Weather effects on birds of different size are mediated by long‐term climate and vegetation type in endangered temperate woodlands

Species occurrence is influenced by a range of factors including habitat attributes, climate, weather, and human landscape modification. These drivers are likely to interact, but their effects are frequently quantified independently. Here, we report the results of a 13‐year study of temperate woodland birds in south‐eastern Australia to quantify how different‐sized birds respond to the interacting effects of: (a) short‐term weather (rainfall and temperature in the 12 months preceding our surveys), (b) long‐term climate (average rainfall and maximum and minimum temperatures over the period 1970–2014), and (c) broad structural forms of vegetation (old‐growth woodland, regrowth woodland, and restoration plantings). We uncovered significant interactions between bird body size, vegetation type, climate, and weather. High short‐term rainfall was associated with decreased occurrence of large birds in old‐growth and regrowth woodland, but not in restoration plantings. Conversely, small bird occurrence peaked in wet years, but this effect was most pronounced in locations with a history of high rainfall, and was actually reversed (peak occurrence in dry years) in restoration plantings in dry climates. The occurrence of small birds was depressed—and large birds elevated—in hot years, except in restoration plantings which supported few large birds under these circumstances. Our investigation suggests that different mechanisms may underpin contrasting responses of small and large birds to the interacting effects of climate, weather, and vegetation type. A diversity of vegetation cover is needed across a landscape to promote the occurrence of different‐sized bird species in agriculture‐dominated landscapes, particularly under variable weather conditions. Climate change is predicted to lead to widespread drying of our study region, and restoration plantings—especially currently climatically wet areas—may become critically important for conserving bird species, particularly small‐bodied taxa.     

The contribution of tumor and host tissue factor expression to oncogene-driven gliomagenesis

Glioblastoma multiforme (GBM) is an aggressive form of glial brain tumors, associated with angiogenesis, thrombosis, and upregulation of tissue factor (TF), the key cellular trigger of coagulation and signaling. Since TF is upregulated by oncogenic mutations occurring in different subsets of human brain tumors we investigated whether TF contributes to tumourigenesis driven by oncogenic activation of EGFR (EGFRvIII) and RAS pathways in the brain. Here we show that TF expression correlates with poor prognosis in glioma, but not in GBM. In situ, the TF protein expression is heterogeneously expressed in adult and pediatric gliomas. GBM cells harboring EGFRvIII (U373vIII) grow aggressively as xenografts in SCID mice and their progression is delayed by administration of monoclonal antibodies blocking coagulant (CNTO 859) and signaling (10H10) effects of TF in vivo. Mice in which TF gene is disrupted in the neuroectodermal lineage exhibit delayed progression of spontaneous brain tumors driven by oncogenic N-ras and SV40 large T antigen (SV40LT) expressed under the control of sleeping beauty transposase. Reduced host TF levels in low-TF/SCID hypomorphic mice mitigated growth of glioma subcutaneously but not in the brain. Thus, we suggest that tumor-associated TF may serve as therapeutic target in the context of oncogene-driven disease progression in a subset of glioma.     

Biochemical and Biophysical Characterization of the Selenium-binding and Reducing Site in Arabidopsis thaliana Homologue to Mammals Selenium-binding Protein 1

The function of selenium-binding protein 1 (SBP1), present in almost all organisms, has not yet been established. In mammals, SBP1 is known to bind the essential element selenium but the binding site has not been identified. In addition, the SBP family has numerous potential metal-binding sites that may play a role in detoxification pathways in plants. In Arabidopsis thaliana, AtSBP1 over-expression increases tolerance to two toxic compounds for plants, selenium and cadmium, often found as soil pollutants. For a better understanding of AtSBP1 function in detoxification mechanisms, we investigated the chelating properties of the protein toward different ligands with a focus on selenium using biochemical and biophysical techniques. Thermal shift assays together with inductively coupled plasma mass spectrometry revealed that AtSBP1 binds selenium after incubation with selenite (SeO₃²⁻) with a ligand to protein molar ratio of 1:1. Isothermal titration calorimetry confirmed the 1:1 stoichiometry and revealed an unexpectedly large value of binding enthalpy suggesting a covalent bond between selenium and AtSBP1. Titration of reduced Cys residues and comparative mass spectrometry on AtSBP1 and the purified selenium-AtSBP1 complex identified Cys²¹ and Cys²² as being responsible for the binding of one selenium. These results were validated by site-directed mutagenesis. Selenium K-edge x-ray absorption near edge spectroscopy performed on the selenium-AtSBP1 complex demonstrated that AtSBP1 reduced SeO₃²⁻ to form a R-S-Se(II)-S-R-type complex. The capacity of AtSBP1 to bind different metals and selenium is discussed with respect to the potential function of AtSBP1 in detoxification mechanisms and selenium metabolism.     

