[Bioperl-l] Bio::Biblio::IO copyright parsing
Chris Fields
cjfields at illinois.edu
Fri Jul 23 15:08:03 EDT 2010
You should file this as a bug, along with the output. My guess is it has to do with character encoding, but not sure.
chris
On Jul 23, 2010, at 1:54 PM, Yulia Bushmanova wrote:
> Sorry, first email had wrong file attached
>
> Yulia
>
> Yulia Bushmanova wrote:
>> Hi All,
>>
>> I was trying to parse Pubmed xml with Bio::Biblio::IO (v.1.006001) and got following error:
>>
>> not well-formed (invalid token) at line 32, column 48, byte 3095 at /usr/lib/perl5/XML/Parser.pm line 187
>>
>> Looks like parser complains on the copyright sign, if I manually remove it from file parsing goes fine. XML::Parser is version 2.36.
>>
>> Any ideas on how to deal with this error?
>>
>> Thanks in advance,
>> Yulia
>
> <?xml version="1.0"?>
> <!DOCTYPE PubmedArticleSet PUBLIC "-//NLM//DTD PubMedArticle, 1st January 2010//EN" "http://www.ncbi.nlm.nih.gov/corehtml/query/DTD/pubmed_100301.dtd">
> <PubmedArticleSet>
> <PubmedArticle>
> <MedlineCitation Owner="NLM" Status="Publisher">
> <PMID>20643054</PMID>
> <DateCreated>
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> </DateCreated>
> <Article PubModel="Print">
> <Journal>
> <ISSN IssnType="Electronic">1542-0086</ISSN>
> <JournalIssue CitedMedium="Internet">
> <Volume>99</Volume>
> <Issue>2</Issue>
> <PubDate>
> <Year>2010</Year>
> <Month>Jul</Month>
> <Day>21</Day>
> </PubDate>
> </JournalIssue>
> <Title>Biophysical journal</Title>
> </Journal>
> <ArticleTitle>Bimodal Analysis Reveals a General Scaling Law Governing Nondirected and Chemotactic Cell Motility.</ArticleTitle>
> <Pagination>
> <MedlinePgn>367-376</MedlinePgn>
> </Pagination>
> <Abstract>
> <AbstractText>Cell motility is a fundamental process with relevance to embryonic development, immune response, and metastasis. Cells move either spontaneously, in a nondirected fashion, or in response to chemotactic signals, in a directed fashion. Even though they are often studied separately, both forms of motility share many complex processes at the molecular and subcellular scale, e.g., orchestrated cytoskeletal rearrangements and polarization. In addition, at the cellular level both types of motility include persistent runs interspersed with reorientation pauses. Because there is a great range of variability in motility among different cell types, a key challenge in the field is to integrate these multiscale processes into a coherent framework. We analyzed the motility of Dictyostelium cells with bimodal analysis, a method that compares time spent in persistent versus reorientation mode. Unexpectedly, we found that reorientation time is coupled with persistent time in an inverse correlation and, surprisingly, the inverse correlation holds for both nondirected and chemotactic motility, so that the full range of Dictyostelium motility can be described by a single scaling relationship. Additionally, we found an identical scaling relationship for three human cell lines, indicating that the coupling of reorientation and persistence holds across species and making it possible to describe the complexity of cell motility in a surprisingly general and simple manner. With this new perspective, we analyzed the motility of Dictyostelium mutants, and found four in which the coupling between two modes was altered. Our results point to a fundamental underlying principle, described by a simple scaling law, unifying mechanisms of eukaryotic cell motility at several scales.</AbstractText>
> <CopyrightInformation>Copyright © 2010 Biophysical Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
> </Abstract>
> <Affiliation>Department of Pharmacology, Vanderbilt University, Nashville, Tennessee.</Affiliation>
> <AuthorList>
> <Author>
> <LastName>Gruver</LastName>
> <ForeName>J Scott</ForeName>
> <Initials>JS</Initials>
> </Author>
> <Author>
> <LastName>Potdar</LastName>
> <ForeName>Alka A</ForeName>
> <Initials>AA</Initials>
> </Author>
> <Author>
> <LastName>Jeon</LastName>
> <ForeName>Junhwan</ForeName>
