<?xml version='1.0'?>
<!DOCTYPE art SYSTEM 'http://www.biomedcentral.com/xml/article.dtd'>
<art>
   <ui>gb-spotlight-20020715-02</ui>
   <ji>GBJ</ji>
   <fm>
      <dochead>Research news</dochead>
      <bibl>
         <title>
            <p>DOG patrol</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Weitzman</snm>
               <mi>B</mi>
               <fnm>Jonathan</fnm>
               <email>jonathanweitzman@hotmail.com</email>
            </au>
         </aug>
         <source>Genome Biology</source>
         <issn>1465-6906</issn>
         <pubdate>2002</pubdate>
         <volume>3</volume>
         <fpage>spotlight-20020715-02</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/gb-spotlight-20020715-02</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>15</day>
               <month>7</month>
               <year>2002</year>
            </date>
         </pub>
      </history>
      <cpyrt>
         <year>2002</year>
         <collab>BioMed Central Ltd</collab>
      </cpyrt>
      <shortabs>
         <p>A helicase protein, named DOG-1, is important for maintaining the stability of guanine-rich tracts of DNA.</p>
      </shortabs>
   </fm>
   <meta>
      <classifications>
         <classification type="news" subtype="status">Archive</classification>
      </classifications>
   </meta>
   <bdy>
      <sec>
         <st>
            <p/>
         </st>
         <p>The importance of maintaining <abbr bid="B1">genome integrity</abbr> is highlighted by diseases that arise upon loss of the mechanisms that ensure correct DNA replication and repair. In an Advanced Online Publication in <abbr bid="B2"><it>Nature Genetics</it></abbr>, Cheung <it>et al.</it> describe a mutator phenotype in <it>Caenorhabditis elegans</it> that is associated with deletions in polyguanine tracts and is caused by disruption of a new gene that they have nicknamed <it>dog</it>-1 (for deletions of guanine-rich DNA) (<it>Nature Genetics </it>8 July 2002, DOI:10.1038/ng928). The <it>dog</it>-1 gene encodes a protein containing a DEAH helicase domain. Disruptions within the <it>dog</it>-1 gene, or RNAi experiments, led to variable deletions of G-rich tracts around the <it>C. elegans</it> genome, without affecting other repeat structures or telomeres. Deletions were generally observed in tracts containing more than 22 guanine nucleotides. Cheung <it>et al.</it> propose that DOG-1 is important for resolving secondary structures of G-rich DNA and predict that homologs may exist in other species.</p>
      </sec>
   </bdy>
   <bm>
      <refgrp>
         <bibl id="B1">
            <note>Genome maintenance mechanisms for preventing cancer.</note>
            <xrefbib>
               <pubid idtype="pmpid" link="fulltext">11357144</pubid>
            </xrefbib>
         </bibl>
         <bibl id="B2">
            <url>http://www.nature.com/ng/</url>
            <note>
               <it>Nature Genetics</it>
            </note>
         </bibl>
      </refgrp>
   </bm>
</art>
