A potential tradeoff between feeding rate and aversive learning determines intoxication in a Caenorhabditis elegans host-pathogen system

Microbes Infect. 2020 Sep;22(8):340-348. doi: 10.1016/j.micinf.2020.01.002. Epub 2020 Jan 31.

Abstract

Despite being the first line of defense against infection, little is known about how host-pathogen interactions determine avoidance. Caenorhabditis elegans can become infected by chemoattractant-producing bacteria through ingestion. The worms can learn to associate these chemoattractants with harm through aversive learning. As a result, the worms will avoid the pathogen. Evolutionary constraints have likely shaped the attraction, intoxication and learning dynamics between bacteria and C. elegans, but these have not been explored. Using bacteria engineered to express an acylhomoserine lactone chemoattractant and a nematicidal protein, we explored how manipulating the amount of attractant produced by the bacteria affects learning and intoxication in mixed stage populations of C. elegans. We found that increasing the production rate of the chemoattractant increased the feeding rate in C. elegans, but decreased the time required for C. elegans to learn to avoid the chemoattractant. Learning generally coincided with a decreased feeding rate. We also observed that the percentage of intoxicated worms was maximized at intermediate production rates of the attractant. We propose that interactions between attractant driven feeding rate and aversive learning are likely responsible for this trend. Our results increase our understanding of behavioral avoidance in C. elegans and have implications in understanding host-pathogen dynamics that shape avoidance.

Keywords: Acylhomoserine lactone; Avoidance; Crystal toxin protein; Evolutionary tradeoff; Feeding rate; Learning deficient.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acyl-Butyrolactones / analysis
  • Acyl-Butyrolactones / metabolism
  • Animals
  • Avoidance Learning*
  • Bacillus thuringiensis Toxins / genetics
  • Bacillus thuringiensis Toxins / metabolism
  • Bacillus thuringiensis Toxins / toxicity
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism
  • Biological Evolution
  • Caenorhabditis elegans / microbiology*
  • Caenorhabditis elegans / physiology*
  • Endotoxins / genetics
  • Endotoxins / metabolism
  • Endotoxins / toxicity
  • Escherichia coli / genetics
  • Escherichia coli / metabolism
  • Feeding Behavior*
  • Gene Expression
  • Hemolysin Proteins / genetics
  • Hemolysin Proteins / metabolism
  • Hemolysin Proteins / toxicity
  • Host-Pathogen Interactions
  • Reaction Time
  • Transcription Factors / genetics
  • Transcription Factors / metabolism

Substances

  • Acyl-Butyrolactones
  • Bacillus thuringiensis Toxins
  • Bacterial Proteins
  • Endotoxins
  • Hemolysin Proteins
  • LuxI protein, Bacteria
  • Transcription Factors
  • insecticidal crystal protein, Bacillus Thuringiensis