Biochemistry of Flower Senescence - Postharvest Biology and Technology of Fruits, Vegetables, and Flowers - page 69

addition, the cytokinin-mediated delay of senescence in leaves has been linked to activity
of invertases (Balibrea Lara et al., 2004) (enzymes that hydrolyze sucrose into glucose and
fructose), and since petals share many molecular and hormonal features with leaves, this may
also prove to be the case for flowers. The complexity of interactions known to occur between
sugars and plant hormone pathways in plants has been outlined in a review (Gibson, 2004).
Sugars are also known to modulate plant growth and development (Rolland et al., 2002), and
in flowers the breakdown of long-chain carbohydrates (e.g., fructan and starch) is one of the
main drivers of petal opening (Bieleski, 2000). Functional analyses of sucrose transporter
proteins have shown that these proteins load sucrose into the sieve elements of source or-
gans, and that their activity is critical for the normal growth, development, and reproduction
of Arabidopsis plants (Gottwald et al., 2000). The activity of petal-specific phloem-loading
sucrose transporters has been postulated to achieve the rapid transition from sink to source
in relation to phloem movement (Bieleski, 2000), as floral tissues shift from mature to senes-
cence states. Sugar signaling has also been implicated in the regulation of gene expression
in plants (van Meeteren et al., 2000), and sugar-feeding treatments alter the expression of
senescence-related cysteine protease and

-galactosidase genes in Sandersonia cut flowers
(O'Donoghue et al., 2005). The integration of sugar or polyols-containing pulsing solutions
into postharvest regimes is effective for maintaining quality and delaying the onset of senes-
cence in gladiolus (Arora and Singh, 2006) and many other cut flowers. Experimentation
suggests that sugars have a role not only as an energy source but also in regulating gene
expression.

β

4.13 Membrane permeability

A consistent feature of senescence is the loss of differential permeability of cell membranes
(Thompson, 1988). Deterioration of cellular membranes causes increased membrane per-
meability, loss of ionic gradients, and decreased function of key membrane proteins (e.g.,
ion pumps) (Paliyath and Droillard, 1992). Changes in the properties of membranes, such
as increases in microviscosity, alterations in saturation/desaturation ratios of fatty acids,
and peroxidation of lipids, are known to occur during petal senescence, with a causal
link to reactive oxygen species, which are often elevated as a result of stress and have
been implicated in the progression of petal senescence. Membrane deterioration is com-
monly associated with progressive decreases in membrane phospholipid content through
phospholipase activity. Increased lipase (lipolytic acyl hydrolase) and lipoxygenase activ-
ity has been linked to the onset of membrane leakiness in carnation (Hong et al., 2000)
and rose (Fukuchi-Mizutani et al., 2000), respectively, but a loss of membrane function in
Alstroemeria occurs without increased activity of lipoxygenase (Leverentz et al., 2002),
suggesting that loss of membrane integrity can be achieved in a number of ways. In petals,
phosphatidylcholine and phosphatidylethanolamine make up 75% of the membranes' phos-
pholipids (Borochov and Woodson, 1989). A senescence-induced lipase with lipolytic acyl
hydrolase activity has been identified from carnation flowers (Hong et al., 2000). The
abundance of the lipase mRNA increases just as carnation petals begin to in roll and is
enhanced by treatment with ethylene. Understanding the cause of membrane breakdown
in senescing tissues also has implications for signal transduction chains, as the compo-
nents of these chains are often associated with membranes. These aspects are addressed in
Chapter 9.