RT Journal Article
SR Electronic
T1 Inhibition of jasmonate-mediated plant defences by the fungal metabolite higginsianin B
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 651562
DO 10.1101/651562
A1 Jean-Félix Dallery
A1 Marlene Zimmer
A1 Vivek Halder
A1 Mohamed Suliman
A1 Sandrine Pigné
A1 Géraldine Le Goff
A1 Despoina D. Gianniou
A1 Ioannis P. Trougakos
A1 Jamal Ouazzani
A1 Debora Gasperini
A1 Richard J. O’Connell
YR 2019
UL http://biorxiv.org/content/early/2019/05/30/651562.abstract
AB 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.Highlight A diterpene secondary metabolite produced by a fungal pathogen suppresses plant jasmonate defense signalling by preventing the proteasomal degradation of JAZ repressor proteins.