Age Determination of Pheasants (Phasianus Colchicus) using Discriminant Analysis

Most gallinaceous birds can be identified as juveniles or adults using the outermost primaries (P9 and P10) which are retained until after the first breeding season and are often identifiable by colour and wear. The pheasant Phasianus colchicus, however, moults all ten primary feathers during its post-juvenile moult so alternative techniques are required. To date the method most widely used on live birds is measurement of the shaft diameter of the proximal primary feather, P1, which is replaced first before the bird is fully-grown. Using a known-age sample of 752 free-living pheasants, this study presents a discriminant function analysis using proximal primary feather measurements and other morphological characteristics to achieve a greater level of accuracy of ageing. Ageing accuracy was high, especially for males, at over 95%. The model was less accurate for females, with 83% and 94% respectively for the two year groups. When our model was applied to an independent data set of unknown-age birds 85% were classified. Less than 3% could not be aged accurately and the remainder were unclassified due to missing measurements. Our model offers a reliable method of ageing pheasants, both live and dead, however researchers are cautioned to potential year, origin (stock) and site effects

Slug is a direct Notch target required for initiation of cardiac cushion cellularization

Snail family proteins are key regulators of epithelial-mesenchymal transition, but their role in endothelial-to-mesenchymal transition (EMT) is less well studied. We show that Slug, a Snail family member, is expressed by a subset of endothelial cells as well as mesenchymal cells of the atrioventricular canal and outflow tract during cardiac cushion morphogenesis. Slug deficiency results in impaired cellularization of the cardiac cushion at embryonic day (E)–9.5 but is compensated by increased Snail expression at E10.5, which restores cardiac cushion EMT. We further demonstrate that Slug, but not Snail, is directly up-regulated by Notch in endothelial cells and that Slug expression is required for Notch-mediated repression of the vascular endothelial cadherin promoter and for promoting migration of transformed endothelial cells. In contrast, transforming growth factor β (TGF-β) induces Snail but not Slug. Interestingly, activation of Notch in the context of TGF-β stimulation results in synergistic up-regulation of Snail in endothelial cells. Collectively, our data suggest that combined expression of Slug and Snail is required for EMT in cardiac cushion morphogenesis

Identification of transcripts with enriched expression in the developing and adult pancreas

The expression profile of different developmental stages of the murine pancreas and predictions of transcription factor interactions, provides a framework for pancreas regulatory networks and development

Habitat correlates of Eurasian woodcock Scolopax rusticola abundance in a declining resident population

In Europe, woodland bird populations have been declining since at least the 1970s, and in Britain, around one third of woodland bird species have undergone declines over this period. Habitat change has been highlighted as a possible cause, but for some species clear evidence of this is lacking owing to an incomplete knowledge of the species’ habitat requirements. Here, we analyse national data to explain the variation in abundance of a declining woodland bird, the Eurasian Woodcock. A nationwide, species-specific survey of breeding Woodcock was conducted in 2003 and 2013 at 807 and 823 randomly selected 1-km squares respectively. The counts were compared with a range of landscape-scale habitat variables as well as local habitat measures recorded by surveyors, using generalised linear mixed models. Habitat variables were measured at a variety of spatial scales using ring buffers, although our analyses show that strong collinearity between scales hinders interpretation. At large landscape scales, breeding Woodcock abundance was correlated with total woodland area and the way this interacted with woodland type. Woodcock were more abundant in woods containing a more heterogeneous mix of woodland habitat types and in woods further from urban areas. On a smaller spatial scale, Woodcock were less likely to be found at sites dominated by beech Fagus spp. and more likely to occur in woods containing birch Betula spp. The Woodcock’s association with large, heterogeneous woods and the apparent attractiveness of certain woodland types present the most relevant topics for future research into the role of habitat change in long-term declines

Habitat geometry rather than visual acuity limits the visibility of a ground-nesting bird's clutch to terrestrial predators

This is the final version. Available on open access from Wiley via the DOI in this record. Data availability statement: The dryad doi: https://datadryad.org/stash/share/2yJJ6xuGiKF7Ey6H2y1rAwyqJVGYFdBgFisTb4NN34I. All data and plots for the main text and supplementary material can be found within our dryad archive. ImageJ scripts for running RNL and 3D analyses with the MICA toolbox and ImageJ can be downloaded from our GitHub: https://github.com/GeorgeHancock471/3D_RNL_Tools.The nests of ground-nesting birds rely heavily on camouflage for their survival, and predation risk, often linked to ecological changes from human activity, is a major source of mortality. Numerous ground-nesting bird populations are in decline, so understanding the effects of camouflage on their nesting behavior is relevant to their conservation concerns. Habitat three-dimensional (3D) geometry, together with predator visual abilities, viewing distance, and viewing angle, determine whether a nest is either visible, occluded, or too far away to detect. While this link is intuitive, few studies have investigated how fine-scale geometry is likely to help defend nests from different predator guilds. We quantified nest visibility based on 3D occlusion, camouflage, and predator visual modeling in northern lapwings, Vanellus vanellus, on different land management regimes. Lapwings selected local backgrounds that had a higher 3D complexity at a spatial scale greater than their entire clutches compared to local control sites. Importantly, our findings show that habitat geometry-rather than predator visual acuity-restricts nest visibility for terrestrial predators and that their field habitats, perceived by humans as open, are functionally closed with respect to a terrestrial predator searching for nests on the ground. Taken together with lapwings' careful nest site selection, our findings highlight the importance of considering habitat geometry for understanding the evolutionary ecology and management of conservation sites for ground-nesting birds.Natural Environment Research Council (NERC)Game and Wildlife Conservation Trus

Notch Initiates the Endothelial-to-Mesenchymal Transition in the Atrioventricular Canal through Autocrine Activation of Soluble Guanylyl Cyclase

