Characterization of an alarm pheromone secreted by amphibian tadpoles that induces behavioral inhibition and suppression of the neuroendocrine stress axis

Many species assess predation risk through chemical cues, but the tissue source, chemical nature, and mechanisms of production or action of these cues are often unknown. Amphibian tadpoles show rapid and sustained behavioral inhibition when exposed to chemical cues of predation. Here we show that an alarm pheromone is produced by ranid tadpole skin cells, is released into the medium via an active secretory process upon predator attack, and signals predator presence to conspecifics. The pheromone is composed of two components with distinct biophysical properties that must be combined to elicit the behavioral response. In addition to the behavioral response, exposure to the alarm pheromone caused rapid and strong suppression of the hypothalamo-pituitary-adrenal (HPA) axis, as evidenced by a time and dose-dependent decrease in whole body corticosterone content. Reversing the decline in endogenous corticosterone caused by exposure to the alarm pheromone through addition of corticosterone to the aquarium water (50 nM) partially blocked the anti-predator behavior, suggesting that the suppression of the HPA axis promotes the expression and maintenance of a behaviorally quiescent state. To our knowledge this is the first evidence for aquatic vertebrate prey actively secreting an alarm pheromone in response to predator attack. We also provide a neuroendocrine mechanism by which the behavioral inhibition caused by exposure to the alarm pheromone is maintained until the threat subsides.     

Monitoring the invasion of the aquatic bug <Emphasis Type="Italic">Trichocorixa verticalis verticalis</Emphasis> (Hemiptera: Corixidae) in the wetlands of Doñana National Park (SW Spain)

We have detected the presence of the North American native corixid Trichocorixa verticalis verticalis (Fieber, 1851) in Doñana wetlands (SW Spain). We have collected data from different research projects done in the area during the period of 2001–2007. We have sampled 134 different sites in Doñana and we found the exotic corixid in 66 occasions. We have found two reproductive populations that might act as sources for the colonization of other waterbodies in the area. When reproduction occurred T. v. verticalis outcompeted native corixids. Its presence out of the waterbodies where we detected reproduction was in small numbers and probably due to vagrant individuals.     

Serotonin released from amacrine neurons is scavenged and degraded in bipolar neurons in the retina

Among mental disorders, mental retardation has been shown to be caused by various factors including a large array of genetic mutations. On the basis of remarkable progress, the emerging view is that defects in the regulation of synaptic activity and morphogenesis of dendritic spines are apparently common features associated with mutations in several genes implicated in mental retardation. In this review, we will discuss X-linked MR-related gene products that are potentially involved in the normal structure and function of the synapses, with a particular focus on pre- and/or post-synaptic plasticity mechanisms. Progress in understanding the underlying conditions leading to mental retardation will undoubtedly be gained from a closer collaboration of geneticists, physiologists and cognitive neuroscientists, which should enable the establishment of standardized approaches.     

Two-step infection processes can lead to coevolution between functionally independent infection and resistance pathways

There is growing evidence that successful infection of hosts by pathogens requires a series of independent steps. However, how multistep infection processes affect host-pathogen coevolution is unclear. We present a coevolutionary model, inspired by empirical observations from a range of host-pathogen systems, where the infection process consists of the following two steps: the first is for the pathogen to recognize and locate a suitable host, and the second is to exploit the host while evading immunity. Importantly, these two steps conform to different models of infection genetics: inverse-gene-for-gene (IGFG) and gene-for-gene (GFG), respectively. We show that coevolution under this scenario can lead to coupled gene frequency changes across these two systems. In particular, selection often favors pathogens that are infective at the first, IGFG, step and hosts that are resistant at the second, GFG, step. Hence, there may be signals of positive selection between functionally independent systems whenever there are multistep processes determining resistance and infectivity. Such multistep infection processes are a fundamental, but overlooked feature of many host-pathogen interactions, and have important consequences for our understanding of host-pathogen coevolution.     

Mutations of the Gene Encoding Otogelin Are a Cause of Autosomal-Recessive Nonsyndromic Moderate Hearing Impairment

