Postharvest Biology and Technology of Fruits, Vegetables, and Flowers

PROGRAMMED CELL DEATH DURING PLANT SENESCENCE 101
metalloproteinase (At2-MMP) has been proposed (Golldack et al., 2002) based on the
fast degradation of chlorophyll and early senescence phenotype of an Arabidopsis mutant
in which this gene is interrupted by a T-DNA. According to these workers, senescence
“sensor” is either continuously degraded or specifically activated by MMP; MMP-deficient
tissues would be hypersensitized for senescence (Golldack et al., 2002). A role of At2-MMP
in releasing signal molecules that trigger cell death both in senescence and in other plant
PCD processes such as tracheary element (TE) differentiation (Groover and Jones, 1999;
Delorme et al., 2000) has also been proposed.
5.9 Signaling cascades network
The expression of many senescence-regulated genes is also affected in other signaling
pathways, indicating a crosstalk between senescence/PCD and other routes: response to
environmental stress, hormones, N/C status, sugars, and amino acids, etc. In some cases,
this just indicates that different endogenous/environmental signals can activate the senescence
pathways. But several evidences indicate that there could be at least partially parallel
signaling cascades leading to senescence.
An illustration of how the molecular mechanisms underlying senescence is part of a
network of interactions in which both internal and external factors participate has been
presented by He et al. (2001) using a large-scale enhancer trap strategy and expression
analysis in Arabidopsis. Using this approach, He and coworkers identified 147 lines that
showed increased expression in senescent leaves but not in nonsenescent ones, suggesting
that the construct has landed in a senescence-inducible gene. Expression analysis of
these genes show that 63 of them were specific for senescing leaves, but in 62 lines the reporter
gene was also expressed in senescing flowers, siliques, and stems. And in a few lines
(4), there was expression in young tissues. These results indicated that there must be both
common and specific components among the senescence programs operating in different
organs. The effect of different endogenous and environmental factors on the expression of
these enhancer lines was also studied, and it gives support to the idea that each of these
factors (ABA, JA, darkness, ethylene, brassinosteroids, dehydration, age, and others) contributes
to the senescence program by inducing a subset of senescence-associated genes. A
few of the lines showed increased expression by two or more of the factors, and preliminary
attempts to construct the senescence regulatory network were presented (He et al.,
2001).
One consequence of the existence of a complicated network as anticipated by Gan and
Amasino (1997) is the plasticity of the program, that is, the senescence program can always
proceed through other “branches” of the network. Consistently, most of the homozygous
Sel knockouts showed no phenotype, and only a few displayed delayed senescence (He
et al., 2001). Most interestingly, a majority (2/3) of the 43 transcription factors showing
transcriptional activation during senescence (Chen et al., 2002) are also induced by stress
treatments (bacteria, viruses, fungi or cold, high salt, or osmotic depending on the specific
factor). Indeed, pathogens and ethylene are known to induce senescence, and similar genes
have been identified with both stresses.
In other studies, some members of the bZIP gene family of transcription factors that are
characterized by its induction on exposure of the plants to low temperatures increased during
aging/senescence of leaves (Berberich et al., 1999; Yang et al., 2001). Interestingly, tbzF