Inter-aviary distance and visual access influence conservation breeding outcomes in a territorial, endangered bird

Funding for setting up the housing database was provided by the UK’s Biotechnology and Biological Sciences Research Council (BBSRC; grant BB/G023913/2 to C.R.).Species extinctions are becoming a global crisis, affecting biodiversity and ecosystem services, with island populations being particularly vulnerable. In response, conservation managers are increasingly turning to ex situ conservation breeding programs to establish assurance populations and provide a source for release and re-establishment of wild populations. The 'Alalā (Hawaiian crow, Corvus hawaiiensis) is a critically endangered and territorial island corvid that became extinct in the wild in 2002, following a severe and prolonged population decline during the late 20th century. Surviving individuals of the species were brought into captivity to establish an assurance population to serve as a source for reintroduction, which commenced in 2016. We analyzed the extent to which a range of captive housing conditions impact 'Alalā reproductive success, using 19 years of breeding program data. We found that reproductive success was most strongly affected by the distance between aviaries and their closest neighbors and whether breeding pairs had visual access to other adult conspecifics. Pairs located in aviaries that were more spatially isolated and without visual access to conspecifics were more likely to produce fertile eggs than pairs housed in aviaries that were closer to others or those with visual access to other birds. Our results have direct management implications relevant to the design of conservation breeding centers geared towards the recovery of endangered, territorial bird species. Moreover, since suboptimal housing conditions can increase stress levels in captive birds, our findings are also relevant to improving animal welfare for 'Alalā and other species in conservation breeding programs.PostprintPeer reviewe

Animal Welfare in Conservation Breeding: Applications and Challenges

Animal welfare and conservation breeding have overlapping and compatible goals that are occasionally divergent. Efforts to improve enclosures, provide enriching experiences, and address behavioral and physical needs further the causes of animal welfare in all zoo settings. However, by mitigating stress, increasing behavioral competence, and enhancing reproduction, health, and survival, conservation breeding programs must also focus on preparing animals for release into the wild. Therefore, conservation breeding facilities must strike a balance of promoting high welfare, while minimizing the effects of captivity to increase population sustainability. As part of the Hawaii Endangered Bird Conservation Program, San Diego Zoo Global operates two captive breeding facilities that house a number of endangered Hawaiian bird species. At our facilities we aim to increase captive animal welfare through husbandry, nutrition, behavior-based enrichment, and integrated veterinary practices. These efforts help foster a captive environment that promotes the development of species-typical behaviors. By using the “Opportunities to Thrive” guiding principles, we outline an outcome-based welfare strategy, and detail some of the related management inputs, such as transitioning to parental rearing, and conducting veterinary exams remotely. Throughout we highlight our evidence-based approach for evaluating our practices, by monitoring welfare and the effectiveness of our inputs. Additionally we focus on some of the unique challenges associated with improving welfare in conservation breeding facilitates and outline concrete future steps for improving and evaluating welfare outcomes that also meet conservation goals

Expression of Six1 in luminal breast cancers predicts poor prognosis and promotes increases in tumor initiating cells by activation of extracellular signal-regulated kinase and transforming growth factor-beta signaling pathways

Abstract Introduction Mammary-specific overexpression of Six1 in mice induces tumors that resemble human breast cancer, some having undergone epithelial to mesenchymal transition (EMT) and exhibiting stem/progenitor cell features. Six1 overexpression in human breast cancer cells promotes EMT and metastatic dissemination. We hypothesized that Six1 plays a role in the tumor initiating cell (TIC) population specifically in certain subtypes of breast cancer, and that by understanding its mechanism of action, we could potentially develop new means to target TICs. Methods We examined gene expression datasets to determine the breast cancer subtypes with Six1 overexpression, and then examined its expression in the CD24low/CD44+ putative TIC population in human luminal breast cancers xenografted through mice and in luminal breast cancer cell lines. Six1 overexpression, or knockdown, was performed in different systems to examine how Six1 levels affect TIC characteristics, using gene expression and flow cytometric analysis, tumorsphere assays, and in vivo TIC assays in immunocompromised and immune-competent mice. We examined the molecular pathways by which Six1 influences TICs using genetic/inhibitor approaches in vitro and in vivo. Finally, we examined the expression of Six1 and phosphorylated extracellular signal-regulated kinase (p-ERK) in human breast cancers. Results High levels of Six1 are associated with adverse outcomes in luminal breast cancers, particularly the luminal B subtype. Six1 levels are enriched in the CD24low/CD44+ TIC population in human luminal breast cancers xenografted through mice, and in tumorsphere cultures in MCF7 and T47D luminal breast cancer cells. When overexpressed in MCF7 cells, Six1expands the TIC population through activation of transforming growth factor-beta (TGF-β) and mitogen activated protein kinase (MEK)/ERK signaling. Inhibition of ERK signaling in MCF7-Six1 cells with MEK1/2 inhibitors, U0126 and AZD6244, restores the TIC population of luminal breast cancer cells back to that observed in control cells. Administration of AZD6244 dramatically inhibits tumor formation efficiency and metastasis in cells that express high levels of Six1 ectopically or endogenously. Finally, we demonstrate that Six1 significantly correlates with phosphorylated ERK in human breast cancers. Conclusions Six1 plays an important role in the TIC population in luminal breast cancers and induces a TIC phenotype by enhancing both TGF-β and ERK signaling. MEK1/2 kinase inhibitors are potential candidates for targeting TICs in breast tumors

