Three Pectin Methylesterase Inhibitors Protect Cell Wall Integrity for Arabidopsis Immunity to Botrytis

Abstract

Infection by necrotrophs is a complex process that starts with the breakdown of the cell wall (CW) matrix initiated by CW-degrading enzymes and results in an extensive tissue maceration. Plants exploit induced defense mechanisms based on biochemical modification of the CW components to protect themselves from enzymatic degradation. The pectin matrix is the main CW target of , and pectin methylesterification status is strongly altered in response to infection. The methylesterification of pectin is controlled mainly by pectin methylesterases (PMEs), whose activity is posttranscriptionally regulated by endogenous protein inhibitors (PMEIs). Here, AtPMEI10, AtPMEI11, and AtPMEI12 are identified as functional PMEIs induced in Arabidopsis () during infection. AtPMEI expression is strictly regulated by jasmonic acid and ethylene signaling, while only AtPMEI11 expression is controlled by PME-related damage-associated molecular patterns, such as oligogalacturonides and methanol. The decrease of pectin methylesterification during infection is higher and the immunity to is compromised in ,, and mutants with respect to the control plants. A higher stimulation of the fungal oxalic acid biosynthetic pathway also can contribute to the higher susceptibility of mutants. The lack of expression does not affect hemicellulose strengthening, callose deposition, and the synthesis of structural defense proteins, proposed as CW-remodeling mechanisms exploited by Arabidopsis to resist CW degradation upon infection. We show that PME activity and pectin methylesterification are dynamically modulated by PMEIs during infection. Our findings point to AtPMEI10, AtPMEI11, and AtPMEI12 as mediators of CW integrity maintenance in plant immunity.

A Pectin Methylesterase Inhibitor Enhances Resistance to Verticillium Wilt

“…4E). These 240 results were consistent with a previous report that showed that AtPMEI expression is 241 strictly regulated by JA and ET (Lionetti et al, 2017). In that study, after induction …”

“…In addition, plant resistance to fungal pathogens is compromised in PMEI 403 mutants where PMEI expression is impaired (Lionetti et al, 2017). In agreement with 404 these previous findings, GhPMEI3 was able to restrict fungal mycelial growth.…”

“…4D). GhPMEI3 expression is induced by exogenous 235 OGs, an elicitor involved in various defense responses (Lionetti et al, 2017).…”

“…The pellet that 628 contained the alcohol-insoluble residues was dried overnight in a fume hood at room 629 temperature, and starch was removed by α-amylase treatment (Lionetti et al, 2017).…”

Interplay of apple volatile organic compounds with Neofabraea vagabunda and other post‐harvest pathogens

“…However, differences in the relative abundance of VOCs emitted in common were recorded among these pathogens. In particular, B. cinerea showed the most rapid and intense release of methanol during growth on AA, probably due to its faster mycelial growth rate (data not reported) and the marked pectin demethylation caused by this fungus (Lionetti et al , ); P. expansum emitted the highest amounts of furan, m ‐cresol, ( Z )‐β‐farnesene, geosmin ( trans ‐1,10‐dimethyl‐ trans ‐9‐decanol) and 3‐methylanisole (1‐methoxy‐3‐methylbenzene), in agreement with other reports (Azeem et al , ; Wang et al , ); while C. fioriniae emitted the most abundant concentration of acetaldehyde and ethanol. Unique emission of some minor VOCs was also recorded by a single fungal species.…”