Cytokinin isopentenyladenine and its glucoside isopentenyladenine-9G delay leaf senescence through activation of cytokinin-associated genes.

Cytokinins (CKs) are well-known as a class of phytohormones capable of delaying senescence in detached leaves. However, CKs are often treated as a monolithic group of compounds even though dozens of CK species are present in plants with varied degrees of reported biological activity. One specific type of CK, isopentenyladenine base (iP), has been demonstrated as having roles in delaying leaf senescence, inhibition of root growth, and promoting shoot regeneration. However, its N-glucosides isopentenyladenine-7- and -9-glucoside (iP7G, iP9G) have remained understudied and thought of as inactive cytokinins for several decades, despite their relatively high concentrations in plants such as the model species . Here we show that iP and one of its glucosides, iP9G, are capable of delaying senescence in leaves, though the glucosides having little to no activity in other bioassays. Additionally, we performed the first transcriptomic study of iP-delayed cotyledon senescence which shows that iP is capable of upregulating photosynthetic genes and downregulating catabolic genes in detached cotyledons. Transcriptomic analysis also shows iP9G has limited effects on gene expression, but that the few affected genes are CK-related and are similar to those seen from iP effects during senescence as seen for the type-A response regulator ARR6. These findings suggest that iP9G functions as an active CK during senescence.