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    <responseDate>2026-10-11T09:16:46Z</responseDate>
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    <identifier>10.57760/sciencedb.11423</identifier>
    <datestamp>2024-07-29T11:32:55Z</datestamp>
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<oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:date>2024-07-29</dc:date>
  <dc:title>Two-component system UhpAB facilitates the pathogenicity of avian pathogenic Escherichia coli through biofilm formation and stress responses</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.11423</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>Avian pathogenic Escherichia coli&amp;nbsp;(APEC) is an important zoonotic pathogen that infects avian species by colonizing the gastrointestinal, respiratory, or&amp;nbsp;reproductive tracts, leading to significant economic losses to the poultry industry worldwide and threatening food security and human health. APEC has evolved the two-component signal transduction system&amp;nbsp;(TCS) to adapt and respond to extracellular&amp;nbsp;environmental stresses, which are produced the host invaded by APEC. Here we focus on the effect of the UhpAB TCS on the pathogenicity of APEC. The results in this study showed that the UhpAB system contributed to the pathogenicity of APEC in animal infection model. The electrophoretic mobility shift assays&amp;nbsp;(EMSA) confirmed that UhpAB specifically bound to the promoters&amp;nbsp;of fepG, ldrD, ycgV, and ydeI,&amp;nbsp;and&amp;nbsp;activated their expression&amp;nbsp;using&amp;nbsp;real-time reverse transcription PCR (real-time RT-PCR) experiments. Furthermore, the UhpAB TCS could promote biofilm formation by activating the expression of biofilm master transcriptional regulator encoding gene csgD&amp;nbsp;and enhence stress tolerence&amp;nbsp;by activating the expression of stress protein encoding genes uspA&amp;nbsp;and bhsA,&amp;nbsp;thereby assisting APEC to evade host immune reponses and inflammatory responses, and&amp;nbsp;increasing the pathogenicity&amp;nbsp;of APEC. These&amp;nbsp;findings&amp;nbsp;deepen our understanding&amp;nbsp;of&amp;nbsp;the pathogenic&amp;nbsp;mechanism&amp;nbsp;in&amp;nbsp;APEC&amp;nbsp;and offer new perspectives for further studies on the prevention and&amp;nbsp;control of APEC infection.</dc:description>
  <dc:subject>avian pathogenic Escherichia coli; UhpAB; biofilm formation; stress tolerence; pathogenicity</dc:subject>
  <dc:creator>Lumin Yu</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by-nc/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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