Poster
Anika Damm
University of Cambridge
CAMBRIDGE, UNITED KINGDOM
Clement Pellegrin
University of Cambridge
Cambridge, England, United Kingdom
Alexis L. Sperling
University of Cambridge
Cambridge, England, United Kingdom
Beth Molloy
University of Cambridge
Cambridge, England, United Kingdom
Dio S. Shin
University of Cambridge
Cambridge, England, United Kingdom
Jonathan Long
University of Cambridge
Cambridge, England, United Kingdom
Paul Brett
John Innes Centre
Norwich, England, United Kingdom
Priya Desikan
University of Cambridge
Cambridge, England, United Kingdom
Tochukwu Chisom Iguh
University of Cambridge
Cambridge, England, United Kingdom
Paulo Vieira
Research Molecular Biologist
USDA
Beltsville, Maryland, United States
Joffrey Mejias
INRAE, Université Côte d’Azur, CNRS, ISA
Sophia Antipolis, Provence-Alpes-Cote d'Azur, France
Anil Kumar
Iowa State University
Ames, Iowa, United States
Tom R. Maier
Iowa State University
Ames, Iowa, United States
Thomas J. Baum
Iowa State University
Ames, Iowa, United States
Sebastian Eves-Van Den Akker, PhD
The Crop Science Centre, Department of Plant Sciences, University of Cambridge
Cambridge, England, United Kingdom
Many pathogens secrete discrete and sequential waves of effectors to manipulate their host. However, the regulators and signals that shape this sophisticated trans-kingdom dialogue are poorly understood. Here, we show that a pair of transcription factors in the plant-parasitic cyst nematodes are stimulated by discrete plant signals termed effectostimulins: small, host-specific molecules that vary in natural populations. We use comparative RNAseq analysis to show that these effectostimulin-activated transcription factors work in concert to regulate the sequential deployment of effectors. The nuclear hormone receptor SUGR-1 activates early-stage effector expression required for plant invasion. Subsequently, its homologue DGR-1 represses these early-stage effectors and activates later-stage effectors, defining a critical switch in effector deployment associated with immune suppression. Together, these data allow us to build a conceptual model of effector production, highlighting crucial checkpoints and showing how pathogens adapt to spare resources when they must and promote parasitism only when it counts. Importantly, given that knockdown of sugr-1 reduces root penetration by 80%, blocking the regulators of effector deployment may open novel and generalisable control mechanisms to pathogens that secrete effectors.