The xanthophyll cycle as an early pathogenic target to deregulate guard cells during Sclerotinia sclerotiorum infection. (2nd January 2020)

• Record Type: Journal Article
• Authors: Zeng, Lizhang; Yang, Xiangbo; Zhou, Jun
• Is Part Of: Plant signaling & behavior. Volume 15:Number 1(2020)
• Publication Date: 2020-01-02
• Subjects: Stoma -- oxalic acid -- non-photochemical quenching -- electron transport rate -- the xanthophyll cycle; Plant ecophysiology -- Periodicals; Plant cellular signal transduction -- Periodicals; Plant cellular signal transduction; Plant ecophysiology; Periodicals; Electronic journals; 581
• DOI: 10.1080/15592324.2019.1691704
• Languages: English
• ISSNs: 1559-2316

Abstract

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.