With the impending implications of climate change and global warming, space colonization in the near future will be necessary for the long-term survival of humans. We are examining how exposure to space affects biological aspects of humans by studying a model organism using a CubeSat. A CubeSat is a miniaturized satellite used in space research, built to a set of standardized measurements (10 cm per side), allowing small research projects to be launched simultaneously. We asked the questions: what would the experimental design look like investigating microgravity and UV radiation’s impact on the model organism C. elegans and what is a feasible experiment to design on a CubeSat? In this project we developed this research question to design a molecular biosciences project on a CubeSat. As part of this project, we conducted a literature review to determine 1) how small-scale satellites can be used for this kind of research, 2) what model organism is best suited for our project, and 3) how we can build upon the existing body of knowledge. The literature review, done in consultation with experts in the field, focused on the effects of microgravity and UV radiation on living organisms in the space environment. We didn’t limit our model organism research to C. elegans in the literature review. We used the constraints of the CubeSat to determine our data sampling methods and developed a research question. We anticipate research from our literature review will help us determine the next steps to take in designing our project. We hope to continue this research in preparation for implementing our work in collaboration with UW CubeSat. Research projects and experiments done in CubeSats like this one can advance the research and help address challenges our Earth faces with a rapidly expanding human population and ongoing climate change.

Microtubules play an essential role in neuronal health as they contribute to the regulation of neuronal morphology, transport and polarity. Our post-translational modification of interest, polyglutamylation, involves the elongation of glutamate chains of microtubules by a set of enzymes called glutamylases. Polyglutamylation is involved in the regulation of microtubule functions, however, the specific role of tubulin glutamylation in its impact on neurodegeneration is not well understood. While there are five glutamylases encoded in the C. elegans genome, there are only two carboxypeptidase enzymes, ccpp-1 and ccpp-6, which catalyze the shortening of polyglutamate chains. A deletion of these carboxypeptidases can cause hyperglutamylation since the shortening mechanism is absent. The purpose of this study is to utilize the loss-of-function mutation in carboxypeptidases to investigate the connection between hyperglutamylation and neurodegeneration using C. elegans as a model organism. We will utilize an Alzheimer’s model strain, GMC101, in which an overexpression of amyloid-beta protein in the body-muscle tissue causes a paralysis phenotype.Using GMC101 helps us explore the neurodegenerative effects of hyperglutamylation in the ccpp-1 and ccpp-6 mutants. We will establish baseline data of ccpp-1, ccpp-6 and GMC101 mutant strains using dye filling and paralysis assays to characterize each strain individually. Next, we will develop a double mutant ccpp-1/GMC101 and ccpp-6/GMC101, to investigate whether these mutations improve or worsens the neuronal morphology and the paralysis phenotype. Based on the literature, we expect the double mutant strains to have a worsened paralysis phenotype as well as a worsened neuronal morphology determined through dye filling assays. Investigating the specific contributions of hyperglutamylation to modulating microtubule properties in neurodegeneration is essential since there is a link between an increase in hyperglutamylation enzymatic activity in neurodegenerative regions. Further understanding of this mechanism could contribute toward developing therapeutics involved in polyglutamylation for individuals with neurodegenerative diseases.