dictyNews
Electronic Edition
Volume 50, number 4
March 15, 2024
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Abstracts
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Functional mechanism study of the allelochemical myrigalone A
identifies a group of ultrapotent inhibitors of ethylene
biosynthesis in plants.
George Heslop-Harrison (1), Kazumi Nakabayashi (2),
Ana Espinosa-Ruiz (3), Francesca Robertson (1,2), Robert
Baines (4), Christopher R.L. Thompson (4), Katrin Hermann (5),
David Alabadí (3), Gerhard Leubner-Metzger (2),
Robin S.B. Williams (1)*
1: Centre for Biomedical Sciences, and
2: Centre for Plant Molecular Sciences, Department of Biological
Sciences, Royal Holloway
University of London, Egham, TW20 0EX, UK;
3: Instituto de Biología Molecular y Celular de Plantas (CSIC-UPV),
46022-Valencia, Spain;
4: Centre for Life's Origins and Evolution, Department of Genetics,
Evolution and Environment, University College London, London,
UK;
5: Syngenta, Crop Protection AG, Stein, Switzerland.
Published in Plant Communications (Plant Comm. 5, 100846)
file:///C:/Users/urba264/Documents/Papers/Robin's
%20published%20papers/Heslop%20Harrison%20et%20al%
20PlantComms%202024.pdf
Allelochemicals represent a class of natural products released
by plants as root, leaf, and fruit exudates that interfere with
the growth and survival of neighboring plants. Understanding
how allelochemicals function to regulate plant responses may
provide valuable new approaches to better control plant function.
One such allelochemical, myrigalone A (MyA) produced by Myrica
gale, inhibits seed germination and seedling growth through an
unknown mechanism. Here, we investigate MyA using the tractable
model Dictyostelium discoideum and reveal that its activity
depends on the conserved homolog of the plant ethylene synthesis
protein 1-aminocyclopropane-1-carboxylic acid oxidase (ACO).
Furthermore, in silico modeling predicts the direct binding of MyA
to ACO within the catalytic pocket. In D. discoideum, ablation of
ACO mimics the MyA-dependent developmental delay, which is
partially restored by exogenous ethylene, and MyA reduces ethylene
production. In Arabidopsis thaliana, MyA treatment delays seed
germination, and this effect is rescued by exogenous ethylene. It
also mimics the effect of established ACO inhibitors on root and
hypocotyl extension, blocks ethylene dependent root hair production,
and reduces ethylene production. Finally, in silico binding analyses
identify arrange of highly potent ethylene inhibitors that block
ethylene-dependent response and reduce ethylene production in
Arabidopsis. Thus, we \demonstrate a molecular mechanism by
which the allelochemical MyA reduces ethylene biosynthesis and
identify a range of ultrapotent inhibitors of ethylene-regulated
responses.
Submitted by Robin Williams [[log in to unmask]]
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