The *NSPIRE fellowship is a competitive scholarship program for senior graduate students at Scripps Research. *NSPIRE Fellows will receive a educational allowance stipend and will have the opportunity to present a seminar at the *NSPIRE Symposium. The seminar will not only feature Fellows’ doctoral research, but also highlight their unique educational journey in a way that is compelling to a diverse audience of students, faculty, and staff from CSU San Marcos, Palomar Community College, Mira Costa Community College, and Scripps Research.
I was a first-generation undergraduate student who did not know how far an undergraduate education would take me. Even less so did I know how far science would take me. It is due to my experience of embarking into the unknown that I am delighted to be a *NSPIRE Fellow. During my undergraduate years, I realized the abundance of opportunities that scientific research provides for students. NSPIRE provides a perfect platform in which I can fulfill my passion for motivating undergraduate students to pursue scientific research. My research is focused on understanding how neuroinflammation can contribute to Parkinson’s disease (PD), the second most common neurodegenerative disorder, which is primarily characterized by the loss of dopaminergic (DA) neurons of the substantia nigrapars compacta (SNc). Recently, inflammation and its mediators have been proposed to contribute to the neuronal loss that occurs in PD. Thus, inflammatory regulators could be involved in the loss of DA neurons and play a significant role in the onset and/or progression of PD. I am investigating whether two regulators of immune response, interleukin-13 (IL-13) and its receptor alpha-1 (IL-13Rα1), contribute to the neuronal loss observed in PD. Elucidating the contribution of IL-13 and IL-13Rα1 to DA neuron loss in PD may reveal them as novel targets for the treatment of PD.
One chemical code describes every living thing we know of. I started working on a PhD to study this most fundamental level of biological organization – the balance of chemical reactions that form a living cell. In pursuit of that goal, I picked a research project by accident, realized I knew nothing about how PhDs work, taught myself laser optics from scratch, learned not to feel so dumb all the time, and ended up caring a lot about transcription. Transcription factors regulate the 20,000 genes that keep your cells functioning, so a single transcription factor has a challenge in finding the one gene it’s responsible for. I study the transcription factor CREB (cyclic AMP response element binding protein) and its strategy of searching DNA in order to regulate everything from nutrient metabolism to memory consolidation to viral infection. I want to know how CREB – and transcription factors like it – scan “incorrect” DNA to find their target sites quickly, how these molecules can guess which way to travel, and how transcription factors cooperate to keep cells running. Like CREB, I have also had to guess which way to travel – but I’ve cleared every obstacle so far.
Unlike many of my peers in grad school, I did not embark on an uninterrupted march through the different levels of education. Instead, I encountered bumps and slow downs along the way, often taking the path less traveled to a terminal degree. I am proud to be an *NSPIRE fellow because I believe this program supports what I’ve learned over the years: you don’t have to come from a privileged background to be successful in science. I am elated at the opportunity to share the story of my academic journey as well as my work on the structure and biophysics of molecular motors. My research is focused on understanding the molecular biology of the microtubule severing enzyme spastin. Spastin uses the chemical energy released through ATP hydrolysis to remodel microtubule arrays, and its mutation is the most common cause of the neurodegenerative disease hereditary spastic paraplegia. Using cryo-electron microscopy (cryo-EM), I obtained a 3D structure of the active form of spastin, revealing an allosteric network within the enzyme that couples multiple activities to microtubule severing. This result is important for understanding how spastin performs its function as a cytoskeletal regulator and gives us insight into why its mutation so often results in disease.