ABSTRACT
Bitterness and astringency are the aversive tastes in mammals. In humans, aversion to bitterness and astringency may be reduced depending on the eating experience. However, the cellular and molecular mechanisms underlying plasticity in preference to bitter and astringent tastants remain unknown. This study aimed to investigate the preference plasticity to bitter and astringent tea polyphenols, including catechins and tannic acids, in the model animal Caenorhabditis elegans. C. elegans showed avoidance behavior against epigallocatechin gallate (EGCG), tannic acid, and theaflavin. However, they displayed diminishing avoidance against EGCG depending on their EGCG-feeding regime at larval stages. Additionally, the behavioral plasticity in avoiding EGCG required the transcription factor DAF-16/FOXO. Isoform-specific deletion mutant analysis and cell-specific rescue analysis revealed that the function of daf-16 isoform b in AIY interneurons is necessary for experience-dependent behavioral plasticity to EGCG.
Subject(s)
Caenorhabditis elegans Proteins , Caenorhabditis elegans , Catechin , Forkhead Transcription Factors , Interneurons , Animals , Catechin/analogs & derivatives , Catechin/pharmacology , Caenorhabditis elegans/drug effects , Caenorhabditis elegans Proteins/metabolism , Caenorhabditis elegans Proteins/genetics , Forkhead Transcription Factors/metabolism , Interneurons/drug effects , Interneurons/metabolism , Avoidance Learning/drug effects , Biflavonoids/pharmacology , Taste/drug effects , Tea/chemistry , Behavior, Animal/drug effects , Larva/drug effectsABSTRACT
This study investigates the mechanisms governing experience-dependent tolerance of bitter compounds in Caenorhabditis elegans. The nematodes showed an aversion to nicotinamide, MgCl2, isoleucine, and arginine in a Gα-dependent manner. Worms furthermore displayed diminished avoidance of MgCl2 upon MgCl2-preconditioning at the larval stages. AIY interneurons have been suggested to be involved in experience-dependent behavioral plasticity.