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<p>The receptor-like cytoplasmic kinase BIK1 and its close homologue PBL1 have been widely recognized as central components of plant immunity. However, most genetic studies of BIK1 and PBL1 functions were carried out with single transfer DNA (T-DNA) insertional mutant alleles. Some phenotypes observed in these mutants, for example autoimmunity, have been difficult to reconcile with the proposed role of BIK1 and PBL1 in pattern-triggered immunity. In this study, we generated several new alleles of <i>bik1</i> and <i>pbl1</i> by CRISPR–Cas9-based gene editing and systematically analysed these mutants alongside existing T-DNA insertional lines. These analyses reinforced the central role of <i>BIK1</i> and <i>PBL1</i> in pattern-triggered immunity mediated by both receptor kinases and receptor-like proteins. At the same time, however, we revealed several pleiotropic phenotypes associated with T-DNA insertions that are not necessarily linked to loss of <i>BIK1</i> or <i>PBL1</i> function. Further analyses of newly generated <i>bik1</i> <i>pbl1</i> double mutants uncovered an even greater contribution of these kinases to immune signalling and disease resistance than previously appreciated. These findings clarify longstanding ambiguities surrounding BIK1 and PBL1 functions.</p>

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New alleles of Arabidopsis BIK1 reinforce its predominant role in pattern-triggered immunity and caution interpretations of other reported functions

  • 期刊论文

  • 发表日期：

    2026年1月7日

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  • Beibei Song,
  • Sera Choi,
  • Liang Kong,
  • Sung-Il Kim,
  • Judith Fliegmann,
  • Xiuming Li,
  • Yong Gao,
  • Thomas A. DeFalco,
  • Meijuan Hu,
  • Meng Li,
  • Yan Zhao,
  • Hongze Wang,
  • Shengwei Ma,
  • Libo Shan,
  • Thorsten Nürnberger,
  • Ping He,
  • Cyril Zipfel,
  • Jian-Min Zhou

摘要

The receptor-like cytoplasmic kinase BIK1 and its close homologue PBL1 have been widely recognized as central components of plant immunity. However, most genetic studies of BIK1 and PBL1 functions were carried out with single transfer DNA (T-DNA) insertional mutant alleles. Some phenotypes observed in these mutants, for example autoimmunity, have been difficult to reconcile with the proposed role of BIK1 and PBL1 in pattern-triggered immunity. In this study, we generated several new alleles of bik1 and pbl1 by CRISPR–Cas9-based gene editing and systematically analysed these mutants alongside existing T-DNA insertional lines. These analyses reinforced the central role of BIK1 and PBL1 in pattern-triggered immunity mediated by both receptor kinases and receptor-like proteins. At the same time, however, we revealed several pleiotropic phenotypes associated with T-DNA insertions that are not necessarily linked to loss of BIK1 or PBL1 function. Further analyses of newly generated bik1 pbl1 double mutants uncovered an even greater contribution of these kinases to immune signalling and disease resistance than previously appreciated. These findings clarify longstanding ambiguities surrounding BIK1 and PBL1 functions.