PCMM News

Three Program in Cellular and Molecular Medicine (PCMM) researchers have recently been honored with high-profile fellowships: Jhullian Alston (Ha Lab) won an HHMI Hanna Gray Fellowship, Camille Le Gall (Ploegh Lab) won an American Heart Association Postdoctoral Fellowship, and Molly Parsons (Hur Lab) won an NIH Ruth L. Kirschstein NRSA postdoctoral fellowship.

Jhullian Alston, PhD, a postdoctoral fellow in Taekjip Ha’s laboratory, has been named an HHMI Hanna Gray Fellow. His research focuses on the role of intrinsically disordered protein regions, which lack fixed structure, in transcription factor function. Specifically, he studies disordered transcriptional activation domains in fusion oncoproteins such as PAX3-FOXO1, a driver of the pediatric cancer alveolar rhabdomyosarcoma. By combining single-molecule FRET and computational biophysics, Jhullian investigates how disordered regions and folded domains within PAX3-FOXO1 cooperate to regulate DNA binding and transcriptional activation, with the goal of developing innovative methods to target disordered regions for therapeutic benefit.

Camille Le Gall, PhD, a postdoctoral fellow in Hidde Ploegh’s laboratory, has received the American Heart Association Postdoctoral Fellowship. Malaria is a mosquito-borne disease caused by apicomplexan Plasmodium falciparum (P. falciparum) parasites. Half of the world’s population in developing (sub)tropical regions remains at risk. Infection can lead to stroke and severe cardiovascular complications, either directly or via hematological disorders. In the context of this work, Camille proposes an inexpensive, dual-function therapeutic strategy to provide immediate therapeutic benefit while also inducing long-term immunity to malaria in case of an infection, by using single domain antibodies targeting P. falciparum. Successful outcomes from this work will identify novel strategies for treating malaria that induce long-lasting immune responses.

Molly Parsons, PhD, a postdoctoral fellow in Sun Hur’s laboratory, was awarded an NIH Ruth L. Kirschstein NRSA postdoctoral fellowship. The innate immune effector TRIM56 restricts a surprisingly broad range of viruses, including influenza A, hepatitis B, and HIV-1 viruses, but its antiviral mechanisms are varied and poorly understood. After establishing an antiretroviral functional assay for TRIM56, Molly recently found that the E3 ubiquitin ligase domain significantly contributes to its anti-HIV-1 activity. Additionally, the C-terminal domain of TRIM56 is a putative nucleic acid binding domain. Molly’s initial crosslinking and pulldown experiments suggest that TRIM56 associates with regulatory domains of the HIV-1 RNA genome that are important for translation and for packaging, which suggests possible modes of action and targets for TRIM56-mediated ubiquitination. In this project, Molly will use cellular, biochemical, and structural assays to elucidate a detailed mechanism for TRIM56 antiretroviral activity, and thus provide insight into the innate immune roles of this emerging class of antiviral effectors.

Congratulations to Jhullian, Camille, and Molly!