The term vegetable is used to describe a harvested edible plant product that is a member of the following categories: tubers, bulbs, roots, leaves, flowers, stem and fruit vegetables. Since senescence in fruits is discussed elsewhere in this book, we will confine discussion to the other categories. There are several distinct patterns of natural plant senescence: 1. Overall senescence, 2. Top senescence, 3. Deciduous senescence, 4. Progressive senescence of leaves, and 5. Bottom senescence of storage organs during sprouting. While this scheme is not always applicable to harvested vegetables, there are many similarities, such as tubers resulting from type 2 and then progressing into type 5 senescence. Also, the mechanisms of harvest-induced senescence in asparagus and broccoli are similar to natural deciduous and flower senescence respectively (King and O'Donoghue, 1995; Pogson et al., 1995).
When considering vegetable senescence, researchers often define the onset of substantial senescence as being when the limits of the marketable quality (or appearance) of the vegetable are reached; this is also referred to as storage life. Consequently, in different types of vegetables the criteria for senescence will differ. In leafy vegetables senescence is indicated by substantial chlorophyll loss and wilting. Whereas in roots and storage organs it is indicated by commencement of sprouting and increased pathogen infection (Schouten, 1987). Chlorophyll loss is an indicator of green tissue senescence, since chloroplast pigments, lipids and proteins are typically the first compounds to be degraded (Noodén et al., 1997). This loss becomes significant 24-48 h at 20°C in the dark after detachment for leaves, spinach and broccoli.
Senescence is defined as a series of active degenerative processes of a cell, organ or organism that are under genetic control, whereas aging is considered a passive process of accumulated defects (Noodén, 1988a,b). Aging may advance the induction of senescence, for example leaves of Arabidopsis mutants impaired in photoprotection, appear to be more susceptible to free radical damage and senesce more rapidly (Bjorkman and Niyogi, 1998; Pogson et al., 1998). Senescence requires active synthesis of cytoplasmic proteins and RNA, with over 30 senescence-associated genes (SAGs) being up regulated (Gan and Amasino, 1997). Even when chlorophyll (Chl) loss is 80%, further loss can be halted by inhibitors of cytoplasmic protein synthesis, or at times even reversed, as shown when pods are removed from senescing soybeans (Brady, 1988).
The membranes, enzymes and other cellular components of a typical plant cell are being continually synthesized (metabolites) and degraded (catabolites) (Brady, 1988). In immature tissue, the balance is in favor of synthesis, while in senescing tissues the balance is in favor of degradation. The shift to catabolism enables nutrient reallocation between organs (Emmerling, 1880). However, the nutrient deficiency of a sink organ is generally not the initiator of the senescence response (Noodén et al., 1997). In general it is a combination of environmental or developmental cues initiating changes in hormone fluxes that promote the active degradation of the targeted tissue (Fig. 22-1; Noodén, 1988a). Although in specific instances like asparagus spear senescence, sucrose content may be an early signal for the subsequent degradative pathways (King and O'Donoghue, 1995). Cytokinins, gibberellins and to some extent auxins typically retard senescence, and other phytohormones such as ethylene, ABA and the jasmonates typically increase the rate of senescence (Fig. 22-1);
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