My name is Typhanie Dumontet, I grew up in the central region of France, called ‘Berry’, between the city of Bourges and Montluçon. I did my graduate studies in cell biology, genetics and physiology at the University of Clermont-Ferrand, where I found a passion for endocrinology and the adrenal glands. I love traveling and was very excited to move to the United States in 2018, where I continued studying the adrenal glands as a post-doctoral fellow in Gary Hammer’s lab at the University of Michigan. I am particularly interested in understanding the rules that govern adrenal differentiation and I focus mainly on zone that produces the glucocorticoids. When I am not in lab, I love spending time outside, biking, hiking, skiing and swimming in the Great Lakes. I am now a research investigator and with Gary as a mentor, my long-term goal is to develop the necessary training, skills, and experience to become an independent investigator by implementing new technology and mouse models to address pathologic and therapeutic challenges of adrenal diseases.

My broad research interests are 1) Elucidating the molecular mechanisms regulating the adrenal gland differentiation and its endocrine function and 2) Combining the use of transgenic mouse models with single cell approaches to identify cell type specific disease mechanisms.
The core of my doctoral research aimed to understand the origin of adrenal lesions in Carney Complex, a rare genetic disease that affects organ homeostasis in both connective and endocrine tissues. To address this question, I engineered several mouse models of Carney Complex targeting Prkar1a, the major gene affected in human patients which encodes the PKA regulatory subunit. This work conclusively demonstrated that these adrenal lesions arise in the postnatal adrenal cortex rather than from the fetal organ. Moreover, it highlighted the role of PKA signaling in the developmental process of adrenarche – a pubertal milestone driven by the adrenal cortex but poorly understood due to the lack of available animal models. An additional work built upon these studies highlighted the role of PKA signaling in controlling the process of SUMOylation in adrenocortical cells. By combining additional mouse models, in vitro pharmacological approaches, and endocrine manipulation, our experiments ultimately led us to discover that SUMOylation patterns are altered in adrenal lesions of Carney Complex patients. These results led to two first-author publication (Dumontet et al., 2018. JCI Insight, Dumontet et al., 2019, FASEB) and the mouse models we developed will continue to provide valuable insight for translational research.
During my postdoctoral studies, I combined single cell technology and newly developed mouse models to uncover transcriptional programs participating in adrenal differentiation. I identified the homeodomain protein, HHEX, as the top enriched transcription factor in glucocorticoid-producing cells, called fasciculata cells. However, its role in adrenal homeostasis was unknown. To gain insights into HHEX contribution to adrenal function, I generated adrenal-specific Hhex knockout mouse models and observed that Hhex-deficient mice exhibited a profound glucocorticoid deficiency at baseline. By combining a series of experiment profiling Hhex DNA-binding, RNA sequencing and histology examination of Hhex-deficient adrenals, I provide evidence that HHEX orchestrates the function of the fasciculata cells to promote chronic stress adaptation and protect lipid droplet integrity in males (Dumontet et al., in preparation).