Scholarlink

<p>Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. Fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (<i>At</i>MC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of a catalytically inactive <i>At</i>MC1 in an <i>atmc1</i> background triggers severe autoimmunity partially dependent on the same immune signalling components. Overexpression of the E3 ligase SNIPER1, a master regulator of NLR homeostasis, fully reverts the AtMC1-dependent autoimmunity phenotype, inferring that a broad defect in NLR turnover may underlie the severe phenotype observed. Catalytically inactive <i>At</i>MC1 localizes to punctate structures that are degraded through autophagy. Considering also previous evidence on the proteostatic functions of <i>At</i>MC1, we speculate that Wt <i>At</i>MC1 may either directly or indirectly control NLR protein levels, thereby preventing autoimmunity.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月20日

查看全文
  • Jose Salguero-Linares,
  • Laia Armengot,
  • Joel Ayet,
  • Nerea Ruiz-Solaní,
  • Svenja C Saile,
  • Marta Salas-Gómez,
  • Esperanza Fernandez,
  • Lode Denolf,
  • Fernando Navarrete,
  • Jenna Krumbach,
  • Markus Kaiser,
  • Simon Stael,
  • Frank Van Breusegem,
  • Kris Gevaert,
  • Farnusch Kaschani,
  • Morten Petersen,
  • Farid El Kasmi,
  • Marc Valls,
  • Núria S Coll

摘要

Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. Fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (AtMC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of a catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Overexpression of the E3 ligase SNIPER1, a master regulator of NLR homeostasis, fully reverts the AtMC1-dependent autoimmunity phenotype, inferring that a broad defect in NLR turnover may underlie the severe phenotype observed. Catalytically inactive AtMC1 localizes to punctate structures that are degraded through autophagy. Considering also previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels, thereby preventing autoimmunity.