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pH changes, to determine which signaling events occurred upon catechin
exposure. ROS have been implicated in signal transduction events lead-
ing to downstream responses, such as modulation of gene expression, that
affect several cellular and developmental processes (Huckelhoven and Ko-
gel 2003; Finkel 1998). ROS are also known to accumulate in plant cells
in response to compatible pathogen infections and may damage cellular
structures and nucleic acids, resulting in cell death (Huckelhoven and Ko-
gel 2003). Fluctuations in [Ca
2+
]
cyt
are also known to occur in response
to stress, including high salinity, osmoticum, heavy metals, and oxida-
tive damage (Fasano et al. 2001; Jones et al. 1998). Finally, cytoplasmic
pH changes are associated with signal transduction and regulation of root
growth (Fasano et al.2001; Scott and Allen 1999), and cell viability is closely
tied to homeostasis of cytoplasmic pH.
Bais et al. (2003) showed that all three factors play an important role in the
initial events leading to catechin phytotoxicity. Using the fluorescent dye 6-
carboxy-2
,7
-dichlorodihydrofluorescein diacetate-di(acetoxymethly es-
ter), they determined that within 10 sec, catechin treatment induced a 12-
fold increase in ROS generation in
C. diffusa
and
A. thaliana
seedlings.
Like the pattern of cell death induction, the increase in ROS originated in
the meristematic region of the root tip and moved into the central elon-
gation zone before progressing back through the main axis of the root in
a wavelike fashion. Catechin treatment also resulted in rapid, transient el-
evations in root-tip-localized [Ca
2+
]
cyt
levels. These increases in [Ca
2+
]
cyt
occurred about 30 sec after catechin treatment, following the ROS signal,
but preceding cell death. Approximately 15−20 min after catechin adminis-
tration, consistent with the initial appearance of cell death, the cytosolic pH
dropped from approximately 7.2 to 5.6. These changes most likely reflect
the loss of ion homeostasis associated with cell mortality. Bais et al. (2003)
also demonstrated that exogenous application of an antioxidant, ascorbic
acid, prevented the generation of the initial ROS signal, the subsequent
spike in meristematic [Ca
2+
]
cyt
levels, and cell death, suggesting that the
phytotoxicity of catechin is directly or indirectly due to oxidative stress.
27.3.3
Catechin Exposure Leads to Genome-Wide Changes in
Arabidopsis
Because the model plant
A. thaliana
is susceptible to catechin, Bais et al.
(2003) were able to monitor changes in global gene expression to deter-
mine potential transcriptional events associated with catechin phytotoxic-
ity. Using a 12,000 gene oligoarray, they monitored changes in transcription
10 min, 1 h, and 12 h after
Arabidopsis
roots had been subjected to phyto-
toxic levels of catechin. Within 1 h of treatment a number of genes related
to oxidative stress were upregulated, including glutathione transferase,
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