> <Initials>J</Initials>
> </Author>
> <Author>
> <LastName>Sai</LastName>
> <ForeName>Jiqing</ForeName>
> <Initials>J</Initials>
> </Author>
> <Author>
> <LastName>Anderson</LastName>
> <ForeName>Bridget</ForeName>
> <Initials>B</Initials>
> </Author>
> <Author>
> <LastName>Webb</LastName>
> <ForeName>Donna</ForeName>
> <Initials>D</Initials>
> </Author>
> <Author>
> <LastName>Richmond</LastName>
> <ForeName>Ann</ForeName>
> <Initials>A</Initials>
> </Author>
> <Author>
> <LastName>Quaranta</LastName>
> <ForeName>Vito</ForeName>
> <Initials>V</Initials>
> </Author>
> <Author>
> <LastName>Cummings</LastName>
> <ForeName>Peter T</ForeName>
> <Initials>PT</Initials>
> </Author>
> <Author>
> <LastName>Chung</LastName>
> <ForeName>Chang Y</ForeName>
> <Initials>CY</Initials>
> </Author>
> </AuthorList>
> <Language>ENG</Language>
> <PublicationTypeList>
> <PublicationType>JOURNAL ARTICLE</PublicationType>
> </PublicationTypeList>
> </Article>
> <MedlineJournalInfo>
> <MedlineTA>Biophys J</MedlineTA>
> <NlmUniqueID>0370626</NlmUniqueID>
> <ISSNLinking>0006-3495</ISSNLinking>
> </MedlineJournalInfo>
> </MedlineCitation>
> <PubmedData>
> <History>
> <PubMedPubDate PubStatus="received">
> <Year>2009</Year>
> <Month>12</Month>
> <Day>17</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="revised">
> <Year>2010</Year>
> <Month>3</Month>
> <Day>9</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="accepted">
> <Year>2010</Year>
> <Month>3</Month>
> <Day>11</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="entrez">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>21</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="pubmed">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>21</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="medline">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>21</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> </History>
> <PublicationStatus>ppublish</PublicationStatus>
> <ArticleIdList>
> <ArticleId IdType="pii">S0006-3495(10)00710-1</ArticleId>
> <ArticleId IdType="doi">10.1016/j.bpj.2010.03.073</ArticleId>
> <ArticleId IdType="pubmed">20643054</ArticleId>
> </ArticleIdList>
> </PubmedData>
> </PubmedArticle>
>
>
> <PubmedArticle>
> <MedlineCitation Owner="NLM" Status="Publisher">
> <PMID>20640912</PMID>
> <DateCreated>
> <Year>2010</Year>
> <Month>7</Month>
> <Day>19</Day>
> </DateCreated>
> <Article PubModel="Print-Electronic">
> <Journal>
> <ISSN IssnType="Electronic">1420-9071</ISSN>
> <JournalIssue CitedMedium="Internet">
> <PubDate>
> <Year>2010</Year>
> <Month>Jul</Month>
> <Day>18</Day>
> </PubDate>
> </JournalIssue>
> <Title>Cellular and molecular life sciences : CMLS</Title>
> </Journal>
> <ArticleTitle>Redundant and unique roles of coronin proteins in Dictyostelium.</ArticleTitle>
> <Pagination>
> <MedlinePgn/>
> </Pagination>
> <Abstract>
> <AbstractText>Dictyostelium discoideum harbors a short (CRN12) and a long coronin (CRN7) composed of one and two beta-propellers, respectively. They are primarily present in the cell cortex and cells lacking CRN12 (corA (-)) or CRN7 (corB (-)) have defects in actin driven processes. We compared the characteristics of a mutant cell line (corA (-) /corB (-)) lacking CRN12 and CRN7 with the single mutants focusing on cytokinesis, phagocytosis, chemotaxis and development. Cytokinesis, uptake of small particles, and developmental defects were not enhanced in the corA (-) /corB (-) strain as compared to the single mutants, whereas motility and phagocytosis of yeast particles were more severely impaired. It appears that although both proteins affect the same processes they do not act in a redundant manner. Rather, they often act antagonistically, which is in accordance with their proposed roles in the actin cytoskeleton where CRN12 acts in actin disassembly whereas CRN7 stabilizes actin filaments and protects them from disassembly.</AbstractText>
> </Abstract>
> <Affiliation>Institute for Biochemistry I, Center for Molecular Medicine Cologne (CMMC) and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Medical Faculty, University of Cologne, 50931, Cologne, Germany.</Affiliation>
