Adaptation of a South American malaria vector to laboratory colonization suggests faster-male evolution for mating ability

Background  

Anopheles (Nyssorhynchus) albitarsis (Diptera: Culicidae) is one of the very few South American mosquito vectors of malaria successfully colonized in the laboratory. These vectors are very hard to breed because they rarely mate in artificial conditions. A few years ago a free-mating laboratory colony of An. albitarsis sensu stricto was established after about 30 generations of artificial-mating. To begin to understand the process of adaptation of these malaria vectors to the laboratory we have compared the insemination rates of colony mosquitoes to those from the original population in both artificial and free-mating crosses. We also carried out crossing experiments between the two types of mosquitoes for a preliminary analysis of the genetic basis of such adaptation.     

The Association of the Vanin-1 N131S Variant with Blood Pressure Is Mediated by Endoplasmic Reticulum-Associated Degradation and Loss of Function

High blood pressure (BP) is the most common cardiovascular risk factor worldwide and a major contributor to heart disease and stroke. We previously discovered a BP-associated missense SNP (single nucleotide polymorphism)–rs2272996–in the gene encoding vanin-1, a glycosylphosphatidylinositol (GPI)-anchored membrane pantetheinase. In the present study, we first replicated the association of rs2272996 and BP traits with a total sample size of nearly 30,000 individuals from the Continental Origins and Genetic Epidemiology Network (COGENT) of African Americans (P = 0.01). This association was further validated using patient plasma samples; we observed that the N131S mutation is associated with significantly lower plasma vanin-1 protein levels. We observed that the N131S vanin-1 is subjected to rapid endoplasmic reticulum-associated degradation (ERAD) as the underlying mechanism for its reduction. Using HEK293 cells stably expressing vanin-1 variants, we showed that N131S vanin-1 was degraded significantly faster than wild type (WT) vanin-1. Consequently, there were only minimal quantities of variant vanin-1 present on the plasma membrane and greatly reduced pantetheinase activity. Application of MG-132, a proteasome inhibitor, resulted in accumulation of ubiquitinated variant protein. A further experiment demonstrated that atenolol and diltiazem, two current drugs for treating hypertension, reduce the vanin-1 protein level. Our study provides strong biological evidence for the association of the identified SNP with BP and suggests that vanin-1 misfolding and degradation are the underlying molecular mechanism.     

An overview of foodborne pathogen detection: In the perspective of biosensors

Food safety is a global health goal and the foodborne diseases take a major crisis on health. Therefore, detection of microbial pathogens in food is the solution to the prevention and recognition of problems related to health and safety. For this reason, a comprehensive literature survey has been carried out aiming to give an overview in the field of foodborne pathogen detection. Conventional and standard bacterial detection methods such as culture and colony counting methods, immunology-based methods and polymerase chain reaction based methods, may take up to several hours or even a few days to yield an answer. Obviously this is inadequate, and recently many researchers are focusing towards the progress of rapid methods. Although new technologies like biosensors show potential approaches, further research and development is essential before biosensors become a real and reliable choice. New bio-molecular techniques for food pathogen detection are being developed to improve the biosensor characteristics such as sensitivity and selectivity, also which is rapid, reliable, effective and suitable for in situ analysis. This paper not only offers an overview in the area of microbial pathogen detection but it also describes the conventional methods, analytical techniques and recent developments in food pathogen detection, identification and quantification, with an emphasis on biosensors.     

Ultrastructural localization of amiloride-sensitive sodium channels and Na+,K(+)-ATPase in the rat's olfactory epithelial surface

Several studies have indicated that olfactory responses are impeded by amiloride. Therefore, it was of interest to see whether, and if so which, olfactory epithelial cellular compartments have amiloride- sensitive structures. Using ultrastructural methods that involved rapid freezing, freeze-substitution and low temperature embedding of olfactory epithelia, this study shows that, in the rat, this tissue is immunoreactive to antibodies against amiloride sensitive Na(+)- channels. However, microvilli of olfactory supporting cells, as opposed to receptor cilia, contained most of the immunoreactive sites. Apices from which the microvilli sprout and receptor cell dendritic knobs had much less if any of the amiloride-antibody binding sites. Using a direct ligand-binding cytochemical method, this study also confirms earlier ones that showed that olfactory receptor cell cilia have Na+, K(+)-ATPase. It is proposed that supporting cell microvilli and the receptor cilia themselves have mechanisms, different but likely complementary, that participate in regulating the salt concentration around the receptor cell cilia. In this way, both structures help to provide the ambient mucous environment for receptor cells to function properly. This regulation of the salt concentration of an ambient fluid environment is a function that the olfactory epithelium shares with cells of transporting epithelia, such as those of kidney.      

The neuroprotective agent, valproic acid, regulates the mitogen-activated protein kinase pathway through modulation of protein kinase A signalling in Dictyostelium discoideum

Activation of the mitogen-activated protein kinase (MAPK) cascade gives rise to a neuroprotective effect in a variety of cell types. The bipolar disorder treatment, valproic acid (VPA), increases the activity of this pathway by modulating extracellular signal-regulated kinase 2 (ERK2) phosphorylation through an unknown mechanism. To investigate the molecular basis of this effect, we have used the biomedical model system Dictyostelium discoideum to dissect this signalling pathway. We find that, similar to mammalian systems, VPA causes a transient increase in the activation of the MAPK signalling pathway, as shown by ERK2 phosphorylation. We show that the MAP kinase and phosphatase, protein kinase A (PKA) and glycogen synthase kinase signalling pathways all function in controlling the levels of phospho-ERK2 (pERK2). We find that VPA induces elevated pERK2 levels through attenuation of the PKA signalling pathway. Interestingly, pERK2 levels are also controlled by another bipolar disorder drug, lithium, providing a common effect of these two drugs. This work therefore suggests a conserved pathway in eukaryotes that is targeted by neuroprotective and bipolar disorder drugs and allows us to propose a model for this neuroprotective effect.