The field of synaptic plasticity, long-term potentiation (LTP) and long-term depression (LTD) presumed to comprise a fine cellular basis for learning and memory is connected with such genetics processes as neuron-specific transcription, epigenetic chromatin remodeling, trafficking of mRNAs from soma to the remote sites of their local translation in axons and dendrites. All these processes are result from a multilevel organization of the genetic material in the nucleus of a nerve cell. Drosophila is a helpful model organism to determine the sequence of events in this system of hierarchical relationships. Drosophila LIMK1 gene (agnostic) with a specific chromosome architecture around the gene capable of generating miRNAs, recapitulates many features both of Williams syndrome and of neurodegenerative disorders. LIMK1 being the key enzyme of actin remodeling. This signal cascade involving receptors of neurotransmitters – small Rho GTPases ( RhoA, Cdc42 and Rac1) –LIM kinase 1 (LIMK1) - cofilin – actin – is believed to play the main role in dendrite- and synaptogenesis. Conditioned courtship suppression paradigm was used to asses learning acquisition and medium-term memory formation in Drosophila mutant agnX1 characterized by existence of the spontaneous mutation agnX1 in limk1 gene harbored by the agnostic locus. Learning acquisition appeared to be normal in intact control. However, a failure of 3-h memory formation was observed in Drosophila mutant agnX1 in normal conditions. We used heat shock (HS) as a stress factor. HS led to restoration of medium-term memory in this mutant. Thus stress influences for agnX1 mutant are necessary and sufficient for restoration of ability to memory formation.
This work was supported by the grant of the Russian Foundation for Basic Research (No 15-04-07738).