SummaryThe heart is the most common site of congenital defects, and valvuloseptal defects are the most common of the cardiac anomalies seen in the newborn. The process of endothelial-to-mesenchymal transition (EndMT) in the cardiac cushions is a required step during early valve development, and Notch signaling is required for this process. Here we show that Notch activation induces the transcription of both subunits of the soluble guanylyl cyclase (sGC) heterodimer, GUCY1A3 and GUCY1B3, which form the nitric oxide receptor. In parallel, Notch also promotes nitric oxide (NO) production by inducing Activin A, thereby activating a PI3-kinase/Akt pathway to phosphorylate eNOS. We thus show that the activation of sGC by NO through a Notch-dependent autocrine loop is necessary to drive early EndMT in the developing atrioventricular canal (AVC)

Flavones induce neutrophil apoptosis by down-regulation of Mcl-1 via a proteasomal-dependent pathway

Neutrophil apoptosis and subsequent nonphlogistic clearance by surrounding phagocytes are key to the successful resolution of neutrophilic inflammation, with dysregulated apoptosis reported in multiple human inflammatory diseases. Enhancing neutrophil apoptosis has proresolution and anti-inflammatory effects in preclinical models of inflammation. Here we investigate the ability of the flavones apigenin, luteolin, and wogonin to induce neutrophil apoptosis in vitro and resolve neutrophilic inflammation in vivo. Human neutrophil apoptosis was assessed morphologically and by flow cytometry following incubation with apigenin, luteolin, and wogonin. All three flavones induced time- and concentration-dependent neutrophil apoptosis (apigenin, EC(50)=12.2 μM; luteolin, EC(50)=14.6 μM; and wogonin, EC(50)=28.9 μM). Induction of apoptosis was caspase dependent, as it was blocked by the broad-spectrum caspase inhibitor Q-VD-OPh and was associated with both caspase-3 and caspase-9 activation. Flavone-induced apoptosis was preceded by down-regulation of the prosurvival protein Mcl-1, with proteasomal inhibition preventing flavone-induced Mcl-1 down-regulation and apoptosis. The flavones abrogated the survival effects of mediators that prolong neutrophil life span, including lipoteichoic acid, peptidoglycan, dexamethasone, and granulocyte-macrophage colony stimulating factor, by driving apoptosis. Furthermore, wogonin enhanced resolution of established neutrophilic inflammation in a zebrafish model of sterile tissue injury. Wogonin-induced resolution was dependent on apoptosis in vivo as it was blocked by caspase inhibition. Our data show that the flavones induce neutrophil apoptosis and have potential as neutrophil apoptosis-inducing anti-inflammatory, proresolution agents.—Lucas, C. D., Allen, K. C., Dorward, D. A., Hoodless, L. J., Melrose, L. A., Marwick, J. A., Tucker, C. S., Haslett, C., Duffin, R., Rossi, A. G. Flavones induce neutrophil apoptosis by down-regulation of Mcl-1 via a proteasomal-dependent pathway

A systematic screen for genes expressed in definitive endoderm by Serial Analysis of Gene Expression (SAGE)

BACKGROUND: The embryonic definitive endoderm (DE) gives rise to organs of the gastrointestinal and respiratory tract including the liver, pancreas and epithelia of the lung and colon. Understanding how DE progenitor cells generate these tissues is critical to understanding the cause of visceral organ disorders and cancers, and will ultimately lead to novel therapies including tissue and organ regeneration. However, investigation into the molecular mechanisms of DE differentiation has been hindered by the lack of early DE-specific markers. RESULTS: We describe the identification of novel as well as known genes that are expressed in DE using Serial Analysis of Gene Expression (SAGE). We generated and analyzed three longSAGE libraries from early DE of murine embryos: early whole definitive endoderm (0–6 somite stage), foregut (8–12 somite stage), and hindgut (8–12 somite stage). A list of candidate genes enriched for expression in endoderm was compiled through comparisons within these three endoderm libraries and against 133 mouse longSAGE libraries generated by the Mouse Atlas of Gene Expression Project encompassing multiple embryonic tissues and stages. Using whole mount in situ hybridization, we confirmed that 22/32 (69%) genes showed previously uncharacterized expression in the DE. Importantly, two genes identified, Pyy and 5730521E12Rik, showed exclusive DE expression at early stages of endoderm patterning. CONCLUSION: The high efficiency of this endoderm screen indicates that our approach can be successfully used to analyze and validate the vast amount of data obtained by the Mouse Atlas of Gene Expression Project. Importantly, these novel early endoderm-expressing genes will be valuable for further investigation into the molecular mechanisms that regulate endoderm development

The Drosophila Mitochondrial Translation Elongation Factor G1 Contains a Nuclear Localization Signal and Inhibits Growth and DPP Signaling

Mutations in the human mitochondrial elongation factor G1 (EF-G1) are recessive lethal and cause death shortly after birth. We have isolated mutations in iconoclast (ico), which encodes the highly conserved Drosophila orthologue of EF-G1. We find that EF-G1 is essential during fly development, but its function is not required in every tissue. In contrast to null mutations, missense mutations exhibit stronger, possibly neomorphic phenotypes that lead to premature death during embryogenesis. Our experiments show that EF-G1 contains a secondary C-terminal nuclear localization signal. Expression of missense mutant forms of EF-G1 can accumulate in the nucleus and cause growth and patterning defects and animal lethality. We find that transgenes that encode mutant human EF-G1 proteins can rescue ico mutants, indicating that the underlying problem of the human disease is not just the loss of enzymatic activity. Our results are consistent with a model where EF-G1 acts as a retrograde signal from mitochondria to the nucleus to slow down cell proliferation if mitochondrial energy output is low