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Nitrogen (N) deficiency critically impairs leaf photosynthetic capacity and triggers premature senescence. However, the physiological metabolism underlying N deficiency-induced leaf senescence and its relationship with the varying mineral nutrients and reactive oxygen (ROS) concentration in leaf tissues are not well understood. In this paper, the premature senescence of flag leaves (psf) mutant and its wild type (WT) were employed to clarify the senescent-associated changes in the contents of several mineral elements, including potassium (K), manganese (Mn), magnesium (Mg), and iron (Fe) in leaf and root tissues under different N regimes. The roles of K and Mn in regulating ROS generation during N deficiency-induced senescence were further verified by exogenous K and Mn treatments. Results showed that N deficiency accelerated leaf senescence and led to a significant increase in ROS and Mn content in both leaf and root tissues, concurrently with N deficiency-induced declines in K, Mg and Fe contents in senescing leaves. In contrast, sufficient N supply delayed leaf senescence and reduced ROS and Mn accumulation in leaf tissues. The changes in ROS and Mn under varying N conditions exhibited an inverse relationship with the variations in K, Mg, and Fe. K deficiency exacerbated N starvation-induced leaf senescence and promoted ROS accumulation by suppressing antioxidant enzyme activity. Conversely, exogenous K incubation at higher concentration inhibited excessive ROS accumulation and retarded leaf senescence under N deficiency. Furthermore, the elevated Mn accumulation under N-deficiency impaired ROS scavenging capacity of antioxidant enzymes, leading to oxidative stress and excessive ROS. Increased Mn levels in leaves and roots further aggravated N deficiency-induced leaf senescence by triggering ROS burst. N deficiency upregulated the expression of key K+ transporter genes (OsHAK1 and OsHAK5) and stimulated K+ efflux from leaf tissues. The elevated accumulation of Mn coupled with the loss of K in senescing leaves acts as an important regulatory mechanism driving N deficiency-induced leaf senescence.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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