Testing evolutionary models of senescence: traditional approaches and future directions

From an evolutionary perspective, the existence of senescence is a paradox. Why has senescence not been more effectively selected against given its associated decreases in Darwinian fitness? Why does senescence exist and how has it evolved? Three major theories offer explanations: (1) the theory of mutation accumulation suggested by PB Medawar; (2) the theory of antagonistic pleiotropy suggested by GC Williams; and (3) the disposable soma theory suggested by TBL Kirkwood. These three theories differ in the underlying causes of aging that they propose but are not mutually exclusive. This paper compares the specific biological predictions of each theory and discusses the methods and results of previous empirical tests. Lifespan is found to be the most frequently used estimate of senescence in evolutionary investigations. This measurement acts as a proxy for an individual’s rate of senescence, but provides no information on an individual’s senescent state or “biological age” throughout life. In the future, use of alternative longitudinal measures of senescence may facilitate investigation of previously neglected aspects of evolutionary models, such as intra- and inter-individual heterogeneity in the process of aging. DNA methylation data are newly proposed to measure biological aging and are suggested to be particularly useful for such investigations.     

A DNA marker assay based on high-resolution melting curve analysis for distinguishing species of the Festuca–Lolium complex

The grass breeding industry is interested in a fast and cheap method of identifying contamination in seeds of Italian and perennial ryegrass (Lolium perenne L. and L. multiflorum Lam., respectively). This study shows that high-resolution melting curve analysis in combination with an unlabelled probe assay is an effective method of detecting single nucleotide polymorphisms (SNPs) in diverse Italian and perennial ryegrass backgrounds. This method proved efficient in differentiating ryegrass species and reducing the effect of additional DNA sequence polymorphisms close to the target SNP on the melting curve profiles. For the identification of contamination in Italian and perennial ryegrass seed production, high-resolution melting curve analysis shows great potential, as it is a single closed-tube PCR reaction with an easy workflow, providing results in <2 h after DNA extraction.     

I Can't Take My Eyes Off of You: Attentional Allocation to Infant,Child, Adolescent and Adult Faces in Mothers and Non-Mothers

It has been reported previously that infant faces elicit enhanced attentional allocation compared to adult faces in adult women, particularly when these faces are emotional and when the participants are mothers, as compared to non-mothers [1]. However, it remains unclear whether this increased salience of infant faces as compared to adult faces extends to children older than infant age, or whether infant faces have a unique capacity to elicit preferential attentional allocation compared to juvenile or adult faces. Therefore, this study investigated attentional allocation to a variety of different aged faces (infants, pre-adolescent children, adolescents, and adults) in 84 adult women, 39 of whom were mothers. Consistent with previous findings, infant faces were found to elicit greater attentional engagement compared to pre-adolescent, adolescent, or adult faces, particularly when the infants displayed distress; again, this effect was more pronounced in mothers compared to non-mothers. Pre-adolescent child faces were also found to elicit greater attentional engagement compared to adolescent and adult faces, but only when they displayed distress. No preferential attentional allocation was observed for adolescent compared to adult faces. These findings indicate that cues potentially signalling vulnerability, specifically age and sad affect, interact to engage attention. They point to a potentially important mechanism, which helps facilitate caregiving behaviour.     

CD98 increases renal epithelial cell proliferation by activating MAPKs

CD98 heavy chain (CD98hc) is a multifunctional transmembrane spanning scaffolding protein whose extracellular domain binds with light chain amino acid transporters (Lats) to form the heterodimeric amino acid transporters (HATs). It also interacts with β1 and β3 integrins by its transmembrane and cytoplasmic domains. This interaction is proposed to be the mechanism whereby CD98 mediates cell survival and growth via currently undefined signaling pathways. In this study, we determined whether the critical function of CD98-dependent amino acid transport also plays a role in cell proliferation and defined the signaling pathways that mediate CD98-dependent proliferation of murine renal inner medullary collecting duct (IMCD) cells. We demonstrate that downregulating CD98hc expression resulted in IMCD cell death. Utilizing overexpression studies of CD98hc mutants that either lacked a cytoplasmic tail or were unable to bind to Lats we showed that CD98 increases serum-dependent cell proliferation by a mechanism that requires the CD98hc cytoplasmic tail. We further demonstrated that CD98-dependent amino acid transport increased renal tubular epithelial cell proliferation by a mechanism that does not require the CD98hc cytoplasmic tail. Both these mechanisms of increased renal tubular epithelial cell proliferation are mediated by Erk and p38 MAPK signaling. Although increased amino transport markedly activated mTor signaling, this pathway did not alter cell proliferation. Thus, these studies demonstrate that in IMCD cells, the cytoplasmic and extracellular domains of CD98hc regulate cell proliferation by distinct mechanisms that are mediated by common MAPK signaling pathways.