We currently have open Post Doctoral positions available for talented and creative individuals.
Please email inquiries with a cover letter, CV and three references to Dr. Edward Morrisey at: email@example.com
Our interests have focused on the role of critical developmental signaling pathways such as Wnt signaling as well as important transcription factors including Foxp1/2/4 and Gata6. Our data has shown that Wnt signaling is uniquely required for lung endoderm specification. Loss of the critical Wnt ligands Wnt2/2b leads to complete respiratory agenesis as noted by lack of Nkx2.1 expression.
Our lab originally cloned the Foxp1/2/4 subfamily of forkhead transcription factors in 2001. We have shown that these factors play key roles in regulating both lung and cardiac development. Recently, we have shown that Foxp1/4 are essential for restricting secretory lineage differentiation and combined loss of these factors leads to a default differentiation into the goblet cell lineage. We continue to explore the role of these factors in lung development by using a combination of conditional mouse mutants along with genomic analysis to determine how Foxp1/2/4 define the lung endoderm progenitor lineage within the foregut.
Recently we have become interested in the role of chromatin remodeling complexes that regulate lung development and regeneration. We demonstrated that Foxp1/2/4, which act as potent transcriptional repressors, interact with the NuRD chromatin remodeling complex. The repressive activity mediated by Foxp1/2/4 requires histone deactylase (HDAC) activity and HDACs are an essential component of NuRD and other chromatin remodeling complexes. The role of HDACs in development, cellular physiology, and disease states is an area of active investigation in our laboratory.
Our lab has a strong ongoing interest in the role of Wnt signaling in cardiovascular development. We have shown that early Wnt/beta-catenin signaling is required for second heart field (SHF) progenitor expansion. Using a series of unique mouse genetic models we have also shown that the Wnt2 ligand is required for development of the posterior pole of the heart including the inflow tract and pulmonary veins. We have recently fate mapped Wnt2+ cells using a novel Wnt2-creERT2 mouse line and have shown that these cells can contribute to different mesenchymal and vascular lineages in the heart and lung in a temporal specific fashion. We will use the Wnt2-creERT2 mouse line along with other novel tools generated in our lab and other labs to define the importance of Wnt signaling in cardiovascular development as well as in the generation of cardiovascular cell lineages from pluripotent stem cells.