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Hoeberichts et al., 2005). A great deal of recent research in this area has led to review and
reevaluation of senescence and cell death in plant tissues (Rubinstein, 2000; Thomas et al.,
2003; van Doorn and Woltering, 2004). To date, most genetic analyses of floral senescence
have focused on changes that occur in mature flowers just prior to wilting or color change.
However, senescence of one floral organ (e.g., petal) is part of a developmental continuum
in the flower, preceded by tissue differentiation, growth and maturation of the petal, fol-
lowed by growth and development of seeds, and co-coordinated by plant hormones. Cell
death processes are thought to be regulated by anti- and pro-death proteins, which may be
expressed throughout the life of the flower, providing for the most part a highly regulated
homeostatic balance. Future genetic analyses of floral senescence are likely to identify the
proteins that function to maintain a nonsenescent “youthful” state, and the “prosenescence”
proteins which function to progress cell death. The past decade has seen increasingly rapid
isolation and identification of senescence-associated genes from cut flower crops, with a
somewhat slower movement toward understanding the function and significance of the
gene products. Genome-wide searches for regulatory flower senescence genes have now
been made in a number of flower species, for example, Alstroemeria (Breeze et al., 2004),
carnation (Verlinden et al., 2002), chrysanthemum (Narumi et al., 2005), daffodil (Hunter
et al., 2002), daylily (Panavas et al., 1999), rose (Channeliere et al., 2002), Iris (van Doorn
et al., 2003), Sandersonia (Eason et al., 2002), and petunia (Jones et al., 2005). Character-
izing generic patterns of gene expression has identified common processes that are linked
with the progression of flower senescence (e.g., ethylene signaling and proteolysis). This
approach will also be useful in identifying the order of molecular changes associated with
flower senescence, thereby enabling researchers to accurately study cause and effect. This
chapter focuses on molecular and genetic research published within the last one decade that
has increased our understanding of the processes involved in or regulating flower senescence
(e.g., ethylene, water quality, cytokinin, sugar, proteolysis, membranes, and cell walls), and
its significance to the postharvest industry.
4.2 Petal senescence
In petals of cut flowers undergoing senescence, protein content falls, protease activity
increases, lipid fluidity in the membranes declines, and respiration rate increases (van Doorn
and Stead, 1997). Senescing carnation flowers exhibit a climacteric-like rise in ethylene
production, and exposure of carnation flowers to exogenous ethylene induces in-rolling
of petals, triggering ethylene synthesis, and inducing chemical and physical changes in
microsomal membrane lipids of senescing petals (Bartoli et al., 1996). In chrysanthemum,
which is nonclimacteric, ethylene does not play a role in flower senescence, with only
minor changes in protein content and the proportion of major polypeptides, explaining the
long postharvest life of chrysanthemum. Conditions inhibiting the action of that is by the
supply of silver salt, sodium benzoate or boric acid, or the synthesis of ethylene, that is
by the supply of aminooxyacetic acid (AOA), prolong the vase life of carnations (Serrano
et al., 2001); an invertase inhibitor, apparently synthesized in wilting petals of a number of
flowers ( Ipomoea , alstroemeria, carnation, dahlia, gladiolus, petunia, and rose), affects the
senescence of petals by blocking sucrose hydrolysis to glucose and fructose in the senescing
tissue, which may control the translocation of sucrose from wilted petals to other organs
of the flower. Petal abscission in rose petals is not affected by the water status unless the
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