Drivers of low breeding success in the Lesser Spotted Woodpecker Dendrocopos minor in England: testing hypotheses for the decline

Capsule The breeding success of Lesser Spotted Woodpeckers Dendrocopos minor is now lower in England than previously reported and also lower than found in studies elsewhere in Europe.

Aims To quantify the breeding success and identify the causes of nest failure. To test the hypotheses that breeding success is related to aspects of food limitation and parental care, and inclement weather during the nesting period, or to interactions with Great Spotted Woodpeckers.

Methods Nests were monitored in three regions of England, recording survival and causes of failure. We measured aspects of food limitation and parental care, rainfall and Great Spotted Woodpecker interactions at nests, to explore whether there was any evidence that these factors were related to breeding success. We compared results to other studies from the UK and continental Europe.

Results Nest survival was 52%. The average number of chicks produced from successful nests was 2.8. Chick-stage daily nest survival was positively related to provisioning rates, indicating that food supply may be limiting. The most common cause of nest failure was presumed starvation of chicks after the disappearance of an adult. Some females ceased visiting nests, leaving provisioning solely to the male. This behaviour has been reported elsewhere in Europe, but in the present study males were unable to compensate fully by increasing their provisioning rates, leading to poor nest survival. Provisioning rates and chick-stage daily nest survival were negatively associated with rainfall. Nest predation by Great Spotted Woodpeckers occurred but was a less frequent cause of failure. Aggressive interactions were recorded between the two woodpecker species but these were unrelated to breeding parameters.

Conclusions Low breeding success is most probably related to food shortages in the breeding period. Simple population modelling using parameters from the present study and from published work shows that if the low productivity that we have observed is replicated throughout Britain, it would be sufficient to account for the observed population decline. However, the possibility that survival rates are also low cannot be ruled out.     

Critical roles of arginine in growth and biofilm development by Streptococcus gordonii

Streptococcus gordonii is an oral commensal and an early coloniser of dental plaque. In vitro, S. gordonii is conditionally auxotrophic for arginine in monoculture but biosynthesises arginine when coaggregated with Actinomyces oris. Here, we investigated the arginine‐responsive regulatory network of S. gordonii and the basis for conditional arginine auxotrophy. ArcB, the catabolic ornithine carbamoyltransferase involved in arginine degradation, was also essential for arginine biosynthesis. However, arcB was poorly expressed following arginine depletion, indicating that arcB levels may limit S. gordonii arginine biosynthesis. Arginine metabolism gene expression was tightly co‐ordinated by three ArgR/AhrC family regulators, encoded by argR, ahrC and arcR genes. Microarray analysis revealed that > 450 genes were regulated in response to rapid shifts in arginine concentration, including many genes involved in adhesion and biofilm formation. In a microfluidic salivary biofilm model, low concentrations of arginine promoted S. gordonii growth, whereas high concentrations (> 5 mM arginine) resulted in dramatic reductions in biofilm biomass and changes to biofilm architecture. Collectively, these data indicate that arginine metabolism is tightly regulated in S. gordonii and that arginine is critical for gene regulation, cellular growth and biofilm formation. Manipulating exogenous arginine concentrations may be an attractive approach for oral biofilm control.     

A review of the subspecies status of the Icelandic Purple Sandpiper Calidris maritima littoralis

The Icelandic Purple Sandpiper Calidris maritima littoralis (C.L. Brehm, 1831) represents one member of a poorly understood subspecies complex. Currently, differences in size define two other subspecies: Calidris maritima belcheri Engelmoer & Roselaar, 1998, which breeds in north‐eastern Canada along the Hudson Bay and James Bay, and Calidris maritima maritima (Brunnich, 1764), which breeds along the Arctic coasts elsewhere in northern Canada, Greenland, Svalbard, Scotland, and Fennoscandia, to northern central Siberia. There are large size differences amongst populations of C. m. maritima, however. As an Arctic/Alpine breeding bird, C. m. littoralis could provide an interesting perspective on the evolutionary changes following a northwards expansion of a species after glacial retreat. Considering the extent of the ice sheet in the northern hemisphere during the last glaciation, and the short period of time since it ended, the correct attribution of subspecies status for C. m. maritima may reflect either rapid diversification from a single population or ancestral splits of distinct evolutionary lineages that survived in isolation at southern latitudes. We applied morphometric subspecies criteria, diagnosability by Amadon's rule, and genetic analysis of five nuclear introns, and the mitochondrial DNA markers cytochrome oxidase c subunit I (COI) and NADH dehydrogenase subunit 2 (ND2), to geographically separate breeding populations in order to examine the subspecies status of the Icelandic population. The results do not provide support for the subspecies status of the Icelandic population because the nominate and Icelandic subspecies fail to uphold Amadon's rule, and genetic analyses indicate that the study populations derive from a single shared refugium. © 2015 The Linnean Society of London     

