Postharvest Biology and Technology of Fruits, Vegetables, and Flowers

PROGRAMMED CELL DEATH DURING PLANT SENESCENCE 103
benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester (BTH; Weymann et al., 1995;
Rate et al., 1999; Shah et al., 1999; Brodersen et al., 2005). Similarly, nahG inhibits PCD
induction by the mycotoxin fumonisin B1 (Asai et al., 2000). Thus, the clearest links of SA
to PCD induction are based on analysis of NahG plants.
5.11 Regulation of senescence by sugar signaling
Coordination of development with the availability of nutrients, such as soluble sugars, may
help ensure an adequate supply of building materials and energy with which to carry out
specific developmental programs. For example, in vivo and in vitro experiments suggest
that increasing sugar levels delay seed germination and stimulate the induction of flowering
and senescence in at least some plant species. Higher sugar concentrations can also increase
the number of tubers formed by potatoes and can stimulate the formation of adventitious
roots by Arabidopsis. New insights into the mechanisms by which sugar response pathways
interact with other response pathways have been provided by microarray experiments,
examining sugar-regulated gene expression under different light and nitrogen conditions
(Gibson, 2005).
Senescent cells show a decline in photosynthetic rate; furthermore, certain components
of the photosynthetic apparatus are the early target for proteolysis, and the mRNA transcripts
for such proteins are downregulated during senescence. Increasing evidence supports that
sugars, the primary products of photosynthetic activity have, in addition to their essential
roles as substrates and source of energy, important functions in signaling (Rolland et al.,
2002).
The evidence regarding this puzzle is fragmentary and sometimes contradictory. Thus,
sugars are known to repress photosynthetic gene expression (occurring during senescence).
Contents of glucose and fructose in leaves increased with age, while starch content diminished
(Wingler et al., 1998). Moreover, glucose-oversensitive mutants of Arabidopsis such
as hysl/cpr5 are indeed selected by the hypersenescence phenotype (Yoshida et al., 2002b).
Senescent petals also contain enough levels of reducing sugars, and therefore limited respiratory
substrate is unlikely to be a major factor in petal senescence. Sucrose itself may
accumulate at high levels in senescing tissues (Crafts-Brandner et al., 1984), although in
this case sucrose is likely to be synthesized via glyoxylate pathway.
How can sugars act as signals for senescence? Often, a key role on sage signaling
has been attributed to hexokinase (HXK). HXK is known to be a glucose sensor that
monitors sugar levels and responds by modulating gene expression and multiple plant
hormone-signaling pathways. In addition, the expression of HXK correlates well with the
rates of leaf senescence. This could indicate that the plant coordinates the activity sources
and sink organs (carbohydrate importing or exporting sites) according to the internal and
external conditions (Sheen et al., 1999; Smeekens, 2000). Furthermore, the transport of
monosaccharides appears to increase during advanced leaf senescence as shown for the
homolog SFPI (Quirino et al., 2001).
Like other terminally differentiated organs, mature flower petals and leaves contain
highly active invertases, whose activities decrease during senescence and as a consequence,
the ratio of sucrose to reducing sugars increases. It has been proposed that de novo synthesis
of an invertase inhibitor is the reason for the decrease in invertase activity. This will leave
more sucrose available for mobilization to other parts of the plant.