By ResearchSEA
Sunday, November 29, 2009
Internal degradation within plant cells and their
response to aging and disease are linked
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| Comparison of a normal Arabiadopsis plant (left) with two
mutants under nutrient-rich conditions. All plants were grown under
the same environmental conditions for five weeks. |
| Copyright : RIKEN 2009 |
The internal degradation process within cells of higher plants
known as autophagy plays a role in limiting programmed cell death
in response to infection and aging, according to recent findings by
a RIKEN-led research group. The group has also uncovered important
molecular components of the mechanism by which this occurs.
Autophagy is known to form the core of plant responses to
starvation, so understanding how it works has significant
consequences for plant survival under changing environmental
conditions.
During autophagy a part of the cell—often including
organelles, such as endoplasmic reticulum, Golgi bodies and
mitochondria—is engulfed into a vesicle surrounded by a
double membrane. This structure then fuses with and delivers its
contents to another specialized vesicle full of enzymes that break
down the plant molecules into simpler components. The plant can
then use these components to build new molecules. Thus, it was long
thought that autophagy was simply a mechanism for plants to recycle
their molecular resources during times of scarcity.
The ATG genes involved in autophagy, however, are still active
under nutrient-rich conditions. To investigate why, Kohki Yoshimoto
and colleagues at the RIKEN Plant Science Center in Yokohama,
together with researchers from the Japanese National Institute for
Basic Biology and the Max Planck Institute for Plant Breeding
Research in Germany, undertook biochemical, pharmacological and
genetic studies in the plant Arabidopsis of two atg mutants in
which autophagy was defective.
Under nutrient-rich conditions, the researchers found that the
mutant plants grew quite normally, but showed early signs of
senescence or aging and increased sensitivity to infection. In
short, the cells became more likely to undergo programmed cell
death from these two causes. They also displayed a build-up of
salicylic acid (SA), a signaling compound that stimulates others
into action, suggesting that autophagy plays a role in regulating
SA signaling.
The researchers then studied plants that were both SA deficient as
well as atg mutants, and found this combination suppressed the atg
mutant features. The suppression of the mutant characteristics was
restored when they added a compound that triggers the same
receptors as SA. In addition, autophagy could be induced in
wild-type plants by this compound, but not when a critical
downstream protein, NPR1, was missing or defective.
Yoshimoto says the team proposes that: “During aging or
infection, SA signaling is accelerated, but that also induces
autophagy via NPR1, which in turn modulates the SA signaling,
limiting cell death.”
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Journal information
1. Yoshimoto, K., Jikumaru, Y., Kamiya, Y., Kusano, M.,
Consonni, C., Panstruga, R., Ohsumi, Y. & Shirasu, K. Autophagy
negatively regulates cell death by controlling NPR1-dependent
salicylic acid signaling during senescence and the innate immune
response in Arabidopsis. The Plant Cell 21, 2914-2927 (2009).
SOURCE