RESUMEN
Success and persistence in the life sciences is influenced by a student's self-efficacy, sense of belonging, and science identity. It has already been demonstrated that outreach experiences and service learning by graduate students in K-12 schools aid in the graduate students' confidence and intrinsic satisfaction. Others have shown the importance of engaging scientists in outreach activities, both for the benefit of the K-12 student and as a way to engage scientists with the community. We predicted it would also be beneficial for undergraduates to engage in service-learning activities during their coursework because working with K-12 students would solidify their scientific identity and sense of belonging while deepening their understanding of the course content. Consequently, we implemented service projects in our upper-level molecular biology and human physiology courses at a primarily undergraduate institution that focuses on five core values: Christian, Liberal Arts, Excellence, Community, and Service. Outcomes such as the undergraduate students' value of service, confidence in their knowledge of course content, ability to create effective lesson plans, and science identity were measured using anonymous surveys. Overall, students reported that they highly valued and enjoyed this unique experience. This type of activity could be used to increase future scientists' awareness of synergistic activities such as academic service and of the joy found in such activities. Future plans include measuring the effects on the participating high school and elementary school students and visiting schools with a high proportion of students from underserved populations.
RESUMEN
Cystine and cysteine are important molecules for pathways such as redox signaling and regulation, and thus identifying cellular deficits upon deletion of the Saccharomyces cerevisiae cystine transporter Ers1p allows for a further understanding of cystine homeostasis. Previous complementation studies using the human ortholog suggest yeast Ers1p is a cystine transporter. Human CTNS encodes the protein Cystinosin, a cystine transporter that is embedded in the lysosomal membrane and facilitates the export of cystine from the lysosome. When CTNS is mutated, cystine transport is disrupted, leading to cystine accumulation, the diagnostic hallmark of the lysosomal storage disorder cystinosis. Here, we provide biochemical evidence for Ers1p-dependent cystine transport. However, the accumulation of intracellular cystine is not observed when the ERS1 gene is deleted from ers1-Δ yeast, supporting the existence of modifier genes that provide a mechanism in ers1-Δ yeast that prevents or corrects cystine accumulation. Upon comparison of the transcriptomes of isogenic ERS1+ and ers1-Δ strains of S. cerevisiae by DNA microarray followed by targeted qPCR, sixteen genes were identified as being differentially expressed between the two genotypes. Genes that encode proteins functioning in sulfur regulation, cellular respiration, and general transport were enriched in our screen, demonstrating pleiotropic effects of ers1-Δ. These results give insight into yeast cystine regulation and the multiple, seemingly distal, pathways that involve proper cystine recycling.
RESUMEN
The lysosome, an organelle central to macromolecule degradation and recycling, plays a pivotal role in normal cell processes, ranging from autophagy to redox regulation. Not surprisingly, lysosomes are an integral part of the renal epithelial molecular machinery that facilitates normal renal physiology. Two inherited diseases that manifest as kidney dysfunction are Fabry's disease and cystinosis, each of which is caused by a primary biochemical defect at the lysosome resulting from loss-of-function mutations in genes that encode lysosomal proteins. The functions of the lysosomes in the kidney and how lysosomal dysfunction might contribute to Fabry's disease and cystinosis are discussed. Unlike most other pediatric renal diseases, therapies are available for Fabry's disease and cystinosis, but require early diagnosis. Recent analysis of ceroid neuronal lipofuscinosis type 3 (Cln3) null mice, a mouse model of lysosomal disease that is primarily associated with neurological deficits, revealed renal functional abnormalities. As current and future therapeutics increase the life-span of those suffering from diseases like neuronal ceroid lipofuscinosis, it remains a distinct possibility that many more lysosomal disorders that primarily manifest as infant and juvenile neurodegenerative diseases may also include renal disease phenotypes.
