Impact of a Science Art Exhibit on Public Interest and Student Comprehension of Disease Ecology Research.

Art is a common approach for communicating and educating about science, yet it remains unclear the extent to which science art can benefit varied audiences in varied contexts. To examine this gap, we developed an art exhibit based on the findings of two publications in disease ecology. In study 1, we asked visitors with varying formal science, technology, engineering, and math (STEM) education backgrounds to complete a survey about their interest in science research before and after viewing the exhibit. In study 2, we recruited upper-level ecology undergraduate students to receive one of three treatments: engage with the art exhibit, read the abstracts of the papers, or do neither. Students completed a comprehension quiz immediately after their learning treatment and again 2 weeks later to evaluate retention. Following the exhibit, visitors who did not report a career or major in STEM showed a greater increase in research interest than visitors who did report a career or major in STEM. For the ecology undergraduate students, comprehension quiz scores were higher for students in the abstract group than the art exhibit group, while both groups scored higher than the control group. Retention of information did not significantly differ between the three groups. Overall, these findings suggest that science art exhibits are an effective method for increasing the accessibility of science to broader audiences and that audience identifiers (e.g., level of formal education in STEM) play an important role in audience experience of science communication and science education initiatives.

Genetic analysis of KillerRed in C. elegans identifies a shared role of calcium genes in ROS-mediated neurodegeneration.

In C. elegans, neurodegeneration induced by excitotoxicity or aggregation of misfolded proteins is dependent on genes involved in calcium release from the endoplasmic reticulum. Reactive oxygen species (ROS) can also induce neurodegeneration, but the relationship between ROS-mediated neurodegeneration and calcium has not been established. We activated KillerRed in the GABA neurons of C. elegans to produce ROS that leads to functional loss and structural degeneration of these neurons and demonstrated that the severity of neurodegeneration was dependent on extent of KillerRed activation. To genetically examine the role of calcium in ROS-mediated neurodegeneration, we measured functional neurodegeneration in itr-1 (inositol trisphosphate receptor), crt-1 (caltreticulin), and unc-68 (ryanodine receptor) mutants. Similar to other neurotoxic conditions, neurodegeneration triggered by KillerRed was reduced in itr-1 and crt-1 mutants. Somewhat unexpectedly, genetic or pharmacological disruption of unc-68 had a minimal effect on neurodegeneration. Our results indicate ROS-mediated neurodegeneration occurs through a conserved calcium regulated mechanism and suggest that components of the degeneration process have different sensitivities to ROS.