> <AuthorList>
> <Author>
> <LastName>Shina</LastName>
> <ForeName>Maria C</ForeName>
> <Initials>MC</Initials>
> </Author>
> <Author>
> <LastName>Müller-Taubenberger</LastName>
> <ForeName>Annette</ForeName>
> <Initials>A</Initials>
> </Author>
> <Author>
> <LastName>Unal</LastName>
> <ForeName>Can</ForeName>
> <Initials>C</Initials>
> </Author>
> <Author>
> <LastName>Schleicher</LastName>
> <ForeName>Michael</ForeName>
> <Initials>M</Initials>
> </Author>
> <Author>
> <LastName>Steinert</LastName>
> <ForeName>Michael</ForeName>
> <Initials>M</Initials>
> </Author>
> <Author>
> <LastName>Eichinger</LastName>
> <ForeName>Ludwig</ForeName>
> <Initials>L</Initials>
> </Author>
> <Author>
> <LastName>Müller</LastName>
> <ForeName>Rolf</ForeName>
> <Initials>R</Initials>
> </Author>
> <Author>
> <LastName>Blau-Wasser</LastName>
> <ForeName>Rosemarie</ForeName>
> <Initials>R</Initials>
> </Author>
> <Author>
> <LastName>Glöckner</LastName>
> <ForeName>Gernot</ForeName>
> <Initials>G</Initials>
> </Author>
> <Author>
> <LastName>Noegel</LastName>
> <ForeName>Angelika A</ForeName>
> <Initials>AA</Initials>
> </Author>
> </AuthorList>
> <Language>ENG</Language>
> <PublicationTypeList>
> <PublicationType>JOURNAL ARTICLE</PublicationType>
> </PublicationTypeList>
> <ArticleDate DateType="Electronic">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>18</Day>
> </ArticleDate>
> </Article>
> <MedlineJournalInfo>
> <MedlineTA>Cell Mol Life Sci</MedlineTA>
> <NlmUniqueID>9705402</NlmUniqueID>
> <ISSNLinking>1420-682X</ISSNLinking>
> </MedlineJournalInfo>
> </MedlineCitation>
> <PubmedData>
> <History>
> <PubMedPubDate PubStatus="received">
> <Year>2010</Year>
> <Month>2</Month>
> <Day>3</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="accepted">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>5</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="revised">
> <Year>2010</Year>
> <Month>5</Month>
> <Day>23</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="aheadofprint">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>18</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="entrez">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="pubmed">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="medline">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> </History>
> <PublicationStatus>aheadofprint</PublicationStatus>
> <ArticleIdList>
> <ArticleId IdType="doi">10.1007/s00018-010-0455-y</ArticleId>
> <ArticleId IdType="pubmed">20640912</ArticleId>
> </ArticleIdList>
> </PubmedData>
> </PubmedArticle>
>
>
> <PubmedArticle>
> <MedlineCitation Owner="NLM" Status="Publisher">
> <PMID>20639697</PMID>
> <DateCreated>
> <Year>2010</Year>
> <Month>7</Month>
> <Day>19</Day>
> </DateCreated>
> <Article PubModel="Print-Electronic">
> <Journal>
> <ISSN IssnType="Electronic">1554-8635</ISSN>
> <JournalIssue CitedMedium="Internet">
> <Volume>6</Volume>
> <Issue>6</Issue>
> <PubDate>
> <Year>2010</Year>
> <Month>Aug</Month>
> <Day>22</Day>
> </PubDate>
> </JournalIssue>
> <Title>Autophagy</Title>
> </Journal>
> <ArticleTitle>A second signal for autophagic cell death?</ArticleTitle>
> <Pagination>
> <MedlinePgn/>
> </Pagination>
> <Abstract>
> <AbstractText>Dictyostelium cells in monolayers in vitro lend themselves well to a study of autophagic cell death (ACD). There is no apoptosis machinery in the protist Dictyostelium, no caspase nor Bcl-2 family members (except a paracaspase whose inactivation does not alter cell death), thus there is no apoptosis that could interfere with, or substitute for, nonapoptotic cell death. Also, Dictyostelium, a eukaryote, has a haploid genome, which facilitates random insertional mutagenesis.</AbstractText>
> </Abstract>
> <Affiliation>Centre d'Immunologie de Marseille-Luminy, Faculté des Sciences de Luminy, Aix Marseille Université, Marseille, France; Institut National de la Santé et de la Recherche Médicale U631, Marseille, France; Centre National de la Recherche Scientifique Unité Mixte de Recherche, Marseille, France.</Affiliation>
