ABSTRACT
Despite the importance of senescence processes, our knowledge of the regulatory mechanisms of senescence is still poor. It is well established that senescence is not a chaotic breakdown, but an orderly loss of normal cell function that is under the control of the nucleus. In contrast to ageing processes, which have a passive and non-regulated degenerative character (for review see Krupinska et al., 2003), senescence is an active and highly regulated process. Senescence is triggered by exogenous and endogenous parameters of which the most important endogenous factors are the age of the leaves and the age and developmental stage of the plant. However, how these two parameters are sensed and translated into molecular signals is still unclear. The photosynthetic activity of leaves of annual plants decreases continuously after full expansion (Batt and Woolhouse, 1975; Hensel et al., 1993). In fast-ageing plants like Arabidopsis, the photosynthesis rate of the leaves decreases by 50% within four to six days of full leaf expansion under continuous light conditions (Hensel et al., 1993). A decline in photosynthetic activity under a certain threshold may act as a senescenceinducing signal (Matile et al., 1992; Smart, 1994). However, autumn senescence in freegrowing aspen (Populus tremula) is exclusively initiated by the photoperiod (Keskitalo et al., 2005). Sugar accumulation, as well as sugar starvation, are discussed as signals to induce senescence; however, changes in the sugar content relative to nitrogen content of leaves during the sink/source transition could also play a role in the induction of leaf senescence (Masclaux et al., 2000; Pourtau et al., 2004; van Doorn, 2004; Wingler et al.,
2004). Besides photoperiod and sugar, senescence is most likely triggered by the interplay of all plant hormones in specific concentrations acting in synergistic or antagonistic ways, and in concert with other signals like sugar, calcium and especially reactive oxygen species (ROS) (Zentgraf 2007).
