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A single mutation in the M-subunit of Rhodospirillum rubrum confers herbicide resistance
G Sopp1, W A Rutherford, W Oettmeier
1Lehrstuhl Biochemie der Pflanzen, Ruhr-Universität, Bochum, Germany.
Abstract:
Cells of the photosynthetic bacterium Rhodospirillum rubrum were rendered resistant against the inhibitor 2-(1-phenyl)ethylamino-3-propionylamino-4-cyano-thiazole (PPCTH). Electron transport in reaction centers prepared from one of the mutants (M6) was neither inhibited by PPCTH and other NH-thiazoles nor terbutryn. These inhibitors are known to bind at the Q(B) site of the L-subunit. Compared to the wild type, chromatophores from M6 exhibited strongly altered Q(B)- Fe2+ and Q(A)- Fe2+ EPR signals. Inhibitor resistance is due to a mutation in the bacterial reaction center M-subunit, where Glu234 is exchanged against Lys. This is the first example of an inhibitor resistance in the Q(B) site caused by a mutation in the M-subunit.
Insights
Researchers developed Rhodospirillum rubrum resistant to PPCTH, a Q(B) site inhibitor. A mutation in the M-subunit (Glu234Lys) caused this resistance, altering electron transport and EPR signals. This study identifies the first M-subunit mutation conferring Q(B) site inhibitor resistance.
Area of Science:
- Photosynthetic bacteria research
- Molecular biology of electron transport
- Biochemistry of reaction centers
Background:
- Photosynthetic bacteria utilize reaction centers for electron transport.
- Inhibitors like PPCTH target the Q(B) site on the L-subunit.
- Understanding inhibitor resistance mechanisms is crucial for studying electron transport.
Purpose of the Study:
- To generate and characterize Rhodospirillum rubrum mutants resistant to the inhibitor PPCTH.
- To investigate the molecular basis of inhibitor resistance at the Q(B) site.
- To identify specific mutations affecting electron transport and inhibitor binding.
Main Methods:
- Generating bacterial mutants of Rhodospirillum rubrum.
- Preparing reaction centers and chromatophores from wild-type and mutant strains.
- Assessing inhibitor sensitivity (PPCTH, NH-thiazoles, terbutryn) on electron transport.
- Analyzing electron paramagnetic resonance (EPR) signals of Q(A) and Q(B) sites.
Main Results:
- A mutant (M6) displayed resistance to PPCTH and related inhibitors.
- Electron transport in M6 reaction centers was unaffected by these inhibitors.
- Mutant M6 showed altered Q(B)-Fe2+ and Q(A)-Fe2+ EPR signals compared to wild type.
- The resistance was linked to a Glu234Lys substitution in the M-subunit of the reaction center.
Conclusions:
- Inhibitor resistance at the Q(B) site can be caused by mutations in the M-subunit.
- The Glu234Lys mutation in the M-subunit is responsible for PPCTH resistance in Rhodospirillum rubrum.
- This finding represents the first documented instance of M-subunit mutation-induced resistance at the Q(B) site.