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.

This is the peer reviewed version of the following article: [Matsuo, H., Fukushima, H., Kurokawa, S., Kawano, E., Okamoto, T., Motose, H. and Takahashi, T. (2022), Loss of function of an Arabidopsis homologue of JMJD6 suppresses the dwarf phenotype of acl5, a mutant defective in thermospermine biosynthesis. FEBS Lett.], which has been published in final form at [https://doi.org/10.1002/1873-3468.14470]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages there of by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.