Cellooligomer/CELLOOLIGOMER RECEPTOR KINASE1 Signaling Exhibits Crosstalk with PAMP-Triggered Immune Responses and Sugar Metabolism in Arabidopsis Roots

Abstract

The degradation of cellulose generates cellooligomers, which function as damage-associated molecular patterns and activate immune and cell wall repair responses via the CELLOOLIGOMER RECEPTOR KINASE1 (CORK1). The most active cellooligomer for the induction of downstream responses is cellotriose, while cellobiose is around 100 times less effective. These short-chain cellooligomers are also metabolized after uptake into the cells. In this study, we demonstrate that CORK1 is mainly expressed in the vascular tissue of the upper, fully developed part of the roots. Cellooligomer/CORK1-induced responses interfere with chitin-triggered immune responses and are influenced by BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE1 and the receptor kinase FERONIA. The pathway also controls sugar transporter and metabolism genes and the phosphorylation state of these proteins. Furthermore, cellotriose-induced ROS production and WRKY30/40 expression are controlled by the sugar transporters SUCROSE-PROTON SYMPORTER1, SUGARS WILL EVENTUALLY BE EXPORTED TRANSPORTER11 (SWEET11), and SWEET12. Our data demonstrate that cellooligomer/CORK1 signaling is integrated into the pattern recognition receptor network and coupled to the primary sugar metabolism in Arabidopsis roots.

Keywords

• cellooligomer
• CELLOOLIGOMER RECEPTOR KINASE1
• BAK1
• FERONIA
• SWEET11
• SWEET12