Lab Team

For Miriam's major project she has been using murine embryonic stem cell directed differentiation toward endoderm and mesoderm lineages to reveal a crucial role of GATA6 during anterior primitive streak-derived progenitor segregation. GATA6 is known to direct by default extra-embryonic endoderm. To promote definitive endoderm fate, she found that GATA6 reinforces the endoderm GRN driven by NODAL while repressing the mesoderm GRN through down-regulation of WNT activity. During progression of mesoderm differentiation, GATA6 induces a switch in the transcriptional output regulated by WNT, promoting lateral mesoderm specification and repression of paraxial mesoderm fate. Thus, this single transcription factor mediates formation of four distinct tissue types, depending on integration of NODAL/WNT activities. 

Romulo directs a research team affiliated with the Evans laboratory. The long-term goal of his research is to better understand the normal and pathological physiology of involuntary muscles. A major emphasis of his research has been elucidating the intrinsic pacemaker mechanisms that trigger rhythmic smooth muscle contractions. He uses the upper urinary tract as a model system, where peristaltic contractions propel fluid away from the kidney. Defects in this process are common and associated with high clinical morbidity. As part of this broader work, his research has also included the development of new technological approaches for studying intact-organ physiology and three-dimensional visualization of tissue architecture.

Rebecca's PhD project seeks to understand how QSER1 and TET1 regulate epigenomic remodeling during cardiac lineage specification from human pluripotent stem cells, with the overarching goal of identifying fundamental epigenetic mechanisms underlying heart development.

Fangfang's major project uses human cardiods and is based on the hypothesis that GATA4 orchestrates human cardiac chamber morphogenesis by directing a coordinated transcriptional program across CM and epicardial lineages, maintaining CM identity and ECM homeostasis while sustaining the paracrine signaling and epithelial-to-mesenchymal transition (EMT) competence required for outer myocardial compaction.