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Key message <p><i>Vitis</i> <i>rupestris</i> metacaspase 5, tethered to microtubules, drives grapevine. Hypersensitive response via calcium-dependent auto-processing, linking cytoskeletal dynamics to defence activation by elicitors.</p> Abstract <p>Metacaspase 5 is a key player for the hypersensitive response of grapevine against biotrophic pathogens and must be activated rapidly as to prevent colonisation. This activation is likely to occur through changes in protein activity. By expressing a GFP fusion of metacaspase 5 from <i>Vitis rupestris</i> in tobacco BY-2 cells, we can show that this protein is bound to microtubules and that the overexpressors are more responsive to the cell-death-inducing elicitors, <i>cis</i>-3-hexenal and harpin. The disruption of microtubules and actin filaments by these elicitors can be blocked by inhibitors of dynamic turnover and stabilisation. Stabilisation of microtubules by taxol can mitigate <i>cis</i>-3-hexenal induced mortality. Mutations of the catalytic or the putative microtubule-binding sites of metacaspase 5 can suppress auto-processing of this enzyme in biochemical assay. Likewise, the response to <i>cis</i>-3-hexenal (cell death, induction of salicylate-related gene expression) is suppressed in cells, whilst the cytoplasmic remodelling is retained. Calcium and the sites for catalysis or microtubule binding are required for both auto-processing and enzyme activity. We arrive at a model, where metacaspase 5 is inactive when tethered to microtubules, but becomes unleashed for auto-processing upon defence-mediated microtubule breakdown.</p>

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Unleash the dogs of death: metacaspase 5, microtubules, and hypersensitive response

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月30日

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  • Xin Zhu,
  • Kunxi Zhang,
  • Peijie Gong,
  • Michael Riemann,
  • Peter Nick

摘要

Key message

Vitis rupestris metacaspase 5, tethered to microtubules, drives grapevine. Hypersensitive response via calcium-dependent auto-processing, linking cytoskeletal dynamics to defence activation by elicitors.

Abstract

Metacaspase 5 is a key player for the hypersensitive response of grapevine against biotrophic pathogens and must be activated rapidly as to prevent colonisation. This activation is likely to occur through changes in protein activity. By expressing a GFP fusion of metacaspase 5 from Vitis rupestris in tobacco BY-2 cells, we can show that this protein is bound to microtubules and that the overexpressors are more responsive to the cell-death-inducing elicitors, cis-3-hexenal and harpin. The disruption of microtubules and actin filaments by these elicitors can be blocked by inhibitors of dynamic turnover and stabilisation. Stabilisation of microtubules by taxol can mitigate cis-3-hexenal induced mortality. Mutations of the catalytic or the putative microtubule-binding sites of metacaspase 5 can suppress auto-processing of this enzyme in biochemical assay. Likewise, the response to cis-3-hexenal (cell death, induction of salicylate-related gene expression) is suppressed in cells, whilst the cytoplasmic remodelling is retained. Calcium and the sites for catalysis or microtubule binding are required for both auto-processing and enzyme activity. We arrive at a model, where metacaspase 5 is inactive when tethered to microtubules, but becomes unleashed for auto-processing upon defence-mediated microtubule breakdown.