Optogenetic upregulation of cyclic adenosine monophosphate during the day increases sleep intensity at night, whereas loss of function of a molecule involved in synaptic pruning, the fragile-X mental retardation protein, increases sleep intensity during the day. Our results show that sleep is not homogenous in insects, and suggest that waking behavior and the associated synaptic plasticity mechanisms determine the timing and intensity of deep sleep stages in Drosophila.

SUMMARY Given the role that sleep plays in modulating plasticity, we hypothesized that increasing sleep would restore memory to canonical memory mutants without specifically rescuing the causal molecular-lesion. Sleep was increased using three independent strategies: activating the dorsal Fan Shaped Body (FB), increasing the expression of Fatty acid binding protein (dFabp) or by administering the GABA-A agonist 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol (THIP). Short-term memory (STM) or Long-term memory (LTM) was evaluated in rutabaga (rut) and dunce (dnc) mutants using Aversive Phototaxic Suppression (APS) and courtship conditioning. Each of the three independent strategies increased sleep and restored memory to rut and dnc mutants. Importantly, inducing sleep also reverses memory defects in a Drosophila model of Alzheimer’s disease. Together these data demonstrate that sleep plays a more fundamental role in modulating behavioral plasticity than previously appreciated and suggests that increasing sleep may benefit patients with certain neurological disorders.

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SummaryIn order to cause disease fungal pathogens must be capable of evading or tolerating the host immune defence system. One commonly utilized evasion mechanism is the ability to continually reside within macrophages of the innate immune system and survive subsequent phagocytic destruction. For intracellular growth to occur, fungal pathogens which typically grow in a filamentous hyphal form in the environment must be able to switch growth to a unicellular yeast growth form in a process known as dimorphic switching. The cue to undergo dimorphic switching relies on the recognition of, and response to, the intracellular host environment. Two-component signalling systems are utilized by eukaryotes to sense and respond to changes in the external environment. This study has investigated the role of the hybrid histidine kinase components encoded by drkA and slnA, in the dimorphic pathogen Penicillium marneffei. Both SlnA and DrkA are required for stress adaptation but are uniquely required for different aspects of asexual development, hyphal morphogenesis and cell wall integrity. Importantly, slnA and drkA are both essential for the generation of yeast cells in vivo, with slnA required for the germination of conidia and drkA required for dimorphic switching during macrophage infection.