Claire Richardson once thought she did not have what it took to be a neural genetics researcher. Not only was neuroscience “too hard,” but she was nervous about other aspects of working in academia: public speaking, presenting her work in seminars, and the “long slog” of research. Despite that, she is now an assistant professor in the UW-Madison Laboratory of Genetics, specializing in cellular and molecular neurobiology and aging. Richardson’s story demonstrates the doubts many potential scientists have and how mentorship and self-development allowed her to break free from self doubt and become a successful career scientist.
Richardson first became aware of the fields of neurology and genetics during her undergraduate studies at Carleton College. However, she did not yet have the confidence to aspire towards a career in these intimidating fields, instead she opted to major in biology and minor in biochemistry. Nevertheless, her undergrad experience provided the building blocks that Richardson needed to think like a scientist, familiarizing herself with the scientific method and establishing critical thinking skills.
Richardson was still unsure about pursuing full-time research when she started her PhD program at MIT, but the people around her slowly changed her mind. “My mentor at MIT, Dennis Kim, was the most important person for helping me to become a career scientist”, Richardson remembers. She explains how being mentored by Dr. Kim, who was “very excited about science and very positive, affirming, and supportive,” and passed these traits down to Richardson and helped her develop as a scientist. This experience was the perfect opportunity for Richardson to develop skills she previously saw as obstacles, such as communicating and presenting, growing her confidence as a scientist.
Richardson attributes part of her success to the encouragement she was given and, as such, aspires to provide a similar mentorship experience to undergraduate and graduate students in her lab. One of the reasons she enjoys working at UW-Madison is the quality of the students she gets the pleasure of working alongside. “I want to make sure that they know that I think that they have so much potential and they can do it,” she explains. “[I want to] see the people who are in my lab through to successfully making research contributions and getting to the next stage of their career.”
The Richardson Lab investigates neural aging and homeostasis of neurons through the nematode C. elegans. The transparent roundworm serves as a beneficial model organism due to its unique facultative life stage, the dauer diapause, where the organism stops aging.
The lab is unique in their study of C. elegans in this alternate facultative state. While the nematode lifespan is around two weeks, they can survive in the dauer life stage for months. Richarson is studying the “ancient signaling pathways that are mediating the decision for the organism” to arrest aging. They are exploring insulin signaling, TGF beta signaling, and hormone signaling, but it is still unclear which of these pathways play a role and in what ways.
Richardson highlights that humans have similar endocrine pathways. She explains that “it’s certainly plausible that if we can show how the endocrine signaling is communicating to subcellular structures…that there would also be a way in which[human] neurons are being regulated by our internal state.” Richardson’s research may well serve as the foundation for learning how to prevent neuron degradation in human medicine.
Beyond the signaling pathways that preserve neurons, Richardson’s lab is studying neuron subcellular structures and how their homeostasis is regulated. She explains that neurons are extremely long-lived cells, but neural subcellular components have a much shorter half-life and must be replenished more frequently. The Richardson Lab is investigating what pathways determine the rate of degradation for the proteins that compose these subcellular structures. Additionally, evidence indicates that protein degradation occurs prior to protein damage; leading to even more questions as to what causes flux in the proteome.
Protein homeostasis occurs similarly across species, “It’s true for us humans, and it’s true for C. elegans,” Richardson explains. It is plausible to infer that the regulation of homeostasis of proteins and subcellular structures may be similar in C. elegans and humans. Understanding what determines the rate of change may help answer further questions about neuron degradation and human health.
While the Richardson Lab is still in its early years, its contributions to the field of neural genetics showcase Richardson’s strong foundations as a scientist despite her early doubts. With the support of her mentors and her own efforts, she is now an accomplished scientist, and it is her time to mentor the next generation of scientists.