
We have integrated information from multiple circadian microarray experiments performed on Arabidopsis thaliana to better estimate the fraction of the plant transcriptome that is circadian regulated.  Analyzing the promoters of clock-controlled genes, we identified circadian clock regulatory elements correlated with phase-specific transcript accumulation.  We have also identified several physiological pathways enriched for clock-regulated changes in transcript abundance, suggesting they may be modulated by the circadian clock.  
Conclusions:
Our analysis suggests that transcript abundance of roughly one third of expressed Arabidopsis thaliana genes is circadian regulated.  We found four promoter elements, enriched in the promoters of genes with four discrete phases, which may contribute to the time-of-day specific changes in the transcript abundance of these genes.  Clock-regulated genes are over-represented among all of the classical plant hormone and multiple stress response pathways, suggesting all of these pathways are influenced by the circadian clock.  Further exploration of the links between the clock and these pathways will lead to a better understanding of how the circadian clock affects plant growth and leads to improved fitness.</description>
			<link>http://genomebiology.com/2008/9/8/R130</link>
			
			 	<dc:creator>Michael F Covington, Julin N Maloof, Marty Straume, Steve A Kay and Stacey L Harmer</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:R130</dc:source>
			<dc:date>2008-08-18</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-r130</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>R130</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-18</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/R129">
            
            <title>Integrative analyses of genetic variation in enzyme activities of primary carbohydrate metabolism reveal distinct modes of regulation in Arabidopsis thaliana</title>
			<description>Background:
Plant primary carbohydrate metabolism is complex and flexible, and is regulated at many levels. Changes of transcript levels do not always lead to changes in enzyme activities, and these do not always affect metabolite levels and fluxes. To analyze interactions between these three levels of function, we have performed parallel genetic analyses of 15 enzyme activities involved in primary carbohydrate metabolism, transcript levels for their encoding structural genes, and a set of relevant metabolites. Quantitative analyses of each trait were performed in the Arabidopsis thaliana Ler x Cvi recombinant inbred line (RIL) population and subjected to correlation and quantitative trait locus (QTL) analysis.
Results:
Traits affecting primary metabolism were often correlated, possibly due to developmental control affecting multiple genes, enzymes, or metabolites. Moreover, the activity QTLs of several enzymes co-localized with the expression QTLs (eQTLs) of their structural genes, or with metabolite accumulation QTLs of their substrates or products. In addition, many trait-specific QTLs were identified, revealing that there is also specific regulation of individual metabolic traits. Regulation of enzyme activities often occurred through multiple loci, involving both cis- and trans-acting transcriptional or post-transcriptional control of structural genes, as well as independently of the structural genes.
Conclusion:
Future studies of the regulatory processes in primary carbohydrate metabolism will benefit from an integrative genetic analysis of gene transcription, enzyme activity, and metabolite content. The multiparallel QTL analyses of the various interconnected transducers of biological information flow, described here for the first time, can assist in determining the cause and consequences of genetic regulation at different levels of complex biological systems.</description>
			<link>http://genomebiology.com/2008/9/8/R129</link>
			
			 	<dc:creator>Joost JB Keurentjes, Ronan Sulpice, Yves Gibon, Marie-Caroline Steinhauser, Jingyuan Fu, Maarten Koornneef, Mark Stitt and Dick Vreugdenhil</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:R129</dc:source>
			<dc:date>2008-08-18</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-r129</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>R129</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-18</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://genomebiology.com/2008/9/8/R128">
            
            <title>MotifCluster: An interactive online tool for clustering and visualizing sequences using shared motifs</title>
			<description>MotifCluster finds related motifs in a set of sequences and clusters the sequences into families using the motifs they contain. MotifCluster, at http://bmf.colorado.edu/motifcluster, lets users test whether proteins are related, cluster sequences by shared conserved motifs, and visualize motifs mapped onto trees, sequences and 3D structures. We demonstrate MotifCluster's accuracy using gold-standard protein superfamilies; using recommended settings, families were assigned to the correct superfamilies with 0.17% false positive and no false negative assignments.</description>
			<link>http://genomebiology.com/2008/9/8/R128</link>
			
			 	<dc:creator>Micah Hamady, Jeremy Widmann, Shelley D Copley and Rob Knight</dc:creator>
			
			<dc:source>Genome Biology 2008, 9:R128</dc:source>
			<dc:date>2008-08-15</dc:date>
			<dc:identifier>doi:10.1186/gb-2008-9-8-r128</dc:identifier>
			
			
							
					<prism:publicationName>Genome Biology</prism:publicationName>
					
			
							
					<prism:issn>1465-6906</prism:issn>
					
			
							
					<prism:volume>9</prism:volume>
					
			
							
					<prism:startingPage>R128</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-15</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
		
    <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
         <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction"/>
         <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution"/>
         <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks"/>
	</cc:License>
</rdf:RDF>
