A Novel Use of Camera Traps to Study Demography and Life History in Wild Animals: A Case Study of Spider Monkeys (Ateles belzebuth)

Demographic and life history data from wild populations of long-lived primate species are difficult to acquire but are critical for evaluating population viability and the success of conservation efforts. Camera trapping provides an opportunity for researchers to monitor wild animal populations indirectly and could help provide demographic and life history data in a way that demands fewer person-hours in the field, is less disruptive to the study population because it requires less direct contact, and may be cost effective. Using data on group composition collected concurrently though both direct observation and camera trap monitoring, we evaluate whether camera traps can provide reliable information on population dynamics (births, disappearances, interbirth intervals, and other demographic variables) for a wild population of white-bellied spider monkeys (Ateles belzebuth), an Endangered species. We placed camera traps focused on the sole access point used by the monkeys to visit a geophagy site located roughly in the center of one group’s home range, and we reviewed all of the photos collected at that site over a roughly 3-yr period to identify the individual monkeys recorded in the pictures. Group composition based on 2947 photos containing 3977 individual monkey images matched perfectly data collected concurrently through direct observation. The camera traps also provided estimates of the dates when individuals disappeared from the study group, and of infant births during the study. We conclude that long-term camera trap monitoring of wild populations of white-bellied spider monkeys—and other animals that are individually recognizable and that regularly visit predictable resources—can be a useful tool for monitoring their population dynamics indirectly.     

Growth responses to temperature,salinity and nutrient variations,and biomass variation and phenology of Ahnfeltia plicata (Rhodophyta,Ahnfeltiales): a commercially interesting agarophyte from the Magellanic Region,Chile

Ahnfeltia plicata (Hudson) E.M. Fries (Rhodophyta, Ahnfeltiales) is one of the most commercially important agarophytes in the world for its production of agar that is high quality and low in sulfate content. In the Magellanic Region, A. plicata forms extensive beds with high biomass production, which could be commercially exploited for agar production. The purposes of this study were to determine the optimal conditions of temperature, salinity, and culture medium; to evaluate the effects of different types and concentrations of auxins and cytokinins on growth of red and yellow gametophytes; and to provide background information on ecological parameters of natural population of A. plicata. Temperatures of 5, 8, 15, and 23 °C were tested, and the interaction of salinity of 25 and 35 psu with Provasoli enriched medium in half (PES/2) and quarter strength (PES/4), and with von Stosch enriched medium in half (VSES/2) and quarter strength (VSES/4) was also conducted. Concentrations of 5.0 and 50.0 μM of two auxins (indole-3-acetic acid (IAA), 2,4-dichlorophenoxyacetic acid (2,4-D)), and two cytokinins (isopentenyladenine (iP) and benzylaminopurine) were added to VSES medium and gelled with 0.5 % agar. Each treatment was tested with three replicates. Red gametophytes of A. plicata tolerate a range of temperature variation, from 5 to 23 °C, and the optimum temperature for growth was 15 °C. The highest growth rate was observed in salinity of 35 psu with half strength of von Stosch culture medium. Red and yellow gametophytes showed different responses to plant growth regulators, and red gametophytes were more sensitive than yellow ones to the addition of IAA and high concentration of iP. However, growth of red gametophytes of A. plicata was stimulated by 2,4-D. The differential sensitivity of red and yellow gametophytes to plant growth regulators suggests the need to test other types and concentrations of auxins and cytokinins.     

HIV increases the release of dickkopf‐1 protein from human astrocytes by a Cx43 hemichannel‐dependent mechanism

Human immunodeficiency virus‐1 (HIV) is a public health issue and a major complication of the disease is NeuroAIDS. In vivo, microglia/macrophages are the main cells infected. However, a low but significant number of HIV‐infected astrocytes has also been detected, but their role in the pathogenesis of NeuroAIDS is not well understood. Our previous data indicate that gap junction channels amplify toxicity from few HIV‐infected into uninfected astrocytes. Now, we demonstrated that HIV infection of astrocytes results in the opening of connexin43 hemichannels (HCs). HIV‐induced opening of connexin43 HCs resulted in dysregulated secretion of dickkopf‐1 protein (DKK1, a soluble wnt pathway inhibitor). Treatment of mixed cultures of neurons and astrocytes with DKK1, in the absence of HIV infection, resulted in the collapse of neuronal processes. HIV infection of mixed cultures of human neurons and astrocytes also resulted in the collapse of neuronal processes through a DKK1‐dependent mechanism. In addition, dysregulated DKK1 expression in astrocytes was observed in human brain tissue sections of individuals with HIV encephalitis as compared to tissue sections from uninfected individuals. Thus, we demonstrated that HIV infection of astrocytes induces dysregulation of DKK1 by a HC‐dependent mechanism that contributes to the brain pathogenesis observed in HIV‐infected individuals.

     

Phosphoproteomic evaluation of pharmacological inhibition of leucine‐rich repeat kinase 2 reveals significant off‐target effects of LRRK‐2‐IN‐1

Genetic mutations in leucine‐rich repeat kinase 2 (LRRK2) have been linked to autosomal dominant Parkinson's disease. The most prevalent mutation, G2019S, results in enhanced LRRK2 kinase activity that potentially contributes to the etiology of Parkinson's disease. Consequently, disease progression is potentially mediated by poorly characterized phosphorylation‐dependent LRRK2 substrate pathways. To address this gap in knowledge, we transduced SH‐SY5Y neuroblastoma cells with LRRK2 G2019S via adenovirus, then determined quantitative changes in the phosphoproteome upon LRRK2 kinase inhibition (LRRK2‐IN‐1 treatment) using stable isotope labeling of amino acids in c ulture combined with phosphopeptide enrichment and LC‐MS/MS analysis. We identified 776 phosphorylation sites that were increased or decreased at least 50% in response to LRRK2‐IN‐1 treatment, including sites on proteins previously known to associate with LRRK2. Bioinformatic analysis of those phosphoproteins suggested a potential role for LRRK2 kinase activity in regulating pro‐inflammatory responses and neurite morphology, among other pathways. In follow‐up experiments, LRRK2‐IN‐1 inhibited lipopolysaccharide‐induced tumor necrosis factor alpha (TNFα) and C‐X‐C motif chemokine 10 (CXCL10) levels in astrocytes and also enhanced multiple neurite characteristics in primary neuronal cultures. However, LRRK2‐IN‐1 had almost identical effects in primary glial and neuronal cultures from LRRK2 knockout mice. These data suggest LRRK2‐IN‐1 may inhibit pathways of perceived LRRK2 pathophysiological function independently of LRRK2 highlighting the need to use multiple pharmacological tools and genetic approaches in studies determining LRRK2 function.

     

Analysis of Meiosis in SUN1 Deficient Mice Reveals a Distinct Role of SUN2 in Mammalian Meiotic LINC Complex Formation and Function

LINC complexes are evolutionarily conserved nuclear envelope bridges, composed of SUN (Sad-1/UNC-84) and KASH (Klarsicht/ANC-1/Syne/homology) domain proteins. They are crucial for nuclear positioning and nuclear shape determination, and also mediate nuclear envelope (NE) attachment of meiotic telomeres, essential for driving homolog synapsis and recombination. In mice, SUN1 and SUN2 are the only SUN domain proteins expressed during meiosis, sharing their localization with meiosis-specific KASH5. Recent studies have shown that loss of SUN1 severely interferes with meiotic processes. Absence of SUN1 provokes defective telomere attachment and causes infertility. Here, we report that meiotic telomere attachment is not entirely lost in mice deficient for SUN1, but numerous telomeres are still attached to the NE through SUN2/KASH5-LINC complexes. In Sun1^−/− meiocytes attached telomeres retained the capacity to form bouquet-like clusters. Furthermore, we could detect significant numbers of late meiotic recombination events in Sun1^−/− mice. Together, this indicates that even in the absence of SUN1 telomere attachment and their movement within the nuclear envelope per se can be functional.     

Ecohealth as a Field: Looking Forward

This forum paper proposes a reflection on the “field of ecohealth” and on how best to sustain a supportive environment that enables the evolution of diverse partnerships and forms of collaboration in the field. It is based on the results of a preconference workshop held in October 2012, in Kunming, China at the fourth biennial conference of the International Association for Ecology and Health. Attended by 105 persons from 38 countries, this workshop aimed to have a large-group and encompassing discussion about ecohealth as an emerging field, touching on subjects such as actors, processes, structures, standards, and resources. Notes taken were used to conduct a qualitative thematic analysis combined with a semantic network analysis. Commonalities highlighted by these discussions draw a portrait of a field in which human health, complex systems thinking, action, and ecosystem health are considered central issues. The need to reach outside of academia to government and the general public was identified as a shared goal. A disconnect between participants’ main concerns and what they perceived as the main concerns of funding agencies emerged as a primary roadblock for the future.     