Already 40 genes have been identified for autosomal-recessive nonsyndromic hearing impairment (arNSHI); however, many more genes are still to be identified. In a Dutch family segregating arNSHI, homozygosity mapping revealed a 2.4 Mb homozygous region on chromosome 11 in p15.1-15.2, which partially overlapped with the previously described DFNB18 locus. However, no putative pathogenic variants were found in USH1C, the gene mutated in DFNB18 hearing impairment. The homozygous region contained 12 additional annotated genes including OTOG, the gene encoding otogelin, a component of the tectorial membrane. It is thought that otogelin contributes to the stability and strength of this membrane through interaction or stabilization of its constituent fibers. The murine orthologous gene was already known to cause hearing loss when defective. Analysis of OTOG in the Dutch family revealed a homozygous 1 bp deletion, c.5508delC, which leads to a shift in the reading frame and a premature stop codon, p.Ala1838ProfsX31. Further screening of 60 unrelated probands from Spanish arNSHI families detected compound heterozygous OTOG mutations in one family, c.6347C>T (p.Pro2116Leu) and c. 6559C>T (p.Arg2187X). The missense mutation p.Pro2116Leu affects a highly conserved residue in the fourth von Willebrand factor type D domain of otogelin. The subjects with OTOG mutations have a moderate hearing impairment, which can be associated with vestibular dysfunction. The flat to shallow “U” or slightly downsloping shaped audiograms closely resembled audiograms of individuals with recessive mutations in the gene encoding α-tectorin, another component of the tectorial membrane. This distinctive phenotype may represent a clue to orientate the molecular diagnosis.     

Granule matrix property and rapid "kiss-and-run" exocytosis contribute to the different kinetics of catecholamine release from carotid glomus and adrenal chromaffin cells at matched quantal size

Catecholamine-containing small dense core granules (SDCGs, vesicular diameter of ~100 nm) are prominent in carotid glomus (chemosensory) cells and some neurons, but the release kinetics from individual SDCGs has not been studied in detail. In this study, we compared the amperometric signals from glomus cells with those from adrenal chromaffin cells, which also secrete catecholamine but via large dense core granules (LDCGs, vesicular diameter of ~200-250 nm). When exocytosis was triggered by whole-cell dialysis (which raised the concentration of intracellular Ca(2+) ([Ca(2+)](i)) to ~0.5 μmol/L), the proportion of the type of signal that represents a flickering fusion pore was 9-fold higher for glomus cells. Yet, at the same range of quantal size (Q, the total amount of catecholamine that can be released from a granule), the kinetics of every phase of the amperometric spike signals from glomus cells was faster. Our data indicate that the last phenomenon involved at least 2 mechanisms: (i) the granule matrix of glomus cells can supply a higher concentration of free catecholamine during exocytosis; (ii) a modest elevation of [Ca(2+)](i) triggers a form of rapid "kiss-and-run" exocytosis, which is very prevalent among glomus SDCGs and leads to incomplete release of their catecholamine content (and underestimation of their Q value).     

Putative CENP-B paralogues are not present at mammalian centromeres

Although centromere protein B (CENP-B) is a highly conserved mammalian centromere protein, its function remains unknown. The presence of the protein is required to form artificial satellite DNA-based centromeres de novo, yet cenpb knockout mice are viable for multiple generations with no mitotic or meiotic defects, and the protein is not present at fully functional neocentromeres. Previous studies have suggested that the presence of functionally redundant paralogues of CENP-B may explain the lack of a phenotype in knockout mice, and the related Tigger-derived (TIGD) family of proteins has been implicated as the most likely candidate for such paralogues. Here, we describe an investigation of the centromere-binding properties of the three TIGD proteins most highly related to CENP-B through phylogenetic analysis through EGFP fusion studies and immunocytochemistry. Although two of the three proteins bound to human centromeres with low affinity when overexpressed as fusion proteins, the strongest candidate, TIGD3, demonstrated no native centromeric binding when using raised antibodies, either in human cells or in cenpb ^−/− mouse ES cells. We conclude that the existence of functional CENP-B paralogues is highly unlikely and that CENP-B acts alone at the centromere. Based on these data, we suggest a new, meiotic drive model of CENP-B action during centromere repositioning in evolution.     

Blood feeding patterns of mosquitoes: random or structured?

Background

During the non-breeding period, many birds migrate to milder areas, found closer to the equator than their breeding sites. Opposite movements are very rare. In the Southern Ocean, the abundance of ¹³C declines markedly with more southern latitude, providing a characteristic ¹³C isoscape. This can be used as a tracer for the movement of seabirds between breeding and inter-breeding areas, by comparing stable isotope ratios of feathers grown at different times of the year.

Results

We studied seasonal movements of Thin-billed prions (Aves, Procellariiformes), breeding at the Subantarctic Falkland/Malvinas Islands, compared with those of Wilson's storm-petrels breeding in the Antarctic South Shetland Islands. The two species showed opposite migratory movements. While Wilson's storm-petrels moved to warmer waters north of the Drake Passage in winter, Thin-billed prions showed a reversed movement towards more polar waters. Carbon stable isotope ratios in recent and historical feathers indicated that poleward winter movements of Thin-billed prions were less common historically (45% in 1913-1915), and have only recently become dominant (92% in 2003-2005), apparently in response to warming sea temperatures.

Conclusions

This study shows that pelagic seabirds can rapidly change migration strategies within populations, including migration towards more poleward waters in winter.