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<p>Potassium (K) is an essential macronutrient for plant growth and plays a critical role in leaf development. Cultivated peanut (<i>Arachis hypogaea</i> L.) is a globally significant source of edible oil and protein. However, the molecular mechanisms underlying peanut leaf responses to K deficiency remain poorly understood. In this study, we conducted hydroponic experiments to investigate the physiological and transcriptomic responses of leaves from two peanut cultivars—Nonghua 18 (NH18, low-K-tolerant) and Huayu 20 (HY20, K-sensitive)—under varying K concentrations (K0: 0 mM; K1: 0.1 mM; CK: 1 mM, KCl). K deficiency induced oxidative stress in peanut leaves, manifesting as chlorosis and premature senescence. Transcriptomic analysis revealed that K deficiency upregulated the expression of functional genes associated with abscisic acid (ABA) signaling and phenylpropanoid metabolic pathway. Notably, the genes <i>arahy.772I7G</i>, <i>arahy.DCNL5J</i> and <i>arahy.SH86H7</i> were significantly correlated with leaf area. Furthermore, the expression of genes related to the phenylpropanoid metabolic pathway exhibited strong correlations with K concentrations in nutrient solution, antioxidant capacity, and leaf growth. Compared to K0, K1 treatment downregulated genes related to ABA signaling and the phenylpropanoid metabolism pathway in NH18 leaves, reducing reactive oxygen species accumulation and mitigating leaf senescence. In contrast, these genes were upregulated in HY20. These findings suggest that ABA signaling and the phenylpropanoid metabolic pathway play pivotal roles in alleviating oxidative stress in peanut leaves under K deficiency. This study provides a theoretical foundation for further exploration of the molecular mechanisms underlying leaf responses to K deficiency, offering insights into cultivar-specific adaptation strategies.</p>

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Physiological and Transcriptomic Analysis Reveals Response Mechanisms of Peanut Seedling Leaves to Potassium Deficiency Across Different Cultivars

  • 期刊论文

  • 发表日期：

    2025年6月25日

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  • Dongying Zhou,
  • Yuanchun Zhang,
  • Guohu Lan,
  • Chuanbao Ma,
  • Huijie Su,
  • Yuexin Sun,
  • Yingyan Liu,
  • He Zhang,
  • Jing Wang,
  • Chao Zhong,
  • Xinhua Zhao,
  • Haiqiu Yu

摘要

Potassium (K) is an essential macronutrient for plant growth and plays a critical role in leaf development. Cultivated peanut (Arachis hypogaea L.) is a globally significant source of edible oil and protein. However, the molecular mechanisms underlying peanut leaf responses to K deficiency remain poorly understood. In this study, we conducted hydroponic experiments to investigate the physiological and transcriptomic responses of leaves from two peanut cultivars—Nonghua 18 (NH18, low-K-tolerant) and Huayu 20 (HY20, K-sensitive)—under varying K concentrations (K0: 0 mM; K1: 0.1 mM; CK: 1 mM, KCl). K deficiency induced oxidative stress in peanut leaves, manifesting as chlorosis and premature senescence. Transcriptomic analysis revealed that K deficiency upregulated the expression of functional genes associated with abscisic acid (ABA) signaling and phenylpropanoid metabolic pathway. Notably, the genes arahy.772I7G, arahy.DCNL5J and arahy.SH86H7 were significantly correlated with leaf area. Furthermore, the expression of genes related to the phenylpropanoid metabolic pathway exhibited strong correlations with K concentrations in nutrient solution, antioxidant capacity, and leaf growth. Compared to K0, K1 treatment downregulated genes related to ABA signaling and the phenylpropanoid metabolism pathway in NH18 leaves, reducing reactive oxygen species accumulation and mitigating leaf senescence. In contrast, these genes were upregulated in HY20. These findings suggest that ABA signaling and the phenylpropanoid metabolic pathway play pivotal roles in alleviating oxidative stress in peanut leaves under K deficiency. This study provides a theoretical foundation for further exploration of the molecular mechanisms underlying leaf responses to K deficiency, offering insights into cultivar-specific adaptation strategies.