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Published on: March 9, 2014
Chloroplast coupling factor 1: A species-specific receptor for tentoxin
J A Steele1, T F Uchytil, R D Durbin
1Plant Disease Resistance Research Unit, Agricultural Research Service, U.S. Department of Agriculture, Madison, Wisc., 53706.
Tentoxin, a cyclic tetrapeptide, inhibits plant growth by inactivating photophosphorylation and coupling factor 1 (CF(1)) ATPase. This toxin binds to CF(1) in sensitive plants, causing chlorosis.
Area of Science:
- Plant biochemistry
- Molecular biology
- Phytopathology
Background:
- Tentoxin is a phytotoxin known to induce chlorosis in susceptible plants.
- The precise molecular mechanism of tentoxin's action, particularly its interaction with energy transduction pathways, requires further elucidation.
Purpose of the Study:
- To investigate the molecular basis of tentoxin's phytotoxicity.
- To determine the interaction between tentoxin and coupling factor 1 (CF(1)) ATPase in sensitive and insensitive plant species.
Main Methods:
- Assessing the effect of tentoxin on photophosphorylation and CF(1) ATPase activity in lettuce (sensitive) and radish (insensitive).
- Quantifying tentoxin binding to CF(1) using affinity constants.
- Correlating tentoxin sensitivity with chlorosis induction across multiple plant species.
Main Results:
- Tentoxin inactivated photophosphorylation and CF(1) ATPase in sensitive lettuce by binding to CF(1) with high affinity (1.3–20 x 10^7 M⁻¹).
- Insensitive radish required 20-fold more tentoxin for 50% photophosphorylation inhibition, with unaffected CF(1) ATPase and weak tentoxin binding (< 1 x 10⁴ M⁻¹).
- Tentoxin sensitivity of photophosphorylation correlated with chlorosis sensitivity in six other plant species.
Conclusions:
- Tentoxin exerts its phytotoxic effects by inhibiting CF(1) ATPase activity, a process dependent on high-affinity binding to CF(1).
- Differential binding affinity of tentoxin to CF(1) explains the varying sensitivity observed in different plant species.
- The study establishes a direct link between tentoxin's molecular interaction with CF(1) and its physiological impact, chlorosis.
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