Paghpate3387

Insensible evaporative water loss (EWL) at or below thermoneutrality is generally assumed to be a passive physical process. However, some arid zone mammals and a single arid zone bird can control their insensible water loss, so we tested the hypothesis that the same is the case for two parrot species from a mesic habitat. We investigated red-rumped parrots (Psephotus haematonotus) and eastern rosellas (Platycercus eximius), measuring their EWL, and other physiological variables, at a range of relative humidities at ambient temperatures of 20 and 30°C (below and at thermoneutrality). We found that, despite a decrease in EWL with increasing relative humidity, rates of EWL were not fully accounted for by the water vapour deficit between the animal and its environment, indicating that the insensible EWL of both parrots was controlled. It is unlikely that this deviation from physical expectations was regulation with a primary role for water conservation because our mesic-habitat parrots had equivalent regulatory ability as the arid habitat budgerigar (Melopsittacus undulatus). This, together with our observations of body temperature and metabolic rate, instead support the hypothesis that acute physiological control of insensible water loss serves a thermoregulatory purpose for endotherms. Modification of both cutaneous and respiratory avenues of evaporation may be involved, possibly via modification of expired air temperature and humidity, and surface resistance.For flightless arboreal arthropods, moving from the understory into tree canopies is cognitively and energetically challenging because vegetational structures present complex three-dimensional landscapes with substantial gaps. Predation risk and wind-induced perturbations in the canopy may further impede the movement process. In the Australian stick insect Extatosoma tiaratum, first-instar nymphs hatch on the forest floor and disperse toward tree canopies in the daytime. JSH23 Here, we addressed how their tactic responses to environmental cues and movement strategies are adapted to the canopy environment. Newly hatched nymphs ascend with high endurance, travelling >100 m within 60 min. Navigation toward open canopies is underpinned by negative gravitaxis, positive phototaxis and visual responses to vertically oriented contrast patterns. Nymphal E. tiaratum also use directed jumping to cross gaps, and respond to tactile stimulation and potential threat with a self-dropping reflex, resulting in aerial descent. Post-hatch dispersal in E. tiaratum thus consists of visually mediated displacement both on vegetational structures and in the air; within the latter context, gliding is then an effective mechanism enabling recovery after predator- and perturbation-induced descent. These results further support the importance of a diurnal niche, in addition to the arboreal spatial niche, in the evolution of gliding in wingless arboreal invertebrates.Miro (mitochondrial Rho GTPases), a mitochondrial outer membrane protein, facilitates mitochondrial axonal transport along the microtubules to facilitate neuronal function. It plays an important role in regulating mitochondrial dynamics (fusion and fission) and cellular energy generation. Thus, Miro might be associated with the key pathologies of several neurodegenerative diseases (NDs) including Alzheimer's disease (AD). In the present manuscript, we have demonstrated the possible genetic interaction between Miro and AD-related genes such as Tau, Aβ42 and Appl in Drosophila melanogaster Ectopic expression of Tau, Aβ42 and Appl induced a rough eye phenotype, defects in phototaxis and climbing activity, and shortened lifespan in the flies. In our study, we have observed that overexpression of Miro improves the rough eye phenotype, behavioral activities (climbing and phototaxis) and ATP level in AD model flies. Further, the improvement examined in AD-related phenotypes was correlated with decreased oxidative stress, cell death and neurodegeneration in Miro overexpressing AD model flies. Thus, the obtained results suggested that Miro genetically interacts with AD-related genes in Drosophila and has the potential to be used as a therapeutic target for the design of therapeutic strategies for NDs.This article has an associated First Person interview with the first author of the paper.Vps54 is a subunit of the Golgi-associated retrograde protein (GARP) complex, which is involved in tethering endosome-derived vesicles to the trans-Golgi network (TGN). In the wobbler mouse, a model for human motor neuron (MN) disease, reduction in the levels of Vps54 causes neurodegeneration. However, it is unclear how disruption of the GARP complex leads to MN dysfunction. To better understand the role of Vps54 in MNs, we have disrupted expression of the Vps54 ortholog in Drosophila and examined the impact on the larval neuromuscular junction (NMJ). Surprisingly, we show that both null mutants and MN-specific knockdown of Vps54 leads to NMJ overgrowth. Reduction of Vps54 partially disrupts localization of the t-SNARE, Syntaxin-16, to the TGN but has no visible impact on endosomal pools. MN-specific knockdown of Vps54 in MNs combined with overexpression of the small GTPases Rab5, Rab7, or Rab11 suppresses the Vps54 NMJ phenotype. Conversely, knockdown of Vps54 combined with overexpression of dominant negative Rab7 causes NMJ and behavioral abnormalities including a decrease in postsynaptic Dlg and GluRIIB levels without any effect on GluRIIA. Taken together, these data suggest that Vps54 controls larval MN axon development and postsynaptic density composition through a mechanism that requires Rab7.Cystic fibrosis (CF) is a genetic disease characterized by progressive lung and chronic digestive manifestations. We have shown that therapeutic doses of vardenafil, a phosphodiesterase type 5 (PDE5) inhibitor, corrects CF Transmembrane conductance Regulator (CFTR)-dependent chloride transport in respiratory and intestinal tissues of F508del homozygous mice. Here, we studied the effect of vardenafil on CFTR in 16HBE14o- and CFBE41o- cell lines. First, the expression levels of PDE5 mRNA in these cell lines were monitored. The two cell lines were exposed to different drugs (dimethyl sulfoxide, 8-Br-cGMP, forskolin or vardenafil). The cAMP and cGMP intracellular concentrations were measured. Finally, we localised the CFTR by immunolabelling. PDE5 was similarly expressed in both wild-type and in CF cells. A fast and transient rise in cGMP intracellular contents followed treatment with vardenafil, confirming its PDE5 inhibitory effect. We showed that vardenafil promoted both the early steps of the cellular processing and the trafficking of F508del without fully addressing the protein to the plasma membrane.