Glycosyltransferase-Like RSE1 Negatively Regulates Leaf Senescence Through Salicylic Acid Signaling in Arabidopsis

Abstract

Leaf senescence is a developmental process designed for nutrient recycling and relocation to maximize growth competence and reproductive capacity of plants. Thus, plants integrate developmental and environmental signals to precisely control senescence. To genetically dissect the complex regulatory mechanism underlying leaf senescence, we identified an early leaf senescence mutant, <i>rse1</i>. <i>RSE1</i> encodes a putative glycosyltransferase. Loss-of-function mutations in <i>RSE1</i> resulted in precocious leaf yellowing and up-regulation of senescence marker genes, indicating enhanced leaf senescence. Transcriptome analysis revealed that salicylic acid (SA) and defense signaling cascades were up-regulated in <i>rse1</i> prior to the onset of leaf senescence. We found that SA accumulation was significantly increased in <i>rse1.</i> The <i>rse1</i> phenotypes are dependent on <i>SA-INDUCTION DEFICIENT 2</i> (<i>SID2</i>), supporting a role of SA in accelerated leaf senescence in <i>rse1</i>. Furthermore, RSE1 protein was localized to the cell wall, implying a possible link between the cell wall and RSE1 function. Together, we show that RSE1 negatively modulates leaf senescence through an <i>SID2</i>-dependent SA signaling pathway.