I'm currently a postdoctoral research fellow in Dr. Bob Goldstein's lab at the University of North Carolina at Chapel Hill. I'm utilizing my background in developmental biology to understand how cell biological mechanisms are regulated. I co-led a project characterizing the organization of the actomyosin network driving apical constriction during C. elegans gastrulation [Zhang, Medwig-Kinney & Goldstein, 2023]. 

I conducted my dissertation research in Dr. David Matus's lab at Stony Brook University, investigating how invasive cell fate acquisition, differentiation, and maintenance are regulated. During C. elegans somatic gonad development, a specialized uterine cell called the anchor cell (AC) invades the underlying basement membrane utilizing cellular programs that are largely conserved across other contexts of cell invasion [Medwig-Kinney & Matus, 2017].

The AC is specified through a Notch-mediated cell fate decision between two initially equipotent cells, giving rise to the invasive post-mitotic AC and a proliferative ventral uterine (VU) cell. I collaborated with the Pani lab to develop tools [Medwig-Kinney et al., 2022, Pani et al., 2022] to visualize and perturb Notch/Delta signaling.

First, I showed that four pro-invasive transcription factors, FOS-1 (Fos), EGL-43 (EVI/MEL), HLH-2 (E/Daughterless), and NHR-67 (NR2E1/TLX) form a gene regulatory network with two sub-circuits: one controlling G0/G1 cell cycle arrest and another controlling cell cycle independent pro-invasive targets. The regulatory interactions among these transcription factors are dynamic, as these transcription factors function independently to regulate the Notch-mediated AC/VU cell fate decision [Medwig-Kinney & Smith et al., 2020]. Later work I contributed to demonstrated how chromatin modifiers regulate this network [Medwig-Kinney & Palmisano et al., 2021, Smith et al., 2022].

During the second half of my dissertation research, I focused on how the invasive AC and proliferative VU cell fates are maintained. I found that transcriptional regulation of the pro-invasive transcription factor NHR-67 was important for discriminating between these two fates. Additionally, I discovered a second mechanism in which NHR-67 forms putative nuclear condensates that colocalize with homologs of Groucho co-repressors (UNC-37 and LSY-22) and TCF/LEF (POP-1). Perturbation of UNC-37, LSY-22, or POP-1 results in ectopic ACs, leading us to the model that these proteins associate with NHR-67 to repress the default invasive state [Medwig-Kinney et al., 2023].