A single mutation in the M-subunit of Rhodospirillum rubrum confers herbicide 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.