Characterization of a Novel Intestinal Glycerol-3-phosphate Acyltransferase Pathway and Its Role in Lipid Homeostasis

Dietary triglycerides (TG) are absorbed by the enterocytes of the small intestine after luminal hydrolysis into monacylglycerol and fatty acids. Before secretion on chylomicrons, these lipids are reesterified into TG, primarily through the monoacylglycerol pathway. However, targeted deletion of the primary murine monoacylglycerol acyltransferase does not quantitatively affect lipid absorption, suggesting the existence of alternative pathways. Therefore, we investigated the role of the glycerol 3-phosphate pathway in dietary lipid absorption. The expression of glycerol-3-phosphate acyltransferase (GPAT3) was examined throughout the small intestine. To evaluate the role for GPAT3 in lipid absorption, mice harboring a disrupted GPAT3 gene (Gpat3^−/−) were subjected to an oral lipid challenge and fed a Western-type diet to characterize the role in lipid and cholesterol homeostasis. Additional mechanistic studies were performed in primary enterocytes. GPAT3 was abundantly expressed in the apical surface of enterocytes in the small intestine. After an oral lipid bolus, Gpat3^−/− mice exhibited attenuated plasma TG excursion and accumulated lipid in the enterocytes. Electron microscopy studies revealed a lack of lipids in the lamina propria and intercellular space in Gpat3^−/− mice. Gpat3^−/− enterocytes displayed a compensatory increase in the synthesis of phospholipid and cholesteryl ester. When fed a Western-type diet, hepatic TG and cholesteryl ester accumulation was significantly higher in Gpat3^−/− mice compared with the wild-type mice accompanied by elevated levels of alanine aminotransferase, a marker of liver injury. Dysregulation of bile acid metabolism was also evident in Gpat3-null mice. These studies identify GPAT3 as a novel enzyme involved in intestinal lipid metabolism.     

Constitutive and inducible aspects of nitrate-nitrogen uptake by Chlamydomonas reinhardtii

Similarly to higher plant root systems, Chlamydomonas reinhardtii Dangeard (UTEX 90) cells exhibited biphasic NO₃^? uptake kinetics. The uptake pattern was similar in cells cultured in 10 mM NO₃^? (NO₃^?-grown), 0.25 mM NO₃^? (N-limited) or 10 mM NO₃^? followed by an 18-h period of N-deprivation (N-starved). In all cell types there was an apparent phase transition in uptake at 1.1 mM NO₃^?, although there were variations in the uptake V_max of both isotherms. The rate of uptake via isotherm 0 ([NO₃^?]<1.1 mM) in N-limited cells was higher than that of either NO₃^?-grown or N-starved cells. In contrast, NO₃^?-grown and N-limited cells exhibited comparable V_max values when supplied with 1.1 to 1.8 mM NO₃^? (isotherm 1). When supplied with 1.6 mM NO₃^?, both N-limited and N-starved cells exhibited enhanced linear uptake after 60 min of incubation. We ascribed this to an induction phenomenon. This trend was not observed when NO₃^?-grown cells were supplied with 1.6 mM NO₃^?, or when N-limited and N-starved cells were supplied with 0.6 mM NO₃^?. The ‘inducible’ aspect of uptake by N-limited cells was blocked by cycloheximide (10 mg l^?1), but not by actinomycin D (5 mg l^?1), thus indicating the involvement of a translational or post-translational event. To investigate this phenomenon further, we analysed the cell proteins of N-limited cells supplied with either 0.6 or 1.6 mM NO₃^? for 90 min, using two-dimensional gel electrophoresis. Comparison of protein profiles enabled the identification of a single cell membrane-associated polypeptide (21 kDa, pI ca 5.5) and ten soluble fraction polypeptides (17–73 kDa, pI ca 5.0 to 7.1) unique to the high NO₃^? treatment. We propose that the ‘inducible’ portion of NO₃^? uptake may provide the means by which C. reinhardtii cells regulate uptake in accordance with assimilatory capacity.     