> <AuthorList>
> <Author>
> <LastName>Giusti</LastName>
> <ForeName>Corinne</ForeName>
> <Initials>C</Initials>
> </Author>
> <Author>
> <LastName>Luciani</LastName>
> <ForeName>Marie-Françoise</ForeName>
> <Initials>MF</Initials>
> </Author>
> <Author>
> <LastName>Golstein</LastName>
> <ForeName>Pierre</ForeName>
> <Initials>P</Initials>
> </Author>
> </AuthorList>
> <Language>ENG</Language>
> <PublicationTypeList>
> <PublicationType>JOURNAL ARTICLE</PublicationType>
> </PublicationTypeList>
> <ArticleDate DateType="Electronic">
> <Year>2010</Year>
> <Month>8</Month>
> <Day>22</Day>
> </ArticleDate>
> </Article>
> <MedlineJournalInfo>
> <MedlineTA>Autophagy</MedlineTA>
> <NlmUniqueID>101265188</NlmUniqueID>
> <ISSNLinking>1554-8627</ISSNLinking>
> </MedlineJournalInfo>
> </MedlineCitation>
> <PubmedData>
> <History>
> <PubMedPubDate PubStatus="entrez">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="pubmed">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="medline">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> </History>
> <PublicationStatus>aheadofprint</PublicationStatus>
> <ArticleIdList>
> <ArticleId IdType="pii">12750</ArticleId>
> <ArticleId IdType="pubmed">20639697</ArticleId>
> </ArticleIdList>
> </PubmedData>
> </PubmedArticle>
>
>
> <PubmedArticle>
> <MedlineCitation Owner="NLM" Status="Publisher">
> <PMID>20626455</PMID>
> <DateCreated>
> <Year>2010</Year>
> <Month>7</Month>
> <Day>19</Day>
> </DateCreated>
> <Article PubModel="Print-Electronic">
> <Journal>
> <ISSN IssnType="Electronic">1462-2920</ISSN>
> <JournalIssue CitedMedium="Internet">
> <PubDate>
> <Year>2010</Year>
> <Month>Jul</Month>
> <Day>7</Day>
> </PubDate>
> </JournalIssue>
> <Title>Environmental microbiology</Title>
> </Journal>
> <ArticleTitle>The global regulator Crc modulates metabolism, susceptibility to antibiotics and virulence in Pseudomonas aeruginosa.</ArticleTitle>
> <Pagination>
> <MedlinePgn/>
> </Pagination>
> <Abstract>
> <AbstractText>Summary The capacity of a bacterial pathogen to produce a disease in a treated host depends on the former's virulence and resistance to antibiotics. Several scattered pieces of evidence suggest that these two characteristics can be influenced by bacterial metabolism. This potential relationship is particularly important upon infection of a host, a situation that demands bacteria adapt their physiology to their new environment, making use of newly available nutrients. To explore the potential cross-talk between bacterial metabolism, antibiotic resistance and virulence, a Pseudomonas aeruginosa model was used. This species is an important opportunistic pathogen intrinsically resistant to many antibiotics. The role of Crc, a global regulator that controls the metabolism of carbon sources and catabolite repression in Pseudomonas, was analysed to determine its contribution to the intrinsic antibiotic resistance and virulence of P. aeruginosa. Using proteomic analyses, high-throughput metabolic tests and functional assays, the present work shows the virulence and antibiotic resistance of this pathogen to be linked to its physiology, and to be under the control (directly or indirectly) of Crc. A P. aeruginosa strain lacking the Crc regulator showed defects in type III secretion, motility, expression of quorum sensing-regulated virulence factors, and was less virulent in a Dictyostelium discoideum model. In addition, this mutant strain was more susceptible to beta-lactams, aminoglycosides, fosfomycin and rifampin. Crc might therefore be a good target in the search for new antibiotics.</AbstractText>
> </Abstract>
> <Affiliation>Departamento de Biotecnología Microbiana, Centro Nacional de Biotecnología, CSIC, Darwin 3, Cantoblanco, 28049 Madrid, Spain.</Affiliation>
> <AuthorList>
> <Author>
> <LastName>Linares</LastName>
> <ForeName>Juan F</ForeName>
> <Initials>JF</Initials>
> </Author>
> <Author>
> <LastName>Moreno</LastName>
> <ForeName>Renata</ForeName>
