Xiaoying Bai, PhD

  • Recruited to: The University of Texas Southwestern Medical Center
  • Recruited from: Childen's Hospital Boston
  • Award: First-Time, Tenure-Track Faculty Member

Dr. Xiaoying Bai received her PhD from Baylor College of Medicine in 2004. She did her postdoctoral training at the Children’s Hospital Boston and Harvard Medical School in 2005-2011. In January 2012, Dr. Bai joined the UT Southwestern Medical Center as an Assistant Professor in the Cecil H. and Ida Green Center for Reproductive Biology Sciences. Her research focuses on investigating thetranscriptional mechanisms that regulate the differentiation of hematopoietic stem cells and aiming to identify potential therapeutic targets for the treatment of human hematologic disorders.

As a graduate student in Dr. Mitzi Kuroda’s lab at the Baylor College of Medicine, Dr. Bai developed a strong interest in transcriptional regulation by studying Drosophila X-chromosome dosage compensation. Her work led to a discovery of non- coding RNA-dependent epigenetic remodeling of the male X chromosome that contributes to hyper- transcription of X-linked genes. At the end of her PhD training, she moved to Boston with Dr. Kuroda, who was recruited to the Harvard Medical School. Dr. Bai continued her research career in Boston after joining Dr. Leonard Zon’s laboratory at Children’s Hospital Boston as a postdoctoral research fellow. Her research In Dr. Zon’s laboratory focused on the transcription cofactor TIF1γ, whichplays a critical function in vertebrate hematopoiesis. Loss of TIF1γ in the zebrafish mutant resulted in a profound anemia and embryonic death. To understand the molecular mechanism by which TIF1γ regulates hematopoiesis, Dr. Bai took the advantage of the large-scale genetics available in zebrafish and developed a modifier screen strategy to identify molecular pathways interacting with TIF1γ. This is the first genetic modifier screen ever performed in zebrafish. She successfully identified a couple of suppressor mutants that restored red cell gene expression in the TIF1γ mutant. Characterizing one of the suppressor mutants uncovered an essential role of TIF1γ in transcription elongation by coupling the blood-specific transcription factor complex to the basal transcriptional elongation machinery. Her work showed that in TIF1γ mutant cells, RNA polymerase II (Pol II)-mediated transcription elongation is stalled on red cell genes due to the failure of recruiting the positive elongation factor p-TEFb. By removing Pol II stalling factors in the suppressor mutant, she was able to show that transcription elongation was restored on red cell genes, leading to a rescue of anemia in TIF1γ mutant fish. Her genetic study correlates well with recent genome-wide studies showing profound Pol II stalling throughout the metazoan genomes, suggesting that regulation of transcription elongation is a critical step in gene expression. Most importantly, mis-regulated Pol II elongation is found to be tightly linked to multiple human diseases including leukemia. Dr. Bai’s work therefore provides a platform to study the biological role of Pol II elongation during both organogenesis and carcinogenesis. In 2010, Dr. Bai received an NIH/NIDDK Pathway to Independence Award.

At UT Southwestern Medical Center, Dr. Bai will investigate the genetic and epigenetic pathways that regulate gene transcription of normal and malignant hematopoiesis, using zebrafish as a genetic and developmental model in combination with mammalian cell culture systems. Her studies have the potential to reveal new mechanism and therapeutic targets, as well as identify new small molecules that can be used to treat cancers and other diseases.