Programmed Cell Death during Plant Senescence - Postharvest Biology and Technology of Fruits, Vegetables, and Flowers - page 100

Further support for the involvement of the ubiquitin/proteasome pathway during senes-
cence comes from the recent report that a mutant defective in AtATE1 gene, an arginyl-
tRNA:protein arginyltransferase involved in the N-end rule pathway, shows a delayed
senescence phenotype in both cotyledons and rosette leaves of Arabidopsis (Yoshida et al.,
2002a). It is possible that a cytosolic or nuclear component is repressing the progress of
senescence, and this factor is destabilized during senescence by the R-transferase activity
of AtATE1 gene product. Ubiquitinated proteins are not necessarily degraded by the 26S
proteasome: many yeast cell surface receptors use ubiquitination for internalization and
degradation by the vacuolar proteases (Wilkinson, 1999). Whatever the case, this indicates
that the N-end rule has an important role in the progression of leaf senescence.
Changes in membrane potential and internal concentrations of Ca 2 + are part of the
signal transduction pathway in animal PCD, and there are indications that this can also be
the case for plants. The recent identification of a cyclic nucleotide-gated ion channel from
Arabidopsis ( AtCNGC2 ) that shows developmental regulation during the early stages of
senescence in different organs, but not in late stages, indicates that this ion channel may
participate in the signaling of the senescence process (Kohler et al., 2001). Furthermore,
the realization that the Arabidopsis mutant dnd1 , which shows reduced ability to undergo
cell death when exposed to avirulent Pseudomonas syringae , is caused by a mutation in
this same gene AtCNGC2 (Clough et al., 2000) supports its role as a mediator in different
forms of PCD.
Identification of additional regulatory elements controlling senescence in plants may
come from genetic approaches. The identification of several ore (from Oresara, long-lived
in Korean language; Oh et al., 1997) mutants indicates that the search can still be fruitful.
Ore mutants show just delayed senescence and not a complete block in senescence. The
reason for this could be multiple pathways acting in parallel to induce senescence, making
genetic screens difficult or alternatively that all the alleles identified so far are weak alleles.
Ore 2 and 3 came out to be alleles of the ethylene-insensitive mutant ein2 and are therefore
affected in the timing of senescence via the ethylene pathway. The nature of old 1, 2, and
3 (onset of leaf death) mutants of Arabidopsis is not known, but mutations in these genes
confer an early onset of senescence (Jing et al., 2002). Characterization of the molecular
basis for several senescence mutants from maize, soybean, and other plants will further
contribute to our understanding of senescence (Buckner et al., 1998).
5.8 Early signal of senescence pathway
A senescence-associated decrease in membrane fluidity has been detected in all senescing
tissue (Paliyath and Droillard, 1992). Changes in membrane composition occur well before
the appearance of any visible symptoms of senescence in petals. There is a senescence-
associated decline in the phospholipid content due to a decrease in synthesis and an increase
in degradation. The ratio of sterol/phospholipid may increase as much as 2-6 times, and this
leads to a decrease in membrane fluidity, which can be detected by fluorescence polarization
and ESR techniques, preceding any visible symptom of senescence in petals. Changes in
fluidity appear to affect the activity of several membrane-bound proteins such as ATPase
and probably many other activities (Paliyath and Droillard, 1992).
In contrast to animal apoptosis, no specific protease has yet been clearly found
to be involved in the initial events of senescence/PCD. A specific role for a matrix