> <Initials>R</Initials>
> </Author>
> <Author>
> <LastName>Fajardo</LastName>
> <ForeName>Alicia</ForeName>
> <Initials>A</Initials>
> </Author>
> <Author>
> <LastName>Martínez-Solano</LastName>
> <ForeName>Laura</ForeName>
> <Initials>L</Initials>
> </Author>
> <Author>
> <LastName>Escalante</LastName>
> <ForeName>Ricardo</ForeName>
> <Initials>R</Initials>
> </Author>
> <Author>
> <LastName>Rojo</LastName>
> <ForeName>Fernando</ForeName>
> <Initials>F</Initials>
> </Author>
> <Author>
> <LastName>Martínez</LastName>
> <ForeName>José L</ForeName>
> <Initials>JL</Initials>
> </Author>
> </AuthorList>
> <Language>ENG</Language>
> <PublicationTypeList>
> <PublicationType>JOURNAL ARTICLE</PublicationType>
> </PublicationTypeList>
> <ArticleDate DateType="Electronic">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>07</Day>
> </ArticleDate>
> </Article>
> <MedlineJournalInfo>
> <MedlineTA>Environ Microbiol</MedlineTA>
> <NlmUniqueID>100883692</NlmUniqueID>
> <ISSNLinking>1462-2912</ISSNLinking>
> </MedlineJournalInfo>
> </MedlineCitation>
> <PubmedData>
> <History>
> <PubMedPubDate PubStatus="entrez">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>15</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="pubmed">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>16</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="medline">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>16</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> </History>
> <PublicationStatus>aheadofprint</PublicationStatus>
> <ArticleIdList>
> <ArticleId IdType="pii">EMI2292</ArticleId>
> <ArticleId IdType="doi">10.1111/j.1462-2920.2010.02292.x</ArticleId>
> <ArticleId IdType="pubmed">20626455</ArticleId>
> </ArticleIdList>
> </PubmedData>
> </PubmedArticle>
>
>
> <PubmedArticle>
> <MedlineCitation Owner="NLM" Status="Publisher">
> <PMID>20624437</PMID>
> <DateCreated>
> <Year>2010</Year>
> <Month>7</Month>
> <Day>20</Day>
> </DateCreated>
> <Article PubModel="Print-Electronic">
> <Journal>
> <ISSN IssnType="Electronic">1873-5169</ISSN>
> <JournalIssue CitedMedium="Internet">
> <PubDate>
> <Year>2010</Year>
> <Month>Jul</Month>
> <Day>16</Day>
> </PubDate>
> </JournalIssue>
> <Title>Peptides</Title>
> </Journal>
> <ArticleTitle>Synthesis and biological activity of peptides equivalent to the IP22 repeat motif found in proteins from Dictyostelium and Mimivirus.</ArticleTitle>
> <Pagination>
> <MedlinePgn/>
> </Pagination>
> <Abstract>
> <AbstractText>A novel IP22 repeat motif of unknown function was discovered previously that comprises almost the entire structure of cmbB, a calmodulin-binding protein from Dictyostelium discoideum. An analysis of over 2000 IP22 repeats across 130 different proteins from different species allowed us to define a prototypical IP22 repeat: I/LPxxhxxhxhxxxhxxxhxxxx (where L=leucine, I=isoleucine, h=any hydrophobic amino acid, x=any amino acid). Here we describe the synthesis of three peptide variants of the IP22 motif: IP22-1 (IPNSVTSLKFGDGFNQPLTPGT; 22aa); IP22-2 (LPSTLKTISLSNSTDKKIFKNS; 22aa); and, IP22-3 (IPKSLRSLFLGKGYNQPLEF; 20aa) plus a control peptide from the N-term of cmbB (HNMNPFSPQLDEKKNSHIVEY; 21aa). The structure and purity of synthesized peptides were verified by HPLC and mass spectrometry. The peptides all dose-dependently enhanced random cell motility and cAMP-mediated chemotaxis in Dictyostelium but IP22-3 was most effective peaking in activity around 50muM. Fluorescein isothiocyanate (FITC)-conjugated IP22 peptides did not penetrate cells suggesting these peptides affect cell motility via cell surface interactions. Treatment of cells with FITC-IP22 peptides also led to enhanced cell motility equivalent to the non-conjugated peptides. Treatment of IP22-3-stimulated cells with 50muM LY294002, 20muM quinacrine or both suggests that IP22-3 requires both phosphoinositol 3-kinase and phospholipase A2 signaling to elicit its effects, a mechanism unique from EGFL motility enhancing peptides. The mechanism of action and potential uses of IP22 repeat peptides are discussed.</AbstractText>
