Abstract
The acaulis5 (acl5) mutant of Arabidopsis is defective in the synthesis of thermospermine, a structural isomer of spermine, and shows severe dwarf phenotype. Decarboxylated S-adenosylmethionine (dcSAM) is a substrate for these polyamines and is synthesized by S-adenosylmethionine decarboxylase (SAMDC). The Arabidopsis genome has four SAMDC genes, SAMDC1~4. Loss-of-function mutants of SAMDC4/BUD2 show bushy and dwarf phenotype. We have found that SAMDC4/BUD2 is down-regulated by exogenous thermospermine while SAMDC1, 2, and 3 are not.
In this study, we examined whether the dwarf phenotype of bud2 is also suppressed by suppressor mutants of acl5, sac51-d, sac52-d, and sac56-d. Our results revealed that these sac mutants rescue the bud2 phenotype. We also confirmed that bud2 mutants contain no detectable level of thermospermine. These findings suggest that SAMDC4/BUD2 plays a major role in thermospermine sythesis and the dwarf phenotype of bud2 is attributed to the lack in thermospermine.
