4.7 Article

The plant metacaspase AtMC1 in pathogen-triggered programmed cell death and aging: functional linkage with autophagy

Journal

CELL DEATH AND DIFFERENTIATION
Volume 21, Issue 9, Pages 1399-1408

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2014.50

Keywords

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Funding

  1. NIH [RO1GM057171 JLD]
  2. EU-Marie Curie Actions [PCDMC-321738]
  3. Catalan Government [BP_B 00030]
  4. Howard Hughes Medical Institute
  5. Gordon and Betty Moore Foundation [GBMF3030]

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Autophagy is a major nutrient recycling mechanism in plants. However, its functional connection with programmed cell death (PCD) is a topic of active debate and remains not well understood. Our previous studies established the plant metacaspase AtMC1 as a positive regulator of pathogen-triggered PCD. Here, we explored the linkage between plant autophagy and AtMC1 function in the context of pathogen-triggered PCD and aging. We observed that autophagy acts as a positive regulator of pathogen-triggered PCD in a parallel pathway to AtMC1. In addition, we unveiled an additional, pro-survival homeostatic function of AtMC1 in aging plants that acts in parallel to a similar pro-survival function of autophagy. This novel pro-survival role of AtMC1 may be functionally related to its prodomain-mediated aggregate localization and potential clearance, in agreement with recent findings using the single budding yeast metacaspase YCA1. We propose a unifying model whereby autophagy and AtMC1 are part of parallel pathways, both positively regulating HR cell death in young plants, when these functions are not masked by the cumulative stresses of aging, and negatively regulating senescence in older plants.

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