PlMYB3RL homodimer activates PlSGRL to accelerate high-temperature-induced leaf senescence by promoting chlorophyll degradation in herbaceous peony ( Paeonia lactiflora pall.)

Abstract High-temperature stress caused by global warming can induce leaf senescence, which adversely affects plant growth and agricultural productivity worldwide. However, the molecular mechanism of high-temperature-induced leaf senescence remains largely unexplored. In this study, a Stay-green-like protein (PlSGRL) that regulates chlorophyll degradation was identified in herbaceous peony (Paeonia lactiflora Pall.). PlSGRL was localized to the chloroplasts, and its expression was upregulated under high-temperature stress. Virus-induced PlSGRL silencing markedly delayed high-temperature-induced leaf senescence in P. lactiflora, as evidenced by higher chlorophyll content, sustained photosystem II efficiency, and alleviated oxidative damage—reflected in reduced malondialdehyde content, relative electrical conductivity, and reactive oxygen species accumulation. Conversely, PlSGRL overexpression accelerated high-temperature-induced leaf senescence. Subsequently, we identified an atypical MYB transcription factor, PlMYB3RL, that directly promoted PlSGRL expression. PlMYB3RL was localized to the nucleus, and its expression was also upregulated under high-temperature stress. Similarly, PlMYB3RL silencing significantly delayed high-temperature-induced leaf senescence. Additionally, PlMYB3RL formed a homodimer through self-interaction, and this homodimer enhanced the transcriptional activation of PlSGRL in a dose-dependent manner. Collectively, these data demonstrate that the PlMYB3RL homodimer activates PlSGRL expression to promote chlorophyll degradation and leaf senescence under high-temperature stress in P. lactiflora. These findings reveal a novel regulatory module underlying high-temperature-induced leaf senescence in P. lactiflora, providing key gene resources and theoretical support for breeding high-temperature-resistant cultivars.