Dynlacht Lab Research
In the Dynlacht Lab, researchers use multiple complementary approaches to better understand the mechanisms underlying progression through the mammalian cell cycle. In particular, we focus on transcriptional mechanisms that link gene expression with cell cycle progression. A second focus is on understanding another event linked to the cell cycle, namely, duplication of centrosomes.
Novel Approaches Toward Understanding the Epigenetic and Transcriptional Controls Governing Mammalian Differentiation
Our laboratory has dedicated more than 20 years to understanding the role of chromatin and gene expression in cell proliferation and differentiation using stem cell and breast cancer models. We use a combination of biochemical, genomic, and computational methods to dissect the