Senescence mechanisms

Abstract

Senescence in plants is usually viewed as an intemally programmed degeneration leading to death. It is a developmental process that occurs in many different tissues and serves different purposes. Generally, apoptosis refers to programmed death of small numbers of animal cells, and it shows some special features at the cell level. Some senescing plant cells show some symptoms typical of apoptosis, while others do not. This review will focus primarily on leaf senescence with ultimate aim of explaining whole plant senescence (i.e., monocarpic senescence). Traditionally, the ideas on senescence mechanisms fall into two major groupings, nutrient deficiencies (e.g., starvation) and genetic programming (i.e., senescence-promoting and senescence-inhibiting genes). Considerable evidence indicates that nutrient deficiencies are not central senescence program components, while increasing evidence supports genetic programming. Because chlorophyll (Chi) and chloroplast (CP) breakdown are so prominent, leaf senescence is generally measured in terms of Chi loss. Although CP breakdown may not be the proximate cause of leaf cell death, it certainly is important as a source of nutrients for use elsewhere, e.g., for developing reproductive structures in monocarpic plants, and this loss limits assimilatory capacity. The CP is dismantled in an orderly sequence. Individual protein complexes seem to be taken out all at once, not one subunit at a time. Removal of any component, e.g., Chi, seems to destabilize the whole complex. It is of special interest that senescing CPs secrete Chl-containing globules indicating that some CP components are broken down outside the CP. Senescence appears to be imposed on the CP by the nucleus, and all the known senescencealtering genes except one, cytG in soybean, are nuclear. Only the djd2 mutation(s) in soybean prevents a broad range of leaf senescence processes. Exactly, what causes cell death is unclear; however, the selective thiol protease inhibitor, E-64, does delay death, and this suggests that proteases play a key role.

Activities of fructan- and sucrose-metabolizing enzymes in wheat stems subjected to water stress during grain filling

“…We speculate, however, that the slow remobilization of carbon reserves for HN-WW plants may also relate to the delayed senescence. It is generally assumed that cytokinins play a role in retardation of plant senescence (Buchanan-Wollaston 1997; Nooden et al 1997). We observed that the plants at HN contained much higher cytokinin (Z+ZR) levels in leaves than those at NN (Fig.…”

Identification of a transcription factor specifically expressed at the onset of leaf senescence

“…Dierent sets of genes, designated senescence-associated genes (SAGs; Hensel et al 1993;Lohman et al 1994) are up-regulated during senescence and encode proteins involved in the breakdown of cellular components, including ribonucleases, polyubiquitin proteases, and cell wall hydrolases. Other gene products are associated with the mobilization of nutrients and minerals, such as fatty acids, nitrogen compounds and phosphate, out of the senescing tissue and into developing parts of the plants (reviewed in Bleecker and Patterson 1997;Buchanan-Vollaston 1997;Had®eld and Bennett 1997;Nam 1997;Noode n et al 1997;Biswal and Biswal 1999;Quirino et al 2000). However, there is a large overlap of gene expression patterns between senescence and stress-, pathogen-and hormoneresponse (Park et al 1998;Weaver et al 1998;Quirino et al 1999).…”

Abscisic acid and cytokinins in the root exudates and leaves and their relationship to senescence and remobilization of carbon reserves in rice subjected to water stress during grain filling

“…Leaf senescence is usually correlated with a decrease in cytokinins in the leaves (Buchanan-Wollaston 1997; Nooden et al 1997). Treatment with cytokinins has been shown to delay leaf senescence in many plants (van Staden et al 1988).…”