Cytokinin inhibition of leaf senescence

Abstract

The senescence delaying effect of cytokinin is well known, however, the details behind how this process occurs remain unclear. Efforts to improve understanding of this phenomenon have led to the identification in Arabidopsis of specific cytokinin signaling components through which senescence signal responses are regulated. These include the cytokinin receptor (AHK3), the type-B response regulator (ARR2) and the recently identified cytokinin response factor (CRF6). At the mechanistic end of this process, it was found that increased cell-wall invertase activity which occurs in response to cytokinin is both necessary and sufficient for the inhibition of senescence. Yet, a direct link between the signaling and mechanistic steps of a cytokinin regulated senescence process has yet to be demonstrated. This may be in part because the relationship between senescence and primary metabolism implied by the key role of cell-wall invertase is the subject of two apparently opposing bodies of evidence. Here we briefly summarize and propose a model in which cytokinin mediated changes in sink/source relationships leads to delayed senescence which is consistent with existing evidence both for and against sugars as a trigger for developmental senescence.

Keywords: carbon allocation; cell wall invertase; cytokinin; leaf; senescence; sink/source relationships.

Figure 1. Model of an emerging pathway integrating current knowledge of cytokinin regulation of senescence. In Arabidopsis, cytokinin perception by AHK leads to activation of ARR2 and induced expression CRF6. It is unclear whether ARR2 directly regulates CRF6 expression in this process. ARR2 and CRF6 proteins may also interact physically in the regulation of downstream genes. One such gene may be cell-wall invertase which has been shown in tobacco and tomato to be necessary for senescence inhibition.

Figure 2. A futile cycle involving CWINV mimics a high rate of carbon export. (A) Loading of sucrose into phloem when photosynthesis rate is high involves pumping large amounts of sucrose into the apoplasm. From the apoplasm it is taken up by companion cells via sucrose symporters. (B) When photosynthesis rate is decreased, less sucrose is available to be pumped into the apoplasm. (C) Cytokinin stimulation of a futile cycle of sucrose export, hydrolyses, uptake and re-synthesis could maintain high rates of sucrose efflux at the expense of long distance transport.