723 research outputs found

    Host response to cuckoo song is predicted by the future risk of brood parasitism

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    This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Introduction: Risk assessment occurs over different temporal and spatial scales and is selected for when individuals show an adaptive response to a threat. Here, we test if birds respond to the threat of brood parasitism using the acoustical cues of brood parasites in the absence of visual stimuli. We broadcast the playback of song of three brood parasites (Chalcites cuckoo species) and a sympatric non-parasite (striated thornbill, Acanthiza lineata) in the territories of superb fairy-wrens (Malurus cyaneus) during the peak breeding period and opportunistic breeding period. The three cuckoo species differ in brood parasite prevalence and the probability of detection by the host, which we used to rank the risk of parasitism (high risk, moderate risk, low risk). Results: Host birds showed the strongest response to the threat of cuckoo parasitism in accordance with the risk of parasitism. Resident wrens had many alarm calls and close and rapid approach to the playback speaker that was broadcasting song of the high risk brood parasite (Horsfield’s bronze-cuckoo, C. basalis) across the year (peak and opportunistic breeding period), some response to the moderate risk brood parasite (shining bronze-cuckoo, C. lucidus) during the peak breeding period, and the weakest response to the low risk brood parasite (little bronzecuckoo, C. minutillus). Playback of the familiar control stimulus in wren territories evoked the least response. Conclusion: Host response to the threat of cuckoo parasitism was assessed using vocal cues of the cuckoo and was predicted by the risk of future parasitism

    Smad4-dependent pathways control basement membrane deposition and endodermal cell migration at early stages of mouse development

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    <p>Abstract</p> <p>Background</p> <p>Smad4 mutant embryos arrest shortly after implantation and display a characteristic shortened proximodistal axis, a significantly reduced epiblast, as well as a thickened visceral endoderm layer. Conditional rescue experiments demonstrate that bypassing the primary requirement for Smad4 in the extra-embryonic endoderm allows the epiblast to gastrulate. Smad4-independent TGF-β signals are thus sufficient to promote mesoderm formation and patterning. To further analyse essential Smad4 activities contributed by the extra-embryonic tissues, and characterise Smad4 dependent pathways in the early embryo, here we performed transcriptional profiling of Smad4 null embryonic stem (ES) cells and day 4 embryoid bodies (EBs).</p> <p>Results</p> <p>Transcripts from wild-type versus Smad4 null ES cells and day 4 EBs were analysed using Illumina arrays. In addition to several known TGF-β/BMP target genes, we identified numerous Smad4-dependent transcripts that are mis-expressed in the mutants. As expected, mesodermal cell markers were dramatically down-regulated. We also observed an increase in non-canonical potency markers (<it>Pramel7</it>, <it>Tbx3</it>, <it>Zscan4</it>), germ cell markers (<it>Aire</it>, <it>Tuba3a</it>, <it>Dnmt3l</it>) as well as early endoderm markers (<it>Dpp4</it>, <it>H19</it>, <it>Dcn</it>). Additionally, expression of the extracellular matrix (ECM) remodelling enzymes <it>Mmp14 </it>and <it>Mmp9 </it>was decreased in Smad4 mutant ES and EB populations. These changes, in combination with increased levels of <it>laminin alpha1</it>, cause excessive basement membrane deposition. Similarly, in the context of the Smad4 null E6.5 embryos we observed an expanded basement membrane (BM) associated with the thickened endoderm layer.</p> <p>Conclusion</p> <p>Smad4 functional loss results in a dramatic shift in gene expression patterns and in the endodermal cell lineage causes an excess deposition of, or an inability to breakdown and remodel, the underlying BM layer. These structural abnormalities probably disrupt reciprocal signalling between the epiblast and overlying visceral endoderm required for gastrulation.</p

