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The xanthophyll cycle as an early pathogenic target to deregulate guard cells during Sclerotinia sclerotiorum infection.

ABSTRACT: Stomata not only control the important balance between gaseous fluxes and water loss, but also act as a route of invading pathogen entry into the plant. Here, the stomatal opening was observed to be induced by a necrotrophic pathogen Sclerotinia sclerotiorum at the early stages of infection. In contrast to uninfected control, the stomatal pores were still opened in S. sclerotiorum-infected regions after dark adaption. Mutation of violaxanthin de-epoxidase, a key enzyme in the xanthophyll cycle, could partially restore the S. sclerotiorum-induced stomatal opening. Further studies showed that S. sclerotiorum invasion led to a decrease in electron transport rate, but a significant increase in non-photochemical quenching (NPQ). The decay kinetics of NPQ revealed that zeaxanthin epoxidase (ZEP, also known as ABA1) was continuous deactivation in S. sclerotiorum-infected region. HPLC-MS/MS analysis showed a slight increase of jasmonate acid (JA), but a great decrease of abscisic acid (ABA) content in S. sclerotiorum-inoculated tissue. Exogenous application of ABA but not JA could rescue the abnormal stomatal opening. Together, these results suggested that the S. sclerotiorum-induced decrease of ABA biosynthesis reduced stomatal closing via dysfunction of the xanthophyll cycle during early pathogenesis.

SUBMITTER: Zeng L

PROVIDER: S-EPMC7012177 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Manipulation of the Xanthophyll Cycle Increases Plant Susceptibility to Sclerotinia sclerotiorum.

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