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Related Experiment Video

Updated: Jun 4, 2026

Quantification of Plasmid-Mediated Antibiotic Resistance in an Experimental Evolution Approach

Quantification of Plasmid-Mediated Antibiotic Resistance in an Experimental Evolution Approach

Published on: December 14, 2019

A molecular evolutionary concept connecting nonhost resistance, pathogen host range, and pathogen speciation.

Paul Schulze-Lefert¹, Ralph Panstruga

¹Max-Planck Institute for Plant Breeding Research, Department of Plant-Microbe Interactions, Carl-von-Linné-Weg 10, D-50829 Köln, Germany.

Trends in Plant Science

|February 15, 2011

Summary

Plant immunity relies on nucleotide-binding and leucine-rich repeat (NB-LRR) proteins and pattern recognition receptors (PRRs). Their roles in nonhost resistance vary with evolutionary distance, influencing pathogen speciation.

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Area of Science:

Plant pathology
Evolutionary biology
Immunology

Background:

Pathogenic microbes usually infect specific plant species.
Nonhost plants resist pathogens through nonhost disease resistance.
Both host and nonhost immunity use pattern recognition receptors (PRRs) and nucleotide-binding and leucine-rich repeat (NB-LRR) proteins.

Purpose of the Study:

To hypothesize how the roles of NB-LRR and PRR immunity in nonhost resistance change with phylogenetic divergence.
To explore how pathogen effector variations drive host range expansion and speciation.

Main Methods:

The study proposes a hypothesis based on existing knowledge of plant immunity and pathogen evolution.
It integrates concepts of plant-pathogen interactions, evolutionary timescales, and genetic mechanisms.

Main Results:

The relative importance of NB-LRR and PRR immunity in nonhost resistance is hypothesized to correlate with phylogenetic divergence time.
Pathogen effector repertoire variation is proposed as a driver for host range expansion and speciation.

Conclusions:

The balance of plant immune components (NB-LRR and PRR) in nonhost resistance is shaped by evolutionary history.
Pathogen evolution, particularly effector diversification, plays a crucial role in shaping host range and driving pathogen speciation.