Dissertation

Transcriptional regulation of effector-triggered immunity (ETI): from tissue to cells

Plants rely on multilayered immune systems to detect and restrict pathogen invasion while minimizing damage to host tissues. This thesis investigates the regulation, spatial organization, and functional consequences of effector-triggered immunity (ETI) in Arabidopsis thaliana.

Author: H. Chhillar
Date: 03 June 2026
Links: Thesis in Leiden Repository

First, this work demonstrates that the two major ETI signaling branches, EDS1-PAD4-ADR1 and EDS1-SAG101-NRG1, contribute differently to ETI, with one primarily promoting pathogen restriction and growth arrest, and the other predominantly controlling hypersensitive cell death responses. Second, using single-cell transcriptomics combined with chemically induced ETI, this thesis reveals that immune execution is highly cell-type specific. While a shared defense program is broadly activated, individual cell types engage distinct transcriptional modules shaped by local regulatory environments. Epidermis-enriched transcriptional regulators were shown to restrict pathogen invasion into internal tissues, highlighting a spatial division of immune functions. Finally, this thesis demonstrates that hypersensitive response (HR)-associated cell death can be genetically uncoupled from effective pathogen resistance. The Arabidopsis cbp60g sard1 mutant exhibits exaggerated HR but only partial resistance to bacterial and oomycete pathogens, challenging the assumption that strong cell death is universally required for ETI-mediated immunity. Together, these findings refine current models of plant immune regulation and provide frameworks for engineering disease resistance while minimizing growth penalties in crops.