Publikationen in Druck
Dallery, J.-F.; Zimmer, M.; Halder, V.; Suliman, M.; Pigné, S.; Le Goff, G.; Gianniou, D. D.; Trougakos, I. P.; Ouazzani, J.; Gasperini, D.; O’Connell, R. J. Inhibition of jasmonate-mediated plant defences by the fungal metabolite higginsianin B bioRxiv (2019) DOI: 10.1101/651562
Infection of Arabidopsis thaliana by the
ascomycete fungus Colletotrichum higginsianum is characterised by an
early symptomless biotrophic phase followed by a destructive
necrotrophic phase. The fungal genome contains 77 secondary
metabolism-related biosynthetic gene clusters (BGCs), and their
expression during the infection process is tightly regulated. Deleting
CclA, a chromatin regulator involved in repression of some BGCs through
H3K4 trimethylation, allowed overproduction of 3 families of terpenoids
and isolation of 12 different molecules. These natural products were
tested in combination with methyl jasmonate (MeJA), an elicitor of
jasmonate responses, for their capacity to alter defence gene induction
in Arabidopsis. Higginsianin B inhibited MeJA-triggered expression of
the defence reporter VSP1p:GUS, suggesting it may block bioactive JA-Ile
synthesis or signalling in planta. Using the JA-Ile sensor Jas9-VENUS,
we found that higginsianin B, but not three other structurally-related
molecules, suppressed JA-Ile signalling by preventing degradation of JAZ
proteins, the repressors of JA responses. Higginsianin B likely blocks
the 26S proteasome-dependent degradation of JAZ proteins because it
inhibited chymotrypsin- and caspase-like protease activities. The
inhibition of target degradation by higginsianin B also extended to
auxin signalling, as higginsianin B treatment reduced IAA-dependent
expression of DR5p:GUS. Overall, our data indicate that specific fungal
secondary metabolites can act similarly to protein effectors to subvert
plant immune and developmental responses.
Publikation
Schulze, A.; Zimmer, M.; Mielke, S.; Stellmach, H.; Melnyk, C. W.; Hause, B.; Gasperini, D. Shoot-to-root translocation of the jasmonate precursor 12-oxo-phytodienoic acid (OPDA) coordinates plant growth responses following tissue damage bioRxiv (2019) DOI: 10.1101/517193
Multicellular organisms rely upon the movement of signaling molecules across cells, tissues and organs to communicate among distal sites. In plants, herbivorous insects, necrotrophic pathogens and mechanical wounding stimulate the activation of the jasmonate (JA) pathway, which in turn triggers the transcriptional changes necessary to protect plants against those challenges, often at the expense of growth. Although previous evidence indicated that JA species can translocate from damaged into distal sites, the identity of the mobile compound(s), the tissues through which they translocate and the consequences of their relocation remain unknown. Here, we demonstrated that endogenous JA species generated after shoot injury translocate to unharmed roots via the phloem vascular tissue in Arabidopsis thaliana. By wounding wild-type shoots of chimeric plants and by quantifying the relocating compounds from their JA-deficient roots, we uncovered that the JA-Ile precursor 12-oxo-phytodienoic acid (OPDA) is a mobile JA species. Our data also showed that OPDA is a primary mobile compound relocating to roots where, upon conversion to the bioactive hormone, it induces JA-mediated gene expression and root growth inhibition. Collectively, our findings reveal the existence of long-distance transport of endogenous OPDA which serves as a communication molecule to coordinate shoot-to-root responses, and highlight the importance of a controlled distribution of JA species among organs during plant stress acclimation.
Publikation
Schulze, A.; Zimmer, M.; Mielke, S.; Stellmach, H.; Melnyk, C. W.; Hause, B.; Gasperini, D. Wound-Induced Shoot-to-Root Relocation of JA-Ile Precursors Coordinates Arabidopsis Growth Mol Plant 12, 1383-1394, (2019) DOI: 10.1016/j.molp.2019.05.013
Multicellular organisms rely on the movement of
signaling molecules across cells, tissues, and organs to communicate
among distal sites. In plants, localized leaf damage activates jasmonic
acid (JA)-dependent transcriptional reprogramming in both harmed and
unharmed tissues. Although it has been indicated that JA species can
translocate from damaged into distal sites, the identity of the mobile
compound(s), the tissues through which they translocate, and the effect
of their relocation remain unknown. Here, we found that following shoot
wounding, the relocation of endogenous jasmonates through the phloem is
essential to initiate JA signaling and stunt growth in unharmed roots of
Arabidopsis thaliana. By employing grafting experiments and hormone
profiling, we uncovered that the hormone precursor
cis-12-oxo-phytodienoic acid (OPDA) and its derivatives, but not the
bioactive JA-Ile conjugate, translocate from wounded shoots into
undamaged roots. Upon root relocation, the mobile precursors
cooperatively regulated JA responses through their conversion into
JA-Ile and JA signaling activation. Collectively, our findings
demonstrate the existence of long-distance translocation of endogenous
OPDA and its derivatives, which serve as mobile molecules to coordinate
shoot-to-root responses, and highlight the importance of a controlled
redistribution of hormone precursors among organs during plant stress
acclimation.
Publikationen in Druck
Mielke, S.; Gasperini, D. Interplay between Plant Cell Walls and Jasmonate Production Plant Cell Physiol (2019) DOI: 10.1093/pcp/pcz119
Plant cell walls are sophisticated
carbohydrate-rich structures representing the immediate contact surface
with the extracellular environment, often serving as the first barrier
against biotic and abiotic stresses. Notably, a variety of perturbations
in plant cell walls result in upregulated jasmonate (JA) production, a
phytohormone with essential roles in defense and growth responses.
Hence, cell wall-derived signals can initiate intracellular JA-mediated
responses and the elucidation of the underlying signaling pathways could
provide novel insights into cell wall maintenance and remodeling, as
well as advance our understanding on how is JA biosynthesis initiated.
This Mini Review will describe current knowledge about cell wall-derived
damage signals and their effects on JA biosynthesis, as well as provide
future perspectives.