    A Synthesis of Human-related Avian Mortality in Canada

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    Many human activities in Canada kill wild birds, yet the relative magnitude of mortality from different sources and the consequent effects on bird populations have not been systematically evaluated. We synthesize recent estimates of avian mortality in Canada from a range of industrial and other human activities, to provide context for the estimates from individual sources presented in this special feature. We assessed the geographic, seasonal, and taxonomic variation in the magnitude of national-scale mortality and in population-level effects on species or groups across Canada, by combining these estimates into a stochastic model of stage-specific mortality. The range of estimates of avian mortality from each source covers several orders of magnitude, and, numerically, landbirds were the most affected group. In total, we estimate that approximately 269 million birds and 2 million nests are destroyed annually in Canada, the equivalent of over 186 million breeding individuals. Combined, cat predation and collisions with windows, vehicles, and transmission lines caused > 95% of all mortality; the highest industrial causes of mortality were the electrical power and agriculture sectors. Other mortality sources such as fisheries bycatch can have important local or species-specific impacts, but are relatively small at a national scale. Mortality rates differed across species and families within major bird groups, highlighting that mortality is not simply proportional to abundance. We also found that mortality is not evenly spread across the country; the largest mortality sources are coincident with human population distribution, while industrial sources are concentrated in southern Ontario, Alberta, and southwestern British Columbia. Many species are therefore likely to be vulnerable to cumulative effects of multiple human-related impacts. This assessment also confirms the high uncertainty in estimating human-related avian mortality in terms of species involved, potential for population-level effects, and the cumulative effects of mortality across the landscape. Effort is still required to improve these estimates, and to guide conservation efforts to minimize direct mortality caused by human activities on Canada's wild bird populations. As avian mortality represents only a portion of the overall impact to avifauna, indirect effects such as habitat fragmentation and alteration, site avoidance, disturbance, and related issues must also be carefully considered

    Oral versus intra‐vaginal imidazole and triazole anti‐fungal treatment of uncomplicated vulvovaginal candidiasis (thrush)

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    Internal sources: • Health Services Research Unit, University of Aberdeen, UK • Clinical Epidemiology Program, Ottawa Hospital Research Institute, The Ottawa Hospital, Canada (Salary support for Julia Worswick) • Centre of Academic Primary Care, University of Aberdeen, UK External sources: • JMG holds a Tier 1 Canadian Research Chair in Knowledge Transfer and Uptake, Canada • MCW was funded by a Health Foundation Improvement Science Fellowship and the University of Strathclyde, UK • The Health Services Research Unit is funded by the Chief Scientist ODice, Scottish Executive Health Department, UK • The Health Economic Research Unit is funded by the Chief Scientist ODice, Scottish Executive Health Department, UKPeer reviewedPublisher PD

    Dynamic instability of the major urinary protein gene family revealed by genomic and phenotypic comparisons between C57 and 129 strain mice

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    Targeted sequencing, manual genome annotation, phylogenetic analysis and mass spectrometry were used to characterise major urinary proteins (MUPs) and the Mup clusters of two strains of inbred mice

    Paracetamol use in early life and asthma: prospective birth cohort study

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    Objective To determine if use of paracetamol in early life is an independent risk factor for childhood asthma

    Large-scale discovery of male reproductive tract-specific genes through analysis of RNA-seq datasets

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    Robertson, M.J., Kent, K., Tharp, N. et al. Large-scale discovery of male reproductive tract-specific genes through analysis of RNA-seq datasets. BMC Biol 18, 103 (2020). https://doi.org/10.1186/s12915-020-00826-

    Impaired perception of facial motion in autism spectrum disorder

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    Copyright: © 2014 O’Brien et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.This article has been made available through the Brunel Open Access Publishing Fund.Facial motion is a special type of biological motion that transmits cues for socio-emotional communication and enables the discrimination of properties such as gender and identity. We used animated average faces to examine the ability of adults with autism spectrum disorders (ASD) to perceive facial motion. Participants completed increasingly difficult tasks involving the discrimination of (1) sequences of facial motion, (2) the identity of individuals based on their facial motion and (3) the gender of individuals. Stimuli were presented in both upright and upside-down orientations to test for the difference in inversion effects often found when comparing ASD with controls in face perception. The ASD group’s performance was impaired relative to the control group in all three tasks and unlike the control group, the individuals with ASD failed to show an inversion effect. These results point to a deficit in facial biological motion processing in people with autism, which we suggest is linked to deficits in lower level motion processing we have previously reported
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