PRL1 interacts with and stabilizes RPA2A to regulate carbon deprivation-induced senescence in Arabidopsis.

Leaf senescence is a developmental program regulated by both endogenous and environmental cues. Abiotic stresses such as nutrient deprivation can induce premature leaf senescence, which profoundly impacts plant growth and crop yield. However, the molecular mechanisms underlying stress-induced senescence are not fully understood. In this work, employing a carbon deprivation (C-deprivation)-induced senescence assay in Arabidopsis seedlings, we identified PLEIOTROPIC REGULATORY LOCUS 1 (PRL1), a component of the NineTeen Complex, as a negative regulator of C-deprivation-induced senescence. Furthermore, we demonstrated that PRL1 directly interacts with the RPA2A subunit of the single-stranded DNA-binding Replication Protein A (RPA) complex. Consistently, the loss of RPA2A leads to premature senescence, while increased expression of RPA2A inhibits senescence. Moreover, overexpression of RPA2A reverses the accelerated senescence in prl1 mutants, and the interaction with PRL1 stabilizes RPA2A under C-deprivation. In summary, our findings reveal the involvement of the PRL1-RPA2A functional module in C-deprivation-induced plant senescence.