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CaNAC2c acts modulator in the tradeoff among pepper growth, adaptation to high temperature stress and resistance to Ralstonia solanacearum infection
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  • Weiwei Cai,
  • Sheng Yang,
  • Ruijie Wu,
  • Jianshen Cao,
  • Lei Shen,
  • Zhen Wu,
  • Deyi Guan,
  • Ronghua Huang,
  • Shuilin He
Weiwei Cai
Key Laboratory of Applied Genetics of universities in Fujian Province
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Sheng Yang
Key Laboratory of Applied Genetics of universities in Fujian Province
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Ruijie Wu
Key Laboratory of Applied Genetics of universities in Fujian Province
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Jianshen Cao
Key Laboratory of Applied Genetics of universities in Fujian Province
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Lei Shen
Key Laboratory of Applied Genetics of universities in Fujian Province
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Zhen Wu
Key Laboratory of Applied Genetics of universities in Fujian Province
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Deyi Guan
Key Laboratory of Applied Genetics of universities in Fujian Province
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Ronghua Huang
Key Laboratory of Applied Genetics of universities in Fujian Province
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Shuilin He
Key Laboratory of Applied Genetics of universities in Fujian Province
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Abstract

In their natural habitats, plants are inevitably exposed to different biotic and abiotic stresses, to maximize fitness, their adaptation to these stresses should be appropriately coordinated by trade-offs among growth and stress response. However, the involved players and their possible mode of action remain to be investigated. Herein, by approaches of reverse genetics including virus induced gene silencing (VIGS), transient overexpression in pepper or ecoptic overexpression in Nicotiana benthamiana, ChIP-PCR and physiology, CaNAC2c was functionally characterized in trade-offs between growth and immunity against Ralstonia solanacearum inoculation (RSI) or thermotolerance. Our results demonstrate that CaNAC2c remains lower level of transcripts in absence of stress and functions negatively in pepper growth, but is upregulated and functions positively in pepper response to high temperature stress (HTS) and to RSI probably via signaling mediated by ABA and JA, respectively. CaNAC2c functions by directly targeting CaHSFA5 and decreasing H2O2 accumulation upon HTS. On the other hand, it acts positively in pepper response to RSI by upregulating JA- and enhancing accumulation of H2O2, while downregulating SA-signaling mediated PR genes, but does not target or regulate CaHSFA5. In addition, CaNAC2c exhibits redundancy with CaNAC2d in response to challenge of RSI but not to that of HTS, indicating that immunity against RSI is more robust than thermotolerance. These findings collectively unveil that tradeoff between growth and thermotolerance/immunity mediated by CaNAC2c is mainly determined by its differential transcription, while tradeoff between thermotolerance and immunity mediated by CaNAC2c is conferred by its context dependent post-translational regulation.