The LEA protein, ABR, is regulated by ABI5 and involved in dark-induced leaf senescence in Arabidopsis thaliana.

The phytohormone abscisic acid (ABA) modulates plant growth and developmental processes such as leaf senescence. In this study, we investigated the role of the Arabidopsis late embryogenesis abundant (LEA) protein ABR (ABA-response protein) in delaying dark-induced leaf senescence. The ABR gene was up-regulated by treatment with ABA, NaCl and mannitol, as well as by light deprivation. In the dark, abr mutant plants displayed a premature leaf senescence phenotype, and various senescence-associated indicators, such as an increase in chlorophyll degradation and membrane leakiness, were enhanced, whereas 35S:ABR/abr transgenic lines showed a marked delay in dark-induced leaf senescence phenotypes. In vitro and in vivo assays showed that ABI5 bind to the ABR promoter, indicating that ABI5 directly regulates the expression of ABR. The disruption of ABI5 function in abr abi5-1 plants abolished the senescence-accelerating phenotype of the abr mutant, demonstrating that ABI5 is epistatic to ABR. In summary, these results highlight the important role that ABR, which is negatively regulated by ABI5, plays in delaying dark-induced leaf senescence.