---
pmid: '35962471'
title: Loss of function of an Arabidopsis homologue of JMJD6 suppresses the dwarf
  phenotype of acl5, a mutant defective in thermospermine biosynthesis.
authors:
- Matsuo H
- Fukushima H
- Kurokawa S
- Kawano E
- Okamoto T
- Motose H
- Takahashi T
journal: FEBS Lett
year: '2022'
full_text_available: false
doi: 10.1002/1873-3468.14470
pubmed_publication_types:
- Journal Article
publication_type: PRIMARY_RESEARCH
---

# Loss of function of an Arabidopsis homologue of JMJD6 suppresses the dwarf phenotype of acl5, a mutant defective in thermospermine biosynthesis.
**Authors:** Matsuo H, Fukushima H, Kurokawa S, Kawano E, Okamoto T, Motose H, Takahashi T
**Journal:** FEBS Lett (2022)
**DOI:** [10.1002/1873-3468.14470](https://doi.org/10.1002/1873-3468.14470)

## Abstract

1. FEBS Lett. 2022 Dec;596(23):3005-3014. doi: 10.1002/1873-3468.14470. Epub 2022
 Aug 12.

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

Matsuo H(1), Fukushima H(1), Kurokawa S(1), Kawano E(1), Okamoto T(1), Motose
H(1), Takahashi T(1).

Author information:
(1)Graduate School of Natural Science and Technology, Okayama University,
Okayama, Japan.

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.

© 2022 Federation of European Biochemical Societies.

DOI: 10.1002/1873-3468.14470
PMID: 35962471 [Indexed for MEDLINE]