Within-group behavioral variation promotes biased task performance and the emergence of a defensive caste in a social spider

The social spider Anelosimus studiosus exhibits a behavioral polymorphism where colony members express either a passive, tolerant behavioral tendency (social) or an aggressive, intolerant behavioral tendency (asocial). Here we test whether asocial individuals act as colony defenders by deflecting the suite of foreign (i.e., heterospecific) spider species that commonly exploit multi-female colonies. We (1) determined whether the phenotypic composition of colonies is associated with foreign spider abundance, (2) tested whether heterospecific spider abundance and diversity affect colony survival in the field, and (3) performed staged encounters between groups of A. studiosus and their colony-level predator Agelenopsis emertoni (A. emertoni)to determine whether asocial females exhibit more defensive behavior. We found that larger colonies harbor more foreign spiders, and the number of asocial colony members was negatively associated with foreign spider abundance. Additionally, colony persistence was negatively associated with the abundance and diversity of foreign spiders within colonies. In encounters with a colony-level predator, asocial females were more likely to exhibit escalatory behavior, and this might explain the negative association between the frequency of asocial females and the presence of foreign spider associates. Together, our results indicate that foreign spiders are detrimental to colony survival, and that asocial females play a defensive role in multi-female colonies

Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression

From the earliest stages of embryonic development, cells of epithelial and mesenchymal origin contribute to the structure and function of developing organs. However, these phenotypes are not always permanent, and instead, under the appropriate conditions, epithelial and mesenchymal cells convert between these two phenotypes. These processes, termed Epithelial-Mesenchymal Transition (EMT), or the reverse Mesenchymal-Epithelial Transition (MET), are required for complex body patterning and morphogenesis. In addition, epithelial plasticity and the acquisition of invasive properties without the full commitment to a mesenchymal phenotype are critical in development, particularly during branching morphogenesis in the mammary gland. Recent work in cancer has identified an analogous plasticity of cellular phenotypes whereby epithelial cancer cells acquire mesenchymal features that permit escape from the primary tumor. Because local invasion is thought to be a necessary first step in metastatic dissemination, EMT and epithelial plasticity are hypothesized to contribute to tumor progression. Similarities between developmental and oncogenic EMT have led to the identification of common contributing pathways, suggesting that the reactivation of developmental pathways in breast and other cancers contributes to tumor progression. For example, developmental EMT regulators including Snail/Slug, Twist, Six1, and Cripto, along with developmental signaling pathways including TGF-β and Wnt/β-catenin, are misexpressed in breast cancer and correlate with poor clinical outcomes. This review focuses on the parallels between epithelial plasticity/EMT in the mammary gland and other organs during development, and on a selection of developmental EMT regulators that are misexpressed specifically during breast cancer

Translational Suppressors and Antisuppressors Alter the Efficiency of the Ty1 Translational Frameshift

©1999 RNA Society. Published by Cold Spring Harbor LaboratoryCertain viruses, transposons, and cellular genes have evolved specific sequences that induce high levels of specific translational errors. Such “programmed misreading” can result in levels of frameshifting or nonsense codon readthrough that are up to 1,000-fold higher than normal. Here we determine how a number of mutations in yeast affect the programmed misreading used by the yeast Ty retrotransposons. These mutations have previously been shown to affect the general accuracy of translational termination. We find that among four nonsense suppressor ribosomal mutations tested, one (a ribosomal protein mutation) enhanced the efficiency of the Ty1 frameshifting, another (an rRNA mutation) reduced frameshifting, and two others (another ribosomal protein mutation and another rRNA mutation) had no effect. Three antisuppressor rRNA mutations all reduced Ty1 frameshifting; however the antisuppressor mutation in the ribosomal protein did not show any effect. Among nonribosomal mutations, the allosuppressor protein phosphatase mutation enhanced Ty1 frameshifting, whereas the partially inactive prion form of the release factor eRF3 caused a slight decrease, if any effect. A mutant form of the other release factor, eRF1, also had no effect on frameshifting. Our data suggest that Ty frameshifting is under the control of the cellular translational machinery. Surprisingly we find that translational suppressors can affect Ty frameshifting in either direction, whereas antisuppressors have either no effect or cause a decrease