In this work, we highlight the relevance of habituation learning to ASD, identify an unprecedented number of novel habituation players, support an emerging role for inhibitory neurons in habituation, and reveal an opposing, circuit-level-based mechanism for Ras/MAPK signaling.
In this paper, we demonstrate that Kismet-related sleep disturbances are caused by high serotonin during development, paralleling a well-established but genetically unsolved autism endophenotype. Despite their developmental origin, Kismet’s sleep architecture defects can be reversed in adulthood by a behavioral regime resembling human sleep restriction therapy.
The histone methyltransferase G9a regulates tolerance to oxidative stress-induced energy consumption
Here, we investigate the role of G9a in oxidative stress responses. During oxidative stress exposure, G9a mutants show rapid depletion of glycogen energy stores, and an inability to access lipid energy stores. The increased susceptibility of G9a mutant flies to oxidative stress can be rescued simply by providing extra sugar.
Also, we found overactivation of stress response and many other genes. A finding that we confirmed across-species in our latest work:Riahi, H., Fenckova, M., Goruk, K.J. et al. The epigenetic regulator G9a attenuates stress-induced resistance and metabolic transcriptional programs across different stressors and species. (2021) BMC Biology