> <CopyrightInformation>Copyright © 2010. Published by Elsevier Inc.</CopyrightInformation>
> </Abstract>
> <Affiliation>Department of Cell and Systems Biology, University of Toronto at Mississauga, Mississauga, Ontario, Canada, L5L 1C6; Department of Biology, University of Toronto at Mississauga, 3359 Mississauga rd. N., Mississauga, Ontario, Canada, L5L 1C6.</Affiliation>
> <AuthorList>
> <Author>
> <LastName>Catalano</LastName>
> <ForeName>Andrew</ForeName>
> <Initials>A</Initials>
> </Author>
> <Author>
> <LastName>Luo</LastName>
> <ForeName>Wei</ForeName>
> <Initials>W</Initials>
> </Author>
> <Author>
> <LastName>Wang</LastName>
> <ForeName>Yali</ForeName>
> <Initials>Y</Initials>
> </Author>
> <Author>
> <LastName>O'Day</LastName>
> <ForeName>Danton H</ForeName>
> <Initials>DH</Initials>
> </Author>
> </AuthorList>
> <Language>ENG</Language>
> <PublicationTypeList>
> <PublicationType>JOURNAL ARTICLE</PublicationType>
> </PublicationTypeList>
> <ArticleDate DateType="Electronic">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>16</Day>
> </ArticleDate>
> </Article>
> <MedlineJournalInfo>
> <MedlineTA>Peptides</MedlineTA>
> <NlmUniqueID>8008690</NlmUniqueID>
> <ISSNLinking>0196-9781</ISSNLinking>
> </MedlineJournalInfo>
> </MedlineCitation>
> <PubmedData>
> <History>
> <PubMedPubDate PubStatus="received">
> <Year>2010</Year>
> <Month>6</Month>
> <Day>22</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="revised">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>3</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="accepted">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>5</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="entrez">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>14</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="pubmed">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>14</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="medline">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>14</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> </History>
> <PublicationStatus>aheadofprint</PublicationStatus>
> <ArticleIdList>
> <ArticleId IdType="pii">S0196-9781(10)00300-1</ArticleId>
> <ArticleId IdType="doi">10.1016/j.peptides.2010.07.005</ArticleId>
> <ArticleId IdType="pubmed">20624437</ArticleId>
> </ArticleIdList>
> </PubmedData>
> </PubmedArticle>
>
>
> <PubmedArticle>
> <MedlineCitation Owner="NLM" Status="In-Process">
> <PMID>20617172</PMID>
> <DateCreated>
> <Year>2010</Year>
> <Month>07</Month>
> <Day>09</Day>
> </DateCreated>
> <Article PubModel="Electronic">
> <Journal>
> <ISSN IssnType="Electronic">1553-7404</ISSN>
> <JournalIssue CitedMedium="Internet">
> <Volume>6</Volume>
> <PubDate>
> <Year>2010</Year>
> </PubDate>
> </JournalIssue>
> <Title>PLoS genetics</Title>
> <ISOAbbreviation>PLoS Genet.</ISOAbbreviation>
> </Journal>
> <ArticleTitle>Variation, sex, and social cooperation: molecular population genetics of the social amoeba Dictyostelium discoideum.</ArticleTitle>
> <Pagination>
> <MedlinePgn>e1001013</MedlinePgn>
> </Pagination>
> <Abstract>
> <AbstractText>Dictyostelium discoideum is a eukaryotic microbial model system for multicellular development, cell-cell signaling, and social behavior. Key models of social evolution require an understanding of genetic relationships between individuals across the genome or possibly at specific genes, but the nature of variation within D. discoideum is largely unknown. We re-sequenced 137 gene fragments in wild North American strains of D. discoideum and examined the levels and patterns of nucleotide variation in this social microbial species. We observe surprisingly low levels of nucleotide variation in D. discoideum across these strains, with a mean nucleotide diversity (pi) of 0.08%, and no strong population stratification among North American strains. We also do not find any clear relationship between nucleotide divergence between strains and levels of social dominance and kin discrimination. Kin discrimination