Abstract

Plant peroxisomes are multifunctional organelles that show plasticity in number, size, morphology, cellular location and metabolic functions. Many of these changes occur in response to environmental factors and are decisive for the development and defence of the plant. Among them, peroxisomal beta-oxidation-mediated synthesis of jasmonic acid (JA) is a key process in regulating development as well as wound- or pathogen-triggered defence responses. This work seeks for the connection between wound, JA and the proliferation of peroxisomes in Arabidopsis thaliana. The hypolipidemic drug clofibrate (CFB) induced the proliferation of peroxisomes and the expression of the beta-oxidation 3-ketoacyl-CoA thiolase 2 (KAT2) gene, coding for a key enzyme in the biosynthesis of JA, among other wound- and JA-responsive gene transcripts in Arabidopsis leaves. The CFB-activated expression of wound-responsive genes was not dependent on JA synthesis or perception and those responsive to JA required the function of the F-box protein COI1. In turn, wounding neither triggered peroxisome proliferation nor required peroxisome integrity to activate gene expression. Interestingly, cells from JA-treated leaves contained fewer but larger peroxisomes than cells from untreated leaves. The proliferation of peroxisomes, the synthesis of JA and the activation of wound-responsive genes by CFB, although functionally connected, were uncoupled in Arabidopsis.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.