PUBLICATION

The role of the Glucocorticoid Receptor in the Regulation of Diel Rhythmicity

Authors
Jaikumar, G., Slabbekoorn, H., Sireeni, J., Schaaf, M., Tudorache, C.
ID
ZDB-PUB-200606-16
Date
2020
Source
Physiology & behavior   223: 112991 (Journal)
Registered Authors
Schaaf, Marcel J. M.
Keywords
Glucocorticoid receptor, biological clock, clock genes, locomotor behaviour, melatonin, zebrafish larvae
MeSH Terms
  • Animals
  • Circadian Rhythm
  • Gene Expression
  • Glucocorticoids
  • Periodicity
  • Receptors, Glucocorticoid*/genetics
  • Zebrafish*/genetics
PubMed
32497529 Full text @ Physiol. Behav.
Abstract
Virtually all organisms have adapted to the earth's day-night cycles by the evolution of endogenous rhythms that regulate most biological processes. Recent research has highlighted the role of glucocorticoids and the Glucocorticoid receptor (GR) in coordinating clock function across various levels of biological organisation. In the present study, we have explored the role of the GR in the rhythmicity of the biological clock, by comparing 5 day old wildtype zebrafish larvae (gr+) with mutant larvae with a non-functional GR (grs357). The mutants display a weaker rhythmicity in locomotor activity in wildtypes than in mutants, while the rhythmicity of the angular velocity was higher for wildtypes. The melatonin production of the mutants showed a weaker rhythmicity, but surprisingly, there were no differences in the rhythmicity of clock-related gene expression between genotypes that could explain a mechanism for GR functionality at the transcriptional level. Furthermore, our results show that grs357 larvae have a more erratic swimming path, and cover more distance during locomotor activity than wild type larvae, in line with previously described behaviour of this mutant. Therefore, these results suggest that GR affects the diel rhythmicity of zebrafish larvae at the behavioural and endocrine level, but that these effects are not mediated by changes in the expression of clock-related genes.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping