Overcoming early career barriers to interdisciplinary climate change research

Climate-change impacts are among the most serious and complex challenges facing society, affecting both natural and social systems. Addressing these requires a new paradigm of interdisciplinary collaboration which incorporates tools, techniques, and insights from across the social, natural, and engineering sciences. Yet, a wide range of intrinsic and extrinsic hurdles need to be overcome to conduct successful, integrated interdisciplinary research. The results of a bibliometric analysis and survey of early to mid-career scientists from 56 countries who were involved with the interdisciplinary DISsertations initiative for the advancement of Climate Change ReSearch (DISCCRS) emphasize the particular challenges faced by early career researchers. Survey respondents perceive conflict between the need for interdisciplinary climate-change research and its potential detriment to career advancement. However, participation in interventions for early career scientists, such as networking and training symposia, had both perceived and measurable impacts on the likelihood of engagement in climate-centric interdisciplinary research. Respondents also ranked alternative mechanisms for encouraging incorporation of interdisciplinary science at early career stages, prioritizing funding of interdisciplinary seed grants, fellowships, and junior faculty networks, interdisciplinary teamwork and communication training, and interdepartmental symposia. To this we add the suggestion that interdisciplinarity be incorporated into tenure and promotion evaluations through the use of exploratory science mapping tools. Despite the need to foster interdisciplinary research and the availability of multiple prospective solutions, there remain expansive structural challenges to its promotion and recognition which, unless collectively addressed, will continue to hinder its potential growth and application to climate-change science

PTPN2, a Candidate Gene for Type 1 Diabetes, Modulates Interferon-γ–Induced Pancreatic β-Cell Apoptosis

OBJECTIVE: The pathogenesis of type 1 diabetes has a strong genetic component. Genome-wide association scans recently identified novel susceptibility genes including the phosphatases PTPN22 and PTPN2. We hypothesized that PTPN2 plays a direct role in beta-cell demise and assessed PTPN2 expression in human islets and rat primary and clonal beta-cells, besides evaluating its role in cytokine-induced signaling and beta-cell apoptosis. RESEARCH DESIGN AND METHODS: PTPN2 mRNA and protein expression was evaluated by real-time PCR and Western blot. Small interfering (si)RNAs were used to inhibit the expression of PTPN2 and downstream STAT1 in beta-cells, allowing the assessment of cell death after cytokine treatment. RESULTS: PTPN2 mRNA and protein are expressed in human islets and rat beta-cells and upregulated by cytokines. Transfection with PTPN2 siRNAs inhibited basal- and cytokine-induced PTPN2 expression in rat beta-cells and dispersed human islets cells. Decreased PTPN2 expression exacerbated interleukin (IL)-1beta + interferon (IFN)-gamma-induced beta-cell apoptosis and turned IFN-gamma alone into a proapoptotic signal. Inhibition of PTPN2 amplified IFN-gamma-induced STAT1 phosphorylation, whereas double knockdown of both PTPN2 and STAT1 protected beta-cells against cytokine-induced apoptosis, suggesting that STAT1 hyperactivation is responsible for the aggravation of cytokine-induced beta-cell death in PTPN2-deficient cells. CONCLUSIONS: We identified a functional role for the type 1 diabetes candidate gene PTPN2 in modulating IFN-gamma signal transduction at the beta-cell level. PTPN2 regulates cytokine-induced apoptosis and may thereby contribute to the pathogenesis of type 1 diabetes