Abstract
The acaulis5 (acl5) mutant is defective in the synthesis of thermospermine and exhibits a severe dwarf phenotype. To elucidate the role of thermospermine in stem elongation, we have analysed suppressor mutants of acl5 (sac). We have previously shown that SAC51 encodes a bHLH-type transcription factor and that SAC52 encodes a ribosomal protein L10 (RPL10). SAC51 mRNA has five uORFs in its 5' region and sac51-d has a point mutation in the 4th uORF. Our data have suggested that translation of the SAC51 main ORF is negatively regulated by ribosome stalling at the 4th uORF in the absence of thermospermine. Furthermore, the genes responsible for sac53-d and sac56-d encode a receptor for activated C kinase (RACK1) and a ribosomal protein L4 (RPL4), respectively. These are also components of the ribosome. Based on our experiments, we suggest that sac52-d and sac56-d mutants result in an increase in the translation efficiency of the SAC51 main ORF but sac53-d has a distinct effect for overcoming the deficiency of thermospermine.
