Dynamics, mechanisms, and evolution of a highly robust plant immune signaling network
F. KATAGIRI (1), R. Hillmer (2), K. Mase (2), N. Hatsugai (2) (1) University of Minnesota, U.S.A.; (2) University of Minnesota, U.S.A.

Microbial pathogens can evolve much faster than plants to break down the plant immune signaling network. Thus, the immune signaling network needs to be highly robust against perturbations to its internal components, so that its underlying mechanisms are effectively concealed from pathogen evolution. (1) We reduced the network to a network of four major signaling sectors (JA, ET, PAD4, and SA) in Arabidopsis and measured the sector activities and the transcriptome response under all possible combinatorial sector perturbations through a time course after flg22 treatment. We found that the transcriptome response mediated by the network is highly buffered from the sector perturbations. We learned mechanistic rules to dynamically model the network using delay differential equations, which generated various testable hypotheses. (2) We found that another sector (sector X) compensates the four sectors in HR signaling during ETI. Since sector X is inhibited by PTI signaling, apparent genetic requirement difference in RPS2- and RPM1-mediated HR signaling can be explained by their signaling kinetic difference. (3) We investigated the evolution of this highly robust network by asking when the subfamilies for important components of the network were neofunctionalized in larger gene families. In most cases we investigated, the neofunctionalization of the subfamilies apparently occurred during seed plant evolution and mostly completed by the emergence of angiosperms.

Abstract Number: P2-2
Session Type: Plenary