The kinase CRK5 regulates dark-induced senescence and dissipation of energy as heat by inhibiting salicylic acid signaling

CYSTEINE-RICH RECEPTOR-LIKE KINASE 5 (CRK5) is a membrane-localized signaling protein implicated in developmental and stress-responsive pathways. Its promoter contains multiple W-box motifs, suggesting regulation by WRKY transcription factors and a potential role in salicylic acid (SA)-dependent signaling. Since SA simultaneously promotes dark-induced senescence and modulates photo-protective dissipation of absorbed energy in excess (AEE) as heat through its effects on non-photochemical quenching (NPQ), stomatal behavior, and leaf temperature, how these SA-driven processes are coordinated remains unclear. Here, we address the unresolved question of whether CRK5 links SA-signaling to the regulation of both senescence and the dissipation of AEE as heat. We demonstrated that loss of CRK5 function leads to increased SA-accumulation, accelerated dark-induced senescence, reduced NPQ, lower foliar temperature, and impaired photosynthetic performance in Arabidopsis (Arabidopsis thaliana). Transcriptomic analysis revealed extensive deregulation of senescence-associated, SA-responsive, and WRKY genes in crk5, particularly under extended darkness. Crucially, introduction of SA-induction-deficient-2 (sid2) or transgenic line (NahG) into the crk5 background fully reverted these phenotypes, whereas disruption of ethylene signaling, ethylene-insensitive-2 (ein2), did not, demonstrating that CRK5 acts specifically through SA-dependent pathways. A line with constitutively enhanced SA levels, constitutive expressor of PR genes 1 (cpr1), showed similar phenotypes to crk5, and exogenous SA further reduced NPQ and leaf temperature across genotypes, confirming that SA negatively regulates foliar AEE dissipation as heat and photosynthetic efficiency. Together, our results identify CRK5 as a key negative regulator of the SA-signaling pathway, which delays dark-induced senescence while positively regulating photosynthesis, NPQ, and thermal dissipation of AEE as heat. This work reveals a previously unrecognized role of CRK5 in coordinating SA-mediated senescence and photo-protective energy management.

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Journal
PLANT PHYSIOLOGY
Published
2026-02-01
DOI
https://doi.org/10.1093/plphys/kiag046
Primary Topic
Plant Gene Expression Analysis
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article
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article

The kinase CRK5 regulates dark-induced senescence and dissipation of energy as heat by inhibiting salicylic acid signaling

Maria Duszyn, Piotr Gawroński, Anna Rusaczonek, Muhammad Kamran et al.
PLANT PHYSIOLOGY
Plant Gene Expression Analysis
article

The kinase CRK5 regulates dark-induced senescence and dissipation of energy as heat by inhibiting salicylic acid signaling

Maria Duszyn, Piotr Gawroński, Anna Rusaczonek, Muhammad Kamran, Roshanak Zarrin Ghalami, Kinga Gołębiewska, Paweł Burdiak
article en

Abstract

CYSTEINE-RICH RECEPTOR-LIKE KINASE 5 (CRK5) is a membrane-localized signaling protein implicated in developmental and stress-responsive pathways. Its promoter contains multiple W-box motifs, suggesting regulation by WRKY transcription factors and a potential role in salicylic acid (SA)-dependent signaling. Since SA simultaneously promotes dark-induced senescence and modulates photo-protective dissipation of absorbed energy in excess (AEE) as heat through its effects on non-photochemical quenching (NPQ), stomatal behavior, and leaf temperature, how these SA-driven processes are coordinated remains unclear. Here, we address the unresolved question of whether CRK5 links SA-signaling to the regulation of both senescence and the dissipation of AEE as heat. We demonstrated that loss of CRK5 function leads to increased SA-accumulation, accelerated dark-induced senescence, reduced NPQ, lower foliar temperature, and impaired photosynthetic performance in Arabidopsis (Arabidopsis thaliana). Transcriptomic analysis revealed extensive deregulation of senescence-associated, SA-responsive, and WRKY genes in crk5, particularly under extended darkness. Crucially, introduction of SA-induction-deficient-2 (sid2) or transgenic line (NahG) into the crk5 background fully reverted these phenotypes, whereas disruption of ethylene signaling, ethylene-insensitive-2 (ein2), did not, demonstrating that CRK5 acts specifically through SA-dependent pathways. A line with constitutively enhanced SA levels, constitutive expressor of PR genes 1 (cpr1), showed similar phenotypes to crk5, and exogenous SA further reduced NPQ and leaf temperature across genotypes, confirming that SA negatively regulates foliar AEE dissipation as heat and photosynthetic efficiency. Together, our results identify CRK5 as a key negative regulator of the SA-signaling pathway, which delays dark-induced senescence while positively regulating photosynthesis, NPQ, and thermal dissipation of AEE as heat. This work reveals a previously unrecognized role of CRK5 in coordinating SA-mediated senescence and photo-protective energy management.

PLANT PHYSIOLOGYVol. 200(2)
Warsaw University of Life Sciences (PL)
Affordable and clean energy
Openalex Percentile: Top 65%
Plant Gene Expression Analysis
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