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        <identifier>oai:figshare.com:article/33809251</identifier>
        <datestamp>2026-09-15T17:22:32Z</datestamp>
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        <oai_dc:dc xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"  xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
          <dc:title>&lt;p&gt;Sequencing data for phage escapers in Fig 3F.&lt;/p&gt;</dc:title>
          <dc:creator>Sabine Grüschow (2491078)</dc:creator>
          <dc:creator>Peter Wotherspoon (22150942)</dc:creator>
          <dc:creator>Emma Hilton-Balfe (24947692)</dc:creator>
          <dc:creator>Shirley Graham (17199361)</dc:creator>
          <dc:creator>Malcolm F. White (20893636)</dc:creator>
          <dc:subject>Biochemistry</dc:subject>
          <dc:subject>Microbiology</dc:subject>
          <dc:subject>Cell Biology</dc:subject>
          <dc:subject>Genetics</dc:subject>
          <dc:subject>Molecular Biology</dc:subject>
          <dc:subject>Biotechnology</dc:subject>
          <dc:subject>Evolutionary Biology</dc:subject>
          <dc:subject>Immunology</dc:subject>
          <dc:subject>Cancer</dc:subject>
          <dc:subject>Mental Health</dc:subject>
          <dc:subject>Infectious Diseases</dc:subject>
          <dc:subject>Virology</dc:subject>
          <dc:subject>Computational  Biology</dc:subject>
          <dc:subject>evolved counter measures</dc:subject>
          <dc:subject>b &gt;-&lt;/ b</dc:subject>
          <dc:subject>associated rossmann fold</dc:subject>
          <dc:subject>activate cellular defences</dc:subject>
          <dc:subject>phage infection cycle</dc:subject>
          <dc:subject>generates cyclic dinucleotides</dc:subject>
          <dc:subject>cas systems generate</dc:subject>
          <dc:subject>permeabilising effector 2tmβ</dc:subject>
          <dc:subject>generates cyclic tri</dc:subject>
          <dc:subject>div &gt;&lt; p</dc:subject>
          <dc:subject>cyclic nucleotide sponges</dc:subject>
          <dc:subject>type iii crispr</dc:subject>
          <dc:subject>cyclic tri</dc:subject>
          <dc:subject>cyclic nucleotide</dc:subject>
          <dc:subject>phage proteins</dc:subject>
          <dc:subject>cyclic nucleotides</dc:subject>
          <dc:subject>viral tactics</dc:subject>
          <dc:subject>viral response</dc:subject>
          <dc:subject>subvert immunity</dc:subject>
          <dc:subject>signalling pathways</dc:subject>
          <dc:subject>panoptes system</dc:subject>
          <dc:subject>panoptes polymerase</dc:subject>
          <dc:subject>guard systems</dc:subject>
          <dc:subject>growth arrest</dc:subject>
          <dc:subject>findings expand</dc:subject>
          <dc:subject>fascinating component</dc:subject>
          <dc:subject>dimeric state</dc:subject>
          <dc:subject>avoid triggering</dc:subject>
          <dc:subject>acb1 &lt;/</dc:subject>
          <dc:description>&lt;div&gt;&lt;p&gt;Cyclic nucleotide second messengers are used in all domains of life to amplify viral infection signals and activate cellular defences. In prokaryotes, CBASS (cyclic nucleotide&lt;b&gt;-&lt;/b&gt;based antiphage signalling system) and type III CRISPR-Cas systems generate a range of cyclic nucleotides which bind and allosterically activate effector proteins to mount an anti-viral response. Viruses have evolved counter measures to antagonise these signalling pathways in the form of cyclic nucleotide sponges and phosphodiesterases that sequester or degrade these molecules to subvert immunity. Recently, the Panoptes system was shown to function as a guard against these viral tactics. The type I Panoptes polymerase, mCpol, generates cyclic dinucleotides as decoy molecules that, when sequestered by phage proteins, results in the activation of the membrane-permeabilising effector 2TMβ to halt the phage infection cycle. Here, we investigate the type II Panoptes system, demonstrating that it generates cyclic tri-adenylate (cA&lt;sub&gt;3&lt;/sub&gt;) to maintain a CRISPR-associated Rossmann fold-transmembrane (CARF-TM) effector in an inactive, dimeric state. When cA&lt;sub&gt;3&lt;/sub&gt; is sequestered or degraded, the CARF protein undergoes conformational changes. In vivo, the absence of cA&lt;sub&gt;3&lt;/sub&gt; results in membrane disruption and growth arrest. Type II Panoptes provides defence against phages that express the cA&lt;sub&gt;3&lt;/sub&gt;-degrading enzyme Acb1; phage escapers introduce mutations into the &lt;i&gt;acb1&lt;/i&gt; gene to avoid triggering the Panoptes system. These findings expand our understanding of the guard systems that constitute a fascinating component of the bacterial immune system.&lt;/p&gt;&lt;/div&gt;</dc:description>
          <dc:date>2026-09-15T17:22:17Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.1371/journal.pbio.3003934.s011</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/_p_Sequencing_data_for_phage_escapers_in_Fig_3F_p_/33809251</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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