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Yi-Ju Chen, Ph.D.

Technology & Resource Development Scientist

Developing mouse models harboring disease-causing variants and pre-clinical testing platforms to help therapeutics development and research discoveries.

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About Yi-Ju Chen, Ph.D.

Dr. Yi-Ju Chen has a long-standing interest in bench-to-bedside research and extensive experience in cancer, developmental biology, and diabetes. She earned her Ph.D. in Biochemistry and Molecular genetics from University of Illinois at Chicago for her research on elucidating the role of FoxM1 in cell cycle progression, tumorigenesis, and metastasis. She then conducted postdoctoral studies in tissue plasticity and cell fate decision at University of Pennsylvania. By generating a new mouse model, she identified that intestinal stem cells can be reprogrammed into insulin-producing cells in vivo. Her research provides a new avenue to develop therapeutic solutions to diabetes. Furthermore, she applied her cell biology expertise and tissue engineering techniques to develop a biomimetic platform for long-term human islet culture and beta cell research. Dr. Chen joined The Jackson Laboratory at Bar Harbor, ME in October of 2018 as Technology & Resource Development Scientist. She works on new mouse models harboring patient mutations. Most of these mutations are linked to rare & orphan disease, which often lack of research and resources for therapeutics development. Yi-Ju directs studies to investigate these models and establishes the pre-clinical testing platform to help drug discovery and the research community.

Selected Publications

Highlighted Abstract

The Forkhead box m1 (Foxm1) gene is critical for G(1)/S transition and essential for mitotic progression. However, the transcriptional mechanisms downstream of FoxM1 that control these cell cycle events remain to be determined. Here, we show that both early-passage Foxm1(-)(/)(-) mouse embryonic fibroblasts (MEFs) and human osteosarcoma U2OS cells depleted of FoxM1 protein by small interfering RNA fail to grow in culture due to a mitotic block and accumulate nuclear levels of cyclin-dependent kinase inhibitor (CDKI) proteins p21(Cip1) and p27(Kip1). Using quantitative chromatin immunoprecipitation and expression assays, we show that FoxM1 is essential for transcription of the mitotic regulatory genes Cdc25B, Aurora B kinase, survivin, centromere protein A (CENPA), and CENPB. We also identify the mechanism by which FoxM1 deficiency causes elevated nuclear levels of the CDKI proteins p21(Cip1) and p27(Kip1). We provide evidence that FoxM1 is essential for transcription of Skp2 and Cks1, which are specificity subunits of the Skp1-Cullin 1-F-box (SCF) ubiquitin ligase complex that targets these CDKI proteins for degradation during the G(1)/S transition. Moreover, early-passage Foxm1(-)(/)(-) MEFs display premature senescence as evidenced by high expression of the senescence-associated beta-galactosidase, p19(ARF), and p16(INK4A) proteins. Taken together, these results demonstrate that FoxM1 regulates transcription of cell cycle genes critical for progression into S-phase and mitosis.

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