A role for cytokinin in the onset of leaf senescence by ethylene in Arabidopsis

The expression of several Arabidopsis senescence-associated genes (SAGs) was found to be upregulated during leaf development of the onset of leaf death 9 mutant under standard growth conditions. Treatment of the mutant with ethylene resulted in a severe senescence response both phenotypically as well as on transcript level. A RNAi-based strategy to downregulate the expression of a SAG encoding for a hydroxyproline-rich glycoprotein, attenuated the ethylene induced senescence response of old9. Comparison of the old9 transcriptome revealed that 67% of the differentially expressed genes with wild type are cytokinin responsive. Cytokinins are well known for their effect to retard leaf senescence. However, by applying cytokinin early in development the response to ethylene-induced senescence could be enhanced. We argue that the cytokinin effect we observed is the result of increasing the sink strength of young tissue while opposite to that ethylene promotes source strength of old leaves. Therefore we propose that the balance between sink and source tissue can modulate the progression rate and timing of senescence.