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Pierce, J. T.

Publications and source records attributed to Pierce, J. T..

3 recordsLinked to original sources

Experiential diversity training and science learning for college students alongside peers with intellectual and developmental disabilities

Diversity, equity and inclusion (DEI) training can benefit STEM students. However, typical college settings often limit college students exposure to adult peers with intellectual and developmental disabilities (IDDs), a historically marginalized group. To lower this barrier, we developed a continuing education program, Lifelong Learning with Friends (LLWF), aimed at adults with IDDs on a large university campus, which provides diversity training to college students. In this program, undergraduate and graduate students from scientific and education disciplines are recruited to volunteer as peers and helpers. LLWF has reached hundreds of students with and without IDDs each year and more than 1,500 over the past 12 years. In our program, college students gain DEI training through learning sophisticated academic topics, including sciences, alongside adults with IDDs. Almost half (42%) of surveyed LLWF college volunteers did not have prior exposure to people with IDDs. Following program participation, we found that, irrespective of prior exposure, nearly all (98%) of volunteers had elevated their expectations of people with IDDs and reported increased interest in IDDs-focused research, education, social interaction, and advocacy. Additionally, college volunteers reported that they improved their science communication by seeing how science could be taught to a broad audience that includes adults with IDDs. We therefore suggest that other universities may consider our LLWF model to enhance DEI training by expanding opportunities for neurotypical students to befriend and learn science alongside adults with IDDs.

scientific communication and education↗

Activity-dependent regulation of the proapoptotic BH3-only gene egl-1 in a living neuron pair in C. elegans

The BH3-only family of proteins is key for initiating apoptosis in a variety of contexts, and may also contribute to non-apoptotic cellular processes. Historically, the nematode Caenorhabditis elegans has provided a powerful system for studying and identifying conserved regulators of BH3-only proteins. In C. elegans, the BH3-only protein EGL-1 is expressed during development to cell-autonomously trigger most developmental cell deaths. Here we provide evidence that egl-1 is also transcribed after development in the sensory neuron pair URX without inducing apoptosis. We used genetic screening and epistasis analysis to determine that its transcription is regulated in URX by neuronal activity and/or in parallel by orthologs of Protein Kinase G and the Salt-Inducible Kinase family. Because several BH3-only family proteins are also expressed in the adult nervous system of mammals, we suggest that studying egl-1 expression in URX may shed light on mechanisms that regulate conserved family members in higher organisms.

genetics↗

APP-induced patterned neurodegeneration exacerbated by APOE4 in C. elegans

Genetic and epidemiological studies have found that variations in the amyloid precursor protein (APP) and the apoliopoprotein E (APOE) genes represent major modifiers of the progressive neurodegeneration in Alzheimers disease (AD). An extra copy or gain-of-function mutations in APP lower age of AD onset. Compared to the other isoforms (APOE3 and APOE2), the {varepsilon}4 allele of APOE (APOE4) hastens and exacerbates early and late onset forms of AD. Convenient in vivo models to study how APP and APOE4 interact at the cellular and molecular level to influence neurodegeneration are lacking. Here, we show that the nematode C. elegans can model important aspects of AD including age-related, patterned neurodegeneration that is exacerbated by APOE4. Specifically, we found that APOE4, but not APOE3, acts with APP to hasten and expand the pattern of cholinergic neurodegeneration caused by APP. Molecular mechanisms underlying how APP and APOE4 synergize to kill some neurons while leaving others unaffected may be uncovered using this convenient worm model of neurodegeneration.

neuroscience↗