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Aims <p>Pepper (<i>Capsicum annuum</i>) is susceptible to bacterial wilt caused by <i>Ralstonia solanacearum</i> under high temperature and high humidity (HTHH) conditions, leading to severe yield losses. Our previous studies revealed that the abscisic acid (ABA) receptor PYR1 negatively regulates bacterial wilt resistance under normal temperature but exhibits positive regulation under HTHH conditions. We discovered that PYR1 interacts with HT1, a member of the AGC protein kinase C family.</p> Methods <p>To investigate the function of CaHT1 and its interaction with CaPYR1, we performed subcellular localization, bimolecular fluorescence complementation (BiFC), pull-down assays, virus-induced gene silencing (VIGS), transient and stable overexpression, qRT-PCR, and disease index evaluation.</p> Results <p>We found that CaHT1 localizes to the plasma membrane and nucleus and physically interacts with CaPYR1. Silencing CaHT1 increased pepper susceptibility to R. solanacearum, whereas stable overexpression of CaHT1 in both pepper and tobacco enhanced disease resistance.</p> Conclusions <p>This study demonstrates that CaHT1 positively regulates pepper resistance to bacterial wilt under both normal and HTHH conditions, indicating that HT1 achieves its positive regulatory role through protein interaction with PYR1. These findings hold significant implications for elucidating pepper disease resistance mechanisms and genetic improvement.</p> Graphical Abstract <p></p>

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CaHT1 regulates pepper immune response to Ralstonia solanacearum and interacts with CaPYR1

  • 期刊论文

  • 发表日期：

    2026年7月7日

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  • Xiang Zheng,
  • Jingang Lv,
  • Huifang Shi,
  • Lingxian Yi,
  • Daojin Yu

摘要

Aims

Pepper (Capsicum annuum) is susceptible to bacterial wilt caused by Ralstonia solanacearum under high temperature and high humidity (HTHH) conditions, leading to severe yield losses. Our previous studies revealed that the abscisic acid (ABA) receptor PYR1 negatively regulates bacterial wilt resistance under normal temperature but exhibits positive regulation under HTHH conditions. We discovered that PYR1 interacts with HT1, a member of the AGC protein kinase C family.

Methods

To investigate the function of CaHT1 and its interaction with CaPYR1, we performed subcellular localization, bimolecular fluorescence complementation (BiFC), pull-down assays, virus-induced gene silencing (VIGS), transient and stable overexpression, qRT-PCR, and disease index evaluation.

Results

We found that CaHT1 localizes to the plasma membrane and nucleus and physically interacts with CaPYR1. Silencing CaHT1 increased pepper susceptibility to R. solanacearum, whereas stable overexpression of CaHT1 in both pepper and tobacco enhanced disease resistance.

Conclusions

This study demonstrates that CaHT1 positively regulates pepper resistance to bacterial wilt under both normal and HTHH conditions, indicating that HT1 achieves its positive regulatory role through protein interaction with PYR1. These findings hold significant implications for elucidating pepper disease resistance mechanisms and genetic improvement.

Graphical Abstract