Proteomics analysis identifies new components of the fission and budding yeast anaphase-promoting complexes

The anaphase-promoting complex (APC) is a conserved multisubunit ubiquitin ligase required for the degradation of key cell cycle regulators. Components of the APC have been identified through genetic screens in both Schizosaccharomyces pombe and Saccharomyces cerevisiae as well as through biochemical purification coupled with mass spectrometric protein identification. With these approaches, 11 subunits of the core S. cerevisiae APC have been identified. Here, we have applied a tandem affinity purification approach coupled with direct analysis of the purified complexes by mass spectrometry (DALPC) to reveal additional subunits of both the S. pombe and S. cerevisiae APCs. Our data increase the total number of identified APC subunits to 13 in both yeasts and indicate that previous approaches were biased against the identification of small subunits. These results underscore the power of direct analysis of protein complexes by mass spectrometry and set the foundation for further functional and structural studies of the APC.     

Posttranscriptional regulation of colonic epithelial repair by RNA binding protein IMP1/IGF2BP1

Correction to: EMBO Reports (2019) 20: e47074. DOI 10.15252/embr.201847074 | Published online 6 May 2019The authors noticed that the control and disease labels had been inverted in their data analysis resulting in publication of incorrect data in Figure 1C. The corrected figure is displayed below. This change affects the conclusions as detailed below. The authors apologize for this error and any confusion it may have caused.In the legend of 1C, change from, “Differential gene expression analysis of pediatric ileal CD patient samples (n = 180) shows increased (> 4‐fold) IMP1 expression as compared to non‐inflammatory bowel disease (IBD) pediatric samples (n = 43)”.Open in a separate windowFigure 1CCorrected Open in a separate windowFigure 1COriginal To, "Differential gene expression analysis of pediatric ileal CD patient samples (n = 180) shows decreased (> 4‐fold) IMP1 expression as compared to non‐inflammatory bowel disease (IBD) pediatric samples (n = 43)”.In abstract, change from, “Here, we report increased IMP1 expression in patients with Crohn''s disease and ulcerative colitis”.To, “Here, we report increased IMP1 expression in adult patients with Crohn''s disease and ulcerative colitis”.In results, change from, “Consistent with these findings, analysis of published the Pediatric RISK Stratification Study (RISK) cohort of RNA‐sequencing data 38 from pediatric patients with Crohn''s disease (CD) patients revealed that IMP1 is upregulated significantly compared to control patients and that this effect is specific to IMP1 (i.e., other distinct isoforms, IMP2 and IMP3, are not changed; Fig 1C)”.To, “Contrary to our findings in colon tissue from adults, analysis of published RNA‐sequencing data from the Pediatric RISK Stratification Study (RISK) cohort of ileal tissue from children with Crohn’s disease (CD) 38 revealed that IMP1 is downregulated significantly compared to control patients in the RISK cohort and that this effect is specific to IMP1 (i.e., other distinct isoforms, IMP2 and IMP3, are not changed; Fig 1C)”.In discussion, change from, “Indeed, we report that IMP1 is upregulated in patients with Crohn''s disease and ulcerative colitis and that mice with Imp1 loss exhibit enhanced repair following DSS‐mediated damage”.To “Indeed, we report that IMP1 is upregulated in adult patients with Crohn''s disease and ulcerative colitis and that mice with Imp1 loss exhibit enhanced repair following DSS‐mediated damage”.     

X‐chromosome lineages and the settlement of the Americas

Most genetic studies on the origins of Native Americans have examined data from mtDNA and Y‐chromosome DNA. To complement these studies and to broaden our understanding of the origin of Native American populations, we present an analysis of 1,873 X‐chromosomes representing Native American (n = 438) and other continental populations (n = 1,435). We genotyped 36 polymorphic sites, forming an informative haplotype within an 8‐kb DNA segment spanning exon 44 of the dystrophin gene. The data reveal continuity from a common Eurasian ancestry between Europeans, Siberians, and Native Americans. However, the loss of two haplotypes frequent in Eurasia (18.8 and 7%) and the rise in frequency of a third haplotype rare elsewhere, indicate a major population bottleneck in the peopling of the Americas. Although genetic drift appears to have played a greater role in the genetic differentiation of Native Americans than in the latitudinally distributed Eurasians, we also observe a signal of a differentiated ancestry of southern and northern populations that cannot be simply explained by the serial southward dilution of genetic diversity. It is possible that the distribution of X‐chromosome lineages reflects the genetic structure of the population of Beringia, itself issued from founder effects and a source of subsequent southern colonization(s). Am J Phys Anthropol, 2009. © 2009 Wiley‐Liss, Inc.