Augmenting course material to be relevant and accessible to students is a ubiquitous challenge throughout academia. We aimed to design, develop, and evaluate the effectiveness of activities meant to promote the learning of difficult concepts in Anatomy and Physiology. More specifically, we focused on the neurophysiology chapter of an open access Anatomy and Physiology course sponsored by the Carnegie Mellon Open Learning Initiative (OLI). This course is being created for pre-nursing students attending community colleges. We used the six-level schema of Bloom’s Taxonomy, a module addressing the knowledge and development of intellectual skills, to design learning activities that encouraged students to analyze, synthesize, and evaluate concepts rather than simply recall, explain, and define them. By compelling students to work at higher cognitive levels during the learning process, we hypothesized that there would be a corresponding elevation in critical thinking skills and a deeper understanding of the material. Our curriculum design strategy was informed by cognitive science research that shows increases in learning efficacy when students are motivated to work at higher cognitive levels. Assessments were designed to align with these higher cognitive level learning activities. Our learning activities were tested by Anatomy and Physiology students using Carnegie Mellon’s OLI course. The Carnegie Mellon course uses an innovative digital dashboard platform which allowed us to track individual student’s understanding of concepts before, during, and after using our materials so that we were able to analyze their success and effectiveness. We revised our learning activities based on these results.

The mitotic spindle orchestrates proper alignment of chromosomes during cell division. The spindle is composed of microtubules that attach to kinetochores, multi-protein complexes that assemble at the centromeres of chromosomes. Understanding kinetochore function is essential to understanding the process of cell division. Through mass spectrometry analysis, the Davis Lab has found an abundance of the urmylation component Uba4 at the kinetochore. The urmylation pathway is highly similar to ubiquitination, and involves conjugation of a ubiquitin related modifier (Urm1) to proteins and RNAs. The role of urmylation at the kinetochore is not known. We hypothesize that post-translational modification of kinetochore proteins through urmylation is a regulator of chromosome segregation. To examine the effects of urmylation on the kinetochore I will be using an Ncs2 mutant, a protein involved in the urmylation pathway, By fluorescently labeling the kinetochore protein Spc105 and spindle pole body protein Spc110, I am using fluorescence microscopy and computational analysis to look for abnormalities in spindle appearance. These results will help elucidate the role of the urmylation pathway in the regulation of cell division.

The spindle assembly checkpoint is important for detecting errors in spindle assembly during mitosis. When the checkpoint is activated, it arrests the cell cycle so that errors such as unattached kinetochores can be detected and corrected before progressing through the cell cycle. Problems with kinetochore attachment can be detrimental and lead to cells with an abnormal number of chromosomes which can then cause birth defects. Misregulation of the cell cycle can lead to abnormal cell division and cancer. Spindle pole bodies in yeast are functionally equivalent to human centrosomes, which organize microtubules in the cell cycle. Spindle pole bodies increase in size when the cell cycle is arrested at the checkpoint. Mad1 is an essential component of the checkpoint and interacts with the Nup60 protein in the nuclear pore complex, a channel through which information traffics between the nucleus and cytoplasm. The N-terminus of Mad1 protein is required to localize Mad1 to the nuclear pore complex, but is not required for the checkpoint arrest. We found previously that if Nup60 is deleted, the spindle pole bodies do not grow in cells arrested at the checkpoint. Mad1 mutants containing only the C-terminus of the protein will be constructed. I will test if the ability of Mad1 to bind to Nup60 is required for spindle pole body growth. Spindle pole body size will be measured by fluorescence microscopy after arresting the cells in metaphase. I hypothesize that although Mad1 interaction with Nup60 is not required for the cell cycle arrest, it is required to signal spindle pole body growth. If true, then deletion of the Nup60 binding domain of Mad1 should block spindle pole body growth. Discovering what interactions are vital in these cells will give us a deeper understanding of how regulation of the cell cycle is maintained.