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<p>Bacterial transcription activator-like effectors (TALEs) promote pathogenicity by activating host susceptibility (<i>S</i>) genes. To understand the pathogenicity and host adaptation of <i>Xanthomonas citri</i> pv. <i>malvacearum</i> (<i>Xcm</i>), we assemble the genome and the TALE repertoire of three recent <i>Xcm</i> Texas isolates. A newly evolved TALE, Tal7b, activates <i>GhSWEET14a</i> and <i>GhSWEET14b</i>, different from <i>GhSWEET10</i> targeted by a TALE in an early <i>Xcm</i> isolate. Activation of <i>GhSWEET14a</i> and <i>GhSWEET14b</i> results in water-soaked lesions. Transcriptome profiling coupled with TALE-binding element prediction identify a pectin lyase gene as an additional Tal7b target, quantitatively contributing to <i>Xcm</i> virulence alongside <i>GhSWEET14a/b</i>. CRISPR-Cas9 gene editing supports the function of <i>GhSWEETs</i> in cotton bacterial blight and the promise of disrupting the TALE-binding site in <i>S</i> genes for disease management. Collectively, our findings elucidate the rapid evolution of TALEs in <i>Xanthomonas</i> field isolates and highlight the virulence mechanism wherein TALEs induce multiple <i>S</i> genes to promote pathogenicity.</p>

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Activation of three targets by a TAL effector confers susceptibility to bacterial blight of cotton

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月14日

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  • Brendan W. Mormile,
  • Yan Yan,
  • Taran Bauer,
  • Li Wang,
  • Rachel C. Rivero,
  • Sara C. D. Carpenter,
  • Catherine Danmaigona Clement,
  • Kevin L. Cox,
  • Lin Zhang,
  • Xiyu Ma,
  • Terry A. Wheeler,
  • Jane K. Dever,
  • Ping He,
  • Adam J. Bogdanove,
  • Libo Shan

摘要

Bacterial transcription activator-like effectors (TALEs) promote pathogenicity by activating host susceptibility (S) genes. To understand the pathogenicity and host adaptation of Xanthomonas citri pv. malvacearum (Xcm), we assemble the genome and the TALE repertoire of three recent Xcm Texas isolates. A newly evolved TALE, Tal7b, activates GhSWEET14a and GhSWEET14b, different from GhSWEET10 targeted by a TALE in an early Xcm isolate. Activation of GhSWEET14a and GhSWEET14b results in water-soaked lesions. Transcriptome profiling coupled with TALE-binding element prediction identify a pectin lyase gene as an additional Tal7b target, quantitatively contributing to Xcm virulence alongside GhSWEET14a/b. CRISPR-Cas9 gene editing supports the function of GhSWEETs in cotton bacterial blight and the promise of disrupting the TALE-binding site in S genes for disease management. Collectively, our findings elucidate the rapid evolution of TALEs in Xanthomonas field isolates and highlight the virulence mechanism wherein TALEs induce multiple S genes to promote pathogenicity.