experiments, however, show that strains collected from the same location show greater ability to distinguish self from non-self than do strains from different geographic areas. This suggests that a greater ability to recognize self versus non-self may arise among strains that are more likely to encounter each other in nature, which would lead to preferential formation of fruiting bodies with clonemates and may prevent the evolution of cheating behaviors within D. discoideum populations. Finally, despite the fact that sex has rarely been observed in this species, we document a rapid decay of linkage disequilibrium between SNPs, the presence of recombinant genotypes among natural strains, and high estimates of the population recombination parameter rho. The SNP data indicate that recombination is widespread within D. discoideum and that sex as a form of social interaction is likely to be an important aspect of the life cycle.</AbstractText>
> </Abstract>
> <Affiliation>Department of Biology and Center for Genomics and Systems Biology, New York University, New York, New York, United States of America.</Affiliation>
> <AuthorList CompleteYN="Y">
> <Author ValidYN="Y">
> <LastName>Flowers</LastName>
> <ForeName>Jonathan M</ForeName>
> <Initials>JM</Initials>
> </Author>
> <Author ValidYN="Y">
> <LastName>Li</LastName>
> <ForeName>Si I</ForeName>
> <Initials>SI</Initials>
> </Author>
> <Author ValidYN="Y">
> <LastName>Stathos</LastName>
> <ForeName>Angela</ForeName>
> <Initials>A</Initials>
> </Author>
> <Author ValidYN="Y">
> <LastName>Saxer</LastName>
> <ForeName>Gerda</ForeName>
> <Initials>G</Initials>
> </Author>
> <Author ValidYN="Y">
> <LastName>Ostrowski</LastName>
> <ForeName>Elizabeth A</ForeName>
> <Initials>EA</Initials>
> </Author>
> <Author ValidYN="Y">
> <LastName>Queller</LastName>
> <ForeName>David C</ForeName>
> <Initials>DC</Initials>
> </Author>
> <Author ValidYN="Y">
> <LastName>Strassmann</LastName>
> <ForeName>Joan E</ForeName>
> <Initials>JE</Initials>
> </Author>
> <Author ValidYN="Y">
> <LastName>Purugganan</LastName>
> <ForeName>Michael D</ForeName>
> <Initials>MD</Initials>
> </Author>
> </AuthorList>
> <Language>eng</Language>
> <PublicationTypeList>
> <PublicationType>Journal Article</PublicationType>
> <PublicationType>Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
> </PublicationTypeList>
> <ArticleDate DateType="Electronic">
> <Year>2010</Year>
> <Month>07</Month>
> <Day>01</Day>
> </ArticleDate>
> </Article>
> <MedlineJournalInfo>
> <Country>United States</Country>
> <MedlineTA>PLoS Genet</MedlineTA>
> <NlmUniqueID>101239074</NlmUniqueID>
> <ISSNLinking>1553-7390</ISSNLinking>
> </MedlineJournalInfo>
> <CitationSubset>IM</CitationSubset>
> <OtherID Source="NLM">PMC2895654</OtherID>
> </MedlineCitation>
> <PubmedData>
> <History>
> <PubMedPubDate PubStatus="received">
> <Year>2010</Year>
> <Month>3</Month>
> <Day>15</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="accepted">
> <Year>2010</Year>
> <Month>6</Month>
> <Day>1</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="epublish">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>1</Day>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="entrez">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>10</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="pubmed">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>10</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="medline">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>10</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> </History>
> <PublicationStatus>epublish</PublicationStatus>
> <ArticleIdList>
> <ArticleId IdType="doi">10.1371/journal.pgen.1001013</ArticleId>
> <ArticleId IdType="pubmed">20617172</ArticleId>
> <ArticleId IdType="pmc">PMC2895654</ArticleId>
> </ArticleIdList>
> </PubmedData>
> </PubmedArticle>
>
>
> <PubmedArticle>
> <MedlineCitation Owner="NLM" Status="Publisher">
> <PMID>20610381</PMID>
> <DateCreated>
> <Year>2010</Year>
> <Month>7</Month>
> <Day>8</Day>
> </DateCreated>
