Being subject daily to the cycle of day and night due to the earth's rotation along its axis, all living organisms on our planet have developed internal chronometers called circadian clocks which allow them to adapt and anticipate this daily change in their environment.
The team's research focuses on the molecular mechanisms of these circadian clocks especially those involving long non-coding RNA.
Since profound alterations of our body clock can be observed in patients with cerebral diseases, without knowledge of whether these alterations are the cause or consequence of the diseases, the team's mission is also to evaluate the roles played by genes, proteins and long non-coding RNA involved in circadian rhythms, in cerebral diseases especially neurodevelopmental disease such as the Prader Willi syndrome.
GRAN team focuses on two major topics:
- Molecular mechanisms of circadian clock functioning
- Disruption of circadian clocks associated with brain diseases
Issues: hormones/steroids, genes and non-coding RNAs
Tools and techniques: cellular and animal models, molecular biology, biochemistry, immunocytochemistry, in situ hybridization, confocal microscopy, animal behavior, NGS data analysis, bioinformatics and genome editing
" For a better understanding of life’s rhythms "
The team's research aims to better understand the functioning of our internal clocks which allow our organism to be rhythmic over 24 hours. As some diseases in the central nervous system are associated with disturbances in our biological clocks, the team is also assessing the contribution of these rhythmic alterations to the pathophysiology of brain diseases.
The exploratory and innovative nature of the team’s project is based on the proposal to evaluate the involvement of the circadian clock via long non-coding RNA in the pathogenesis of human brain diseases.
1. Characterization of the molecular mechanisms involved in the control of circadian gene expression, especially those involving long non coding RNAs such as Neat1 or Malat1
2. Characterization of circadian anomalies associated with the pathophysiology of Prader-Willi syndrome and identification of the genes involved in these dysfunctions