A chemical biology approach reveals an opposite action between thermospermine and auxin in xylem development in Arabidopsis thaliana

Kaori Yoshimoto, Yoshiteru Noutoshi, Ken Ichiro Hayashi, Ken Shirasu, Taku Takahashi, Hiroyasu Motose

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Thermospermine, a structural isomer of spermine, is produced through the action of ACAULIS5 (ACL5) and suppresses xylem differentiation in Arabidopsis thaliana. To elucidate the molecular basis of the function of thermospermine, we screened chemical libraries for compounds that can modulate xylem differentiation in the acl5 mutant, which is deficient in thermospermine and shows a severe dwarf phenotype associated with excessive proliferation of xylem vessels. We found that the isooctyl ester of a synthetic auxin, 2,4-D, remarkably enhanced xylem vessel differentiation in acl5 seedlings. 2,4-D, 2,4-D analogs and IAA analogs, including 4-chloro IAA (4-Cl-IAA) and IAA ethyl ester, also enhanced xylem vessel formation, while IAA alone had little or no obvious effect on xylem differentiation. These effects of auxin analogs were observed only in the acl5 mutant but not in the wild type, and were suppressed by the anti-auxin, p-chlorophenoxyisobutyric acid (PCIB) and α-(phenyl ethyl-2-one)-IAA (PEO-IAA), and also by thermospermine. Furthermore, the suppressor of acaulis51-d (sac51-d) mutation, which causes SAC51 overexpression in the absence of thermospermine and suppresses the dwarf phenotype of acl5, also suppressed the effect of auxin analogs in acl5. These results suggest that the auxin signaling that promotes xylem differentiation is normally limited by SAC51-mediated thermospermine signaling but can be continually stimulated by exogenous auxin analogs in the absence of thermospermine. The opposite action between thermospermine and auxin may fine-tune the timing and spatial pattern of xylem differentiation.

Original languageEnglish
Pages (from-to)635-645
Number of pages11
JournalPlant and Cell Physiology
Volume53
Issue number4
DOIs
Publication statusPublished - Apr 2012

Fingerprint

Xylem
Indoleacetic Acids
Arabidopsis
xylem
auxins
Arabidopsis thaliana
indole acetic acid
Biological Sciences
xylem vessels
2,4-Dichlorophenoxyacetic Acid
2,4-D
esters
Esters
Clofibric Acid
phenotype
mutants
Small Molecule Libraries
Phenotype
spermine
Spermine

Keywords

  • 2,4-D
  • ACAULIS5
  • Arabidopsis thaliana
  • Auxin
  • Thermospermine
  • Xylem differentiation

ASJC Scopus subject areas

  • Plant Science
  • Physiology
  • Cell Biology

Cite this

A chemical biology approach reveals an opposite action between thermospermine and auxin in xylem development in Arabidopsis thaliana. / Yoshimoto, Kaori; Noutoshi, Yoshiteru; Hayashi, Ken Ichiro; Shirasu, Ken; Takahashi, Taku; Motose, Hiroyasu.

In: Plant and Cell Physiology, Vol. 53, No. 4, 04.2012, p. 635-645.

Research output: Contribution to journalArticle

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abstract = "Thermospermine, a structural isomer of spermine, is produced through the action of ACAULIS5 (ACL5) and suppresses xylem differentiation in Arabidopsis thaliana. To elucidate the molecular basis of the function of thermospermine, we screened chemical libraries for compounds that can modulate xylem differentiation in the acl5 mutant, which is deficient in thermospermine and shows a severe dwarf phenotype associated with excessive proliferation of xylem vessels. We found that the isooctyl ester of a synthetic auxin, 2,4-D, remarkably enhanced xylem vessel differentiation in acl5 seedlings. 2,4-D, 2,4-D analogs and IAA analogs, including 4-chloro IAA (4-Cl-IAA) and IAA ethyl ester, also enhanced xylem vessel formation, while IAA alone had little or no obvious effect on xylem differentiation. These effects of auxin analogs were observed only in the acl5 mutant but not in the wild type, and were suppressed by the anti-auxin, p-chlorophenoxyisobutyric acid (PCIB) and α-(phenyl ethyl-2-one)-IAA (PEO-IAA), and also by thermospermine. Furthermore, the suppressor of acaulis51-d (sac51-d) mutation, which causes SAC51 overexpression in the absence of thermospermine and suppresses the dwarf phenotype of acl5, also suppressed the effect of auxin analogs in acl5. These results suggest that the auxin signaling that promotes xylem differentiation is normally limited by SAC51-mediated thermospermine signaling but can be continually stimulated by exogenous auxin analogs in the absence of thermospermine. The opposite action between thermospermine and auxin may fine-tune the timing and spatial pattern of xylem differentiation.",
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