Molecular variation at the SLC6A3 locus predicts lifetime risk of PTSD in the Detroit Neighborhood Health Study

Recent work suggests that the 9-repeat (9R) allele located in the 3'UTR VNTR of the SLC6A3 gene increases risk of posttraumatic stress disorder (PTSD). However, no study reporting this association to date has been based on population-based samples. Furthermore, no study of which we are aware has assessed the joint action of genetic and DNA methylation variation at SLC6A3 on risk of PTSD. In this study, we assessed whether molecular variation at SLC6A3 locus influences risk of PTSD. Participants (n?=?320; 62 cases/258 controls) were drawn from an urban, community-based sample of predominantly African American Detroit adult residents, and included those who had completed a baseline telephone survey, had provided blood specimens, and had a homozygous genotype for either the 9R or 10R allele or a heterozygous 9R/10R genotype. The influence of DNA methylation variation in the SLC6A3 promoter locus was also assessed in a subset of participants with available methylation data (n?=?83; 16 cases/67 controls). In the full analytic sample, 9R allele carriers had almost double the risk of lifetime PTSD compared to 10R/10R genotype carriers (OR?=?1.98, 95% CI?=?1.02-3.86), controlling for age, sex, race, socioeconomic status, number of traumas, smoking, and lifetime depression. In the subsample of participants with available methylation data, a significant (p?=?0.008) interaction was observed whereby 9R allele carriers showed an increased risk of lifetime PTSD only in conjunction with high methylation in the SLC6A3 promoter locus, controlling for the same covariates. Our results confirm previous reports supporting a role for the 9R allele in increasing susceptibility to PTSD. They further extend these findings by providing preliminary evidence that a "double hit" model, including both a putatively reduced-function allele and high methylation in the promoter region, may more accurately capture molecular risk of PTSD at the SLC6A3 locus.     

Evidence for the Neurotrophic Regulation of Collagen-Tailed Acetylcholinesterase in Immature Skeletal Muscle by β-Endorphin

Abstract: Acetylcholinesterase (AChE) was extracted in a high-saline medium from gastrocnemius muscles of rat embryos and young rats aged 14 days'gestation to 40 days post partum. The molecular forms of the enzyme were separated by low-salt precipitation, followed by velocity sedimentation. During gestation, all molecular forms increased in activity, particularly the 16 S (A₁₂) form. During the first 2 weeks of life, there was a large increase in the activity of soluble AChE (G forms), whilst the activity of insoluble AChE (A forms) was reduced. Denervation of the muscle reversed the change in the relative proportions of the molecular forms. The embryonic pattern of activities of AChE forms persisted in cultures of myotubes obtained at 20 days'gestation and maintained in the absence of spinal cord. When myotubes were maintained in medium previously conditioned by developing spinal cord explants, 16 S AChE declined while the soluble (4 and 6 S) forms increased in activity in a manner resembling that seen in early postnatal muscles in vivo . β-Endorphin (β-EP) immunoreactivity was detected in the spinal cord-conditioned medium and was identified by HPLC and ion-exchange chromatography as β-EP-(l–31) plus its shortened and N -acetylated forms. Cultivation of myotubes in the presence of synthetic camel β-EP resulted in a reversible change in the pattern of AChE forms which was similar to that seen with spinal cord-conditioned medium. These studies provide evidence for the neuroregulation of AChE A and G forms in immature skeletal muscle. A major candidate for this role is β-EP, produced and released by developing spinal cord.