The loss of COP1 delays senescence and inhibits root growth through modulation of sucrose allocation and availability.

Abstract

CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) participates in diverse signaling pathways that regulate plant growth and development, but its role in sucrose-mediated signaling remains unclear. Here, we show that COP1 contributes to leaf senescence and root growth by modulating sucrose allocation and availability in Arabidopsis. Under sucrose-free conditions, cop1 mutants developed chlorotic leaves with reduced chlorophyll content, impaired primary root growth, and decreased starch granule formation in root columella cells. cop1 mutants also showed reduced expression of sucrose transport- and catabolism-related genes in leaves, suggesting impaired source-to-sink sugar allocation and reduced sucrose turnover in source tissues. Consistent with this possibility, exogenous glucose and sucrose supplementation alleviated leaf chlorosis and increased chlorophyll content and primary root growth, while sucrose supplementation also partially restored starch granule formation in root columella cells. Moreover, overexpression of SUCROSE-PROTON SYMPORTER 2, a key sucrose transporter for shoot-to-root sucrose transport that was downregulated in cop1 mutants, partially restored chlorophyll content, primary root growth, and starch granule formation. COP1 loss was also accompanied by reduced brassinosteroid (BR) signaling, including decreased expression of BR-related genes, reduced BRASSINAZOLE-RESISTANT 1 (BZR1) accumulation, attenuated brassinolide (BL) responsiveness, and decreased endogenous BL content, along with decreased expression of ethylene biosynthesis- and senescence-associated genes and delayed leaf senescence. Together, these findings indicate that loss of COP1 disrupts sucrose allocation and availability, with sucrose accumulating in leaves while the delivery of shoot-derived sucrose to roots is limited, thereby impairing starch granule formation and root growth and reducing BR/ethylene-associated senescence responses, ultimately delaying leaf senescence.