Aphids are insect pests that use piercing-sucking mouthparts to navigate into leaf tissues and feed from phloem sap. During feeding and probing, aphids penetrate the rigid plant cell walls and deliver effector proteins mixed with saliva into the host plant cells. Cell wall-damage usually leads to the release of damage-associated molecular patterns (DAMPs), including oligogalacturonides (OGs), which promote PRR-triggered immunity (PTI) against pathogens. Whether OG-induced plant defence responses play a role in aphid-plant interactions is not fully understood. Here we show that OGs are released in aphid-exposed leaves but less so than in non-treated plants indicating that these insects may suppress the accumulation of OGs during feeding. Prior exposure of plants to OGs induces plant defense responses that reduce the ability of M. persicae to colonize plants. This plant defense is suppressed by the aphid effector Mp10 (also known as chemosensory protein 4 or CSP4) that is delivered by aphids into the cytoplasm of plant cells. Mp10 suppresses PTI responses to OGs and a variety of other elicitors. Prolonged leaf exposure to Mp10 leads to chlorosis that is dependent on SGT1 and EDS1, central regulators of intracellular NLR receptor signaling and effector-triggered immunity (ETI). However, we identified other aphid effectors that suppress ETI. Therefore, aphids actively manage the impact of feeding damage by limiting OG release and suppressing cell wall associated immunity.

Aphids curtail the impact of feeding damage by limiting oligogalacturonide release and suppressing cell wall associated immunity / Gravino, Matteo; Pontiggia, Daniela; T Mugford, Sam; Joyce, Joshua; Drurey, Claire; Prince, David; Cervone, Felice; DE LORENZO, Giulia; Hogenhout, Saskia A.. - (2023). (Intervento presentato al convegno 2023 International Society for Molecular Plant-Microbe Interactions (2023 IS-MPMI) tenutosi a Providence, Rhode Island, US.) [10.5281/zenodo.8180698.svg].

Aphids curtail the impact of feeding damage by limiting oligogalacturonide release and suppressing cell wall associated immunity

Daniela Pontiggia
Secondo
;
Giulia De Lorenzo;
2023

Abstract

Aphids are insect pests that use piercing-sucking mouthparts to navigate into leaf tissues and feed from phloem sap. During feeding and probing, aphids penetrate the rigid plant cell walls and deliver effector proteins mixed with saliva into the host plant cells. Cell wall-damage usually leads to the release of damage-associated molecular patterns (DAMPs), including oligogalacturonides (OGs), which promote PRR-triggered immunity (PTI) against pathogens. Whether OG-induced plant defence responses play a role in aphid-plant interactions is not fully understood. Here we show that OGs are released in aphid-exposed leaves but less so than in non-treated plants indicating that these insects may suppress the accumulation of OGs during feeding. Prior exposure of plants to OGs induces plant defense responses that reduce the ability of M. persicae to colonize plants. This plant defense is suppressed by the aphid effector Mp10 (also known as chemosensory protein 4 or CSP4) that is delivered by aphids into the cytoplasm of plant cells. Mp10 suppresses PTI responses to OGs and a variety of other elicitors. Prolonged leaf exposure to Mp10 leads to chlorosis that is dependent on SGT1 and EDS1, central regulators of intracellular NLR receptor signaling and effector-triggered immunity (ETI). However, we identified other aphid effectors that suppress ETI. Therefore, aphids actively manage the impact of feeding damage by limiting OG release and suppressing cell wall associated immunity.
2023
File allegati a questo prodotto
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1696464
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact