Effects of Protein Synthesis Inhibitors on Acetylene Reduction Activity of Lupin Root Nodules

Abstract

Rifampicin and D-threo-chloramphenicol inhibited the incorporation of [³⁵S]methionine into purified bacteroid suspensions, and into the bacteroid fraction but not the plant cytoplasmic fraction of cultured nodules. Cycloheximide and anisomycin inhibited [³⁵S]methionine incorporation into the plant cytoplasmic fraction of cultured nodules; at early times they inhibited incorporation into the bacteroid fraction, but at later times this effect was reversed.

Chloramphenicol, rifampicin, spectinomycin, cycloheximide and anisomycin all prevented the induction of acetylene reduction activity in immature nodules; spectinomycin did not prevent induction in nodules containing a spectinomycin-resistant Rhizobium. Neither rifampicin nor chloramphenicol inhibited the acetylene reduction activity of mature nodules, but cycloheximide and anisomycin caused rapid loss of activity. Cycloheximide did not inhibit the acetylene reduction activity of Rhizobium strain 32H1 in pure cultures.

The results suggest that both plant cytoplasmic protein synthesis and bacteroid protein synthesis are needed for the induction of nitrogenase activity in developing lupin nodules, and that plant cytoplasmic protein synthesis but not bacteroid protein synthesis is needed for the maintenance of nitrogenase activity at high levels.