> <Article PubModel="Print-Electronic">
> <Journal>
> <ISSN IssnType="Electronic">1083-351X</ISSN>
> <JournalIssue CitedMedium="Internet">
> <PubDate>
> <Year>2010</Year>
> <Month>Jul</Month>
> <Day>7</Day>
> </PubDate>
> </JournalIssue>
> <Title>The Journal of biological chemistry</Title>
> </Journal>
> <ArticleTitle>Expression of actin Tyr53Ala in Dictyostelium disrupts the cytoskeleton and inhibits intracellular and intercellular chemotactic-signaling.</ArticleTitle>
> <Pagination>
> <MedlinePgn/>
> </Pagination>
> <Abstract>
> <AbstractText>We showed previously that phosphorylation of Tyr-53, or its mutation to Ala, inhibits actin polymerization in vitro with formation of aggregates of short filaments, and that expression of Y53A-actin in Dictyostelium blocks differentiation and development at the mound stage (Liu et al. (2006) Proc. Natl. Acad. Sci. U.S.A. 103, 13694-13699; Liu et al. (2010) J. Biol. Chem. 285, 9729-9739). We now show that expression of Y53A-actin, which does not affect cell growth, phagocytosis or pinocytosis, inhibits the formation of head-to-tail cell streams during cAMP-induced aggregation, although individual amoebae chemotax normally. We show that expression of Y53A-actin causes a 50% reduction of cell-surface cAMP-receptors, and inhibits cAMP-induced increases in adenylyl cyclase A activity, phosphorylation of ERK2 and actin polymerization. Trafficking of vesicles containing adenylyl cyclase A to the rear of the cell and secretion of the ACA-vesicles are also inhibited. The actin cytoskeleton of cells expressing Y53A-actin is characterized by numerous short filaments, and bundled and aggregated filaments similar to the structures formed by copolymerization of purified Y53A-actin and wild-type actin in vitro. This disorganized actin cytoskeleton may be responsible for the inhibition of intracellular and intercellular cAMP signaling in cells expressing F-Y/A-actin.</AbstractText>
> </Abstract>
> <Affiliation>NHLBI, NIH, United States;</Affiliation>
> <AuthorList>
> <Author>
> <LastName>Shu</LastName>
> <ForeName>Shi</ForeName>
> <Initials>S</Initials>
> </Author>
> <Author>
> <LastName>Liu</LastName>
> <ForeName>Xiong</ForeName>
> <Initials>X</Initials>
> </Author>
> <Author>
> <LastName>Kriebel</LastName>
> <ForeName>Paul W</ForeName>
> <Initials>PW</Initials>
> </Author>
> <Author>
> <LastName>Hong</LastName>
> <ForeName>Myoung-Soon</ForeName>
> <Initials>MS</Initials>
> </Author>
> <Author>
> <LastName>Daniels</LastName>
> <ForeName>Mathew P</ForeName>
> <Initials>MP</Initials>
> </Author>
> <Author>
> <LastName>Parent</LastName>
> <ForeName>Carole A</ForeName>
> <Initials>CA</Initials>
> </Author>
> <Author>
> <LastName>Korn</LastName>
> <ForeName>Edward D</ForeName>
> <Initials>ED</Initials>
> </Author>
> </AuthorList>
> <Language>ENG</Language>
> <PublicationTypeList>
> <PublicationType>JOURNAL ARTICLE</PublicationType>
> </PublicationTypeList>
> <ArticleDate DateType="Electronic">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>7</Day>
> </ArticleDate>
> </Article>
> <MedlineJournalInfo>
> <MedlineTA>J Biol Chem</MedlineTA>
> <NlmUniqueID>2985121R</NlmUniqueID>
> <ISSNLinking>0021-9258</ISSNLinking>
> </MedlineJournalInfo>
> </MedlineCitation>
> <PubmedData>
> <History>
> <PubMedPubDate PubStatus="entrez">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>9</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="pubmed">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>9</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> <PubMedPubDate PubStatus="medline">
> <Year>2010</Year>
> <Month>7</Month>
> <Day>9</Day>
> <Hour>6</Hour>
> <Minute>0</Minute>
> </PubMedPubDate>
> </History>
> <PublicationStatus>aheadofprint</PublicationStatus>
> <ArticleIdList>
> <ArticleId IdType="pii">M110.116277</ArticleId>
> <ArticleId IdType="doi">10.1074/jbc.M110.116277</ArticleId>
> <ArticleId IdType="pubmed">20610381</ArticleId>
> </ArticleIdList>
> </PubmedData>
> </PubmedArticle>
>
>
> </PubmedArticleSet>
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