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Published on: December 11, 2012
Coevolution between pathogen-derived proteinases and proteinase inhibitors of host insects
1Justus-Liebig University of Giessen, Institute of Phytopathology and Applied Zoology at the Interdisciplinary Research Center, Giessen, Germany. Andreas.Vilcinskas@agrar.uni-giessen.de
Abstract:
Virulence is thought to coevolve as a result of reciprocal selection between pathogens and their hosts. This paper focuses on coevolution between microbial proteinases operating as virulence factors and host defense molecules of insects. Owing to shorter generation times and smaller genomes, microbes exhibit a high evolutionary adaptability in comparison with their hosts. Indeed, the latter can only compete with pathogens if they evolve mechanisms providing a comparable genetic plasticity. Gene or domain duplication and shuffling by recombination is the driving force behind the countermeasures in host defense effectors. Recent literature provides evidence for both diversifications of fungal proteinases involved in pathogenesis and expansion host proteinase inhibitors subsets contributing to insect innate immunity. For example, the pathogen-associated spectrum of proteolytic enzymes encompasses thermolysin-like metalloproteinases that putatively promoted the evolution of corresponding host inhibitors of these virulence factors which complement the insect repertoire of antimicrobial defense molecules. Beyond mutual diversification of effector molecules coevolution resulted also in sophisticated molecular adaptations of host insects such as sensing and feedback-loop regulation of microbial metalloproteinases and corresponding countermeasures of pathogens providing evasion of host immunity induced by these virulence factors.
Insights
Pathogen proteinases and insect immune molecules coevolve. Insects develop genetic plasticity through gene duplication and recombination to counter microbial virulence factors, enhancing innate immunity.
Area of Science:
- Evolutionary biology
- Insect immunology
- Microbial pathogenesis
Background:
- Pathogen virulence factors and host defense mechanisms are shaped by coevolutionary pressures.
- Microbial pathogens possess high evolutionary adaptability due to shorter generation times and smaller genomes.
- Insects require comparable genetic plasticity to effectively compete with rapidly evolving pathogens.
Purpose of the Study:
- To investigate the coevolution between microbial proteinases (virulence factors) and insect host defense molecules.
- To explore the molecular mechanisms underlying insect countermeasures against microbial virulence.
- To examine the diversification of proteinases and inhibitors in host-pathogen interactions.
Main Methods:
- Analysis of recent literature on microbial proteinases and insect immune effectors.
- Focus on gene/domain duplication and recombination as drivers of host defense evolution.
- Examination of specific examples like thermolysin-like metalloproteinases and their inhibitors.
Main Results:
- Diversification of fungal proteinases involved in pathogenesis has been observed.
- Expansion of insect proteinase inhibitor subsets contributes to innate immunity.
- Coevolution has led to sophisticated host adaptations, including sensing and feedback regulation of microbial metalloproteinases.
- Pathogens have evolved countermeasures to evade host immunity induced by these factors.
Conclusions:
- Reciprocal selection drives the coevolution of virulence factors and host defenses.
- Insects employ genetic mechanisms like duplication and recombination to enhance immune plasticity.
- Sophisticated molecular adaptations occur on both pathogen and host sides during coevolutionary arms races.
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