PUB13-Mediated Degradation of PBS3 Regulates Salicylic Acid Biosynthesis to Coordinate Plant Immunity and Leaf Longevity

Salicylic acid (SA) is essential for plant immunity, but excessive SA accumulation accelerates leaf senescence, necessitating tight control of its biosynthesis. Although AVRPPHB SUSCEPTIBLE3 (PBS3) is a key enzyme in SA biosynthesis, how PBS3 abundance is regulated to coordinate immunity and longevity remains unclear. Using genetic, biochemical, and physiological analyses, we show that PBS3 functions as a quantitative regulator of the immunity-longevity balance. Loss of PBS3 compromises disease resistance but delays senescence, whereas graded increases in PBS3 abundance progressively enhance pathogen-induced SA accumulation, systemic acquired resistance (SAR), and senescence severity. We further identify the E3 ubiquitin ligase PLANT U-BOX PROTEIN 13 (PUB13) as a direct regulator of PBS3. PUB13 physically associates with PBS3 and promotes its polyubiquitination and degradation through the 26S proteasome pathway. Disruption of PUB13 stabilizes PBS3, resulting in elevated SA accumulation, enhanced SAR, and accelerated leaf senescence. Time-course analyses revealed that pathogen-induced PBS3 accumulation and SA biosynthesis are transient in wild-type plants but remain elevated in pub13 mutants, indicating that PUB13 promotes the attenuation of immune-associated SA production after defense activation. Together, our findings establish the PUB13-PBS3 module as a post-translational mechanism that fine-tunes SA biosynthesis, enabling effective immunity while preventing prolonged SA accumulation and its detrimental effects on plant longevity.