BackgroundAppropriate vertical movement is critical for the survival of flying animals. Although negative geotaxis (moving away from Earth) driven by gravity has been extensively studied, much less is understood concerning a static regulatory mechanism for inducing positive geotaxis (moving toward Earth).ResultsUsing Drosophila melanogaster as a model organism, we showed that geomagnetic field (GMF) induces positive geotaxis and antagonizes negative gravitaxis. Remarkably, GMF acts as a sensory cue for an appetite-driven associative learning behavior through the GMF-induced positive geotaxis. This GMF-induced positive geotaxis requires the three geotaxis genes, such as cry, pyx and pdf, and the corresponding neurons residing in Johnston’s organ of the fly’s antennae.ConclusionsThese findings provide a novel concept with the neurogenetic basis on the regulation of vertical movement by GMF in the flying animals.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-016-0235-1) contains supplementary material, which is available to authorized users.
A primary cilium is an antenna-like structure on the cell surface that plays a crucial role in sensory perception and signal transduction. Mitochondria, the ‘powerhouse’ of the cell, control cell survival, and death. The cellular ability to remove dysfunctional mitochondria through mitophagy is important for cell survival. We show here that mitochondrial stress, caused by respiratory complex inhibitors and excessive fission, robustly stimulates ciliogenesis in different types of cells including neuronal cells. Mitochondrial stress-induced ciliogenesis is mediated by mitochondrial reactive oxygen species generation, subsequent activation of AMP-activated protein kinase and autophagy. Conversely, abrogation of ciliogenesis compromises mitochondrial stress-induced autophagy, leading to enhanced cell death. In mice, treatment with mitochondrial toxin, MPTP elicits ciliary elongation and autophagy in the substantia nigra dopamine neurons. Blockade of cilia formation in these neurons attenuates MPTP-induced autophagy but facilitates dopamine neuronal loss and motor disability. Our findings demonstrate the important role of primary cilia in cellular pro-survival responses during mitochondrial stress.
We have observed a switching transition between bistable memory switching and monostable threshold switching in Pt/NiO/Pt structure. Bistable memory switching could be changed to monostable threshold switching by applying a positive electrical pulse with height of 2 V and width between 10−2 and 10−4 s. The change is reversible by applying a negative electrical pulse with the same height and width. By considering polarity- and width-dependence of the switching transition and compositional difference on electrical properties in NiOx, we have proposed a model in which the migration of oxygen ions (O2−) is responsible for the switching transition in Pt/NiO/Pt structures.
Both bi-stable memory and mono-stable threshold switching are observed in amorphous NbOx films. In addition, the transition between memory and threshold switching can be induced by changing external electrical stress. Raman spectroscopy and transmission electron microscope data show that the NbOx film is self-assembled into a layered structure consisting of a top metal-rich region and a bottom oxygen-rich region. The volume ratio of the two regions depends on the film thickness. Our experimental results suggest that different characteristics of conducting filaments in the two regions result in thickness dependence of switching types and the transition between memory and threshold switching.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.