Delay of Senescence by Cytokinin

Extensive research has identified cytokinins as the most effective senescence-retarding growth regulators. Cytokinins have been known to regulate various aspects of plant growth and development, including cell differentiation, release of lateral buds from apical dominance, and senescence. Much evidence suggests that cytokinins play an important role in senescence (see Chapter 6 for further details). Interestingly, in the transgenic plants expressing the KNOTTED 1 (KN1) gene under the control of the SAG12 promoter (SAG: senescence-associated gene), delayed senescence was accompanied by the increase of cytokinin content in older leaves. Thus, the effect of KN1 on senescence may be mediated through changes in cytokinin levels (Ori et al., 1999). In sorghum, a dominant gene produces a stay-green trait, apparently through promoting cytokinin formation by the roots (Ambler et al, 1992; Walulu et al., 1994).

Arecent observation that a mutation in a putative cytokinin receptor of Arabidopsis delays senescence adds more intriguing support for the role of cytokinin in senescence (Kim, Lim, Woo, Hwang, and Nam, unpublished results).

C. Regulation of Senescence by Ethylene

Ethylene has long been known as an endogenous regulator of senescence, including fruit ripening and flower and leaf senescence. The involvement of ethylene in a senescence process is described in detail in Chapter 8. Many mutations acting on a wide range of steps in ethylene signaling also influence senescence, including leaf senescence, sometimes fairly selectively, sometimes as part of a pleiotropic spectrum. The importance of ethylene in controlling senescence is illustrated by ore3, which is an allele of ein2 (ethylene-insensitive2 mutation) (Oh et al., 1997).

D. Change of Senescence by Brassinosteroid Biosynthesis

Besides promotion of cell elongation and division, brassinosteroids, as other plant hormones, also exhibit broad effects throughout plant development, including retardation of abscission, promotion of ethylene biosynthesis, and enhancement of stress resistance (Fujioka et al., 1997). Thus, it is expected that the genes controlling biosynthesis or perception of brassinosteroids also affect senescence, although the effect of brassinosteroids on plant senescence has not been extensively examined. There is genetic evidence that brassi-nosteroids may be also involved in leaf senescence. The det2 (de-etiolated2) mutation has a defect at an early step in brassinosteroid biosynthesis, and this was reported to confer delayed leaf senescence symptoms, i.e., delayed leaf yellowing (Chory et al., 1991). It will be necessary to further examine the phenotype with other senescence markers to establish that the genes related to synthesis or perception of brassinosteroids alter senescence.

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