Jeffrey D. Steimle, PhD
My name is Jeff Steimle and I am postdoctoral associate in Dr. James Martin’s lab in the Department of Integrative Physiology at the Baylor College of Medicine. During my postdoc career, I have been investigating the role of the paired-like homeodomain transcription factor, PITX2, plays in the patterning of the heart and the consequences mispatterning has for human health, including the risk of developing atrial fibrillation (AF). Early work focused on the molecular and genetic roles of the pulmonary vein myocardium using new technologies such as single nuclei RNA- and ATAC-seq to interrogate both the cell autonomous and non-autonomous roles of PITX2. These efforts have led to upcoming work interrogating PITX2’s role in advanced aging and fibrosis as it contributes to atrial fibrillation manifestation as well as ongoing work investigating the epigenetic and developmental basis of PITX2 in left-right patterning for atrial fibrillation susceptibility. To this end, I have received both an NIH Postdoctoral Fellowship (F32 HL156465) and a NIH Pathway to Independence Award (K99/R00 HL169742).
Prior to my postdoc, I received my Bachelors of Science in Biological Sciences from the University of Notre Dame in 2011. There, I worked in the lab of Dr. Hope Hollocher exploring the molecular consequences of sequence variation in closely related Drosophila species that demonstrate strong clinal variation in melanin production.
After completing college, I matriculated into the University of Chicago where I completed my MS/PhD in Developmental Biology at the University of Chicago in 2019. During my training, I was mentored by and worked in the lab of Dr. Ivan Moskowitz in the Departments of Pediatrics, Pathology, and Human Genetics. There, I focused on understanding the gene regulatory networks governed by Tbx5 in the cardiopulmonary progenitors and posterior second heart field for development of the lungs and atrial septum and how that regulatory network is maintained throughout development and life in the adult lungs. Through my work, we identified a conserved Tbx5-dependent Wnt2/2b signaling event required for the formation of lungs in lunged vertebrates, which signals back to the heart for cardiac septation. This work spawned multiple collaborations, including published work examining the nuanced role of cilia for septation, variation underlying septal defects in the human population, the role Trisomy 21 plays in septal defects, and a repressive role of TBX5 in ventricular septation.
In addition to my cardiovascular development work, my graduate career also included a significant effort examining the patterning of the electrical conduction system of the heart. Prior to this work, we knew that the cardiac transcription factor, Tbx5, was critical for patterning the cardiac conduction system during development, but not how this translated to maintenance in the adult heart. To this aim, we examined the TBX5-TBX3 interactions regulating the highly specialized ventricular conduction system. This work further spawned a fruitful collaboration examining the interplay of PDGF-signaling and TBX5 in ventricular conduction. Furthermore, we examined the regulation of atrial chamber conduction in the context of atrial fibrillation regulated by FOG2, TBX5, and the interactions of these two genes.
Lastly, my graduate research made several advances in understanding epigenetic and transcriptional control during development. In particular, my work on the lineage-specifying transcription factor ETV2 during the fate decision between hematoendothelial and cardiomyogenic lineages, allowed us to resolve the molecular decisions occurring during specification, commitment, and differentiation. This work and related work involving the temporal decisions of differentiation have driven new avenues of research into the molecular decisions underlying gene regulatory networks during development.
J.D. Steimle Research 