Loss of function of an Arabidopsis homologue of JMJD6 suppresses the dwarf phenotype of acl5, a mutant defective in thermospermine biosynthesis.

In Arabidopsis thaliana, the ACL5 gene encodes thermospermine synthase and its mutant, acl5, exhibits a dwarf phenotype with excessive xylem formation. Studies of suppressor mutants of acl5 reveal the involvement of thermospermine in enhancing mRNA translation of the SAC51 gene family. We show here that a mutant, sac59, which partially suppresses the acl5 phenotype, has a point mutation in JMJ22 encoding a D6-class Jumonji C protein (JMJD6). A T-DNA insertion allele, jmj22-2, also partially suppressed the acl5 phenotype while mutants of its closest two homologs JMJ21 and JMJ20 had no such effects, suggesting a unique role for JMJ22 in plant development. We found that mRNAs of the SAC51 family are more stabilized in acl5 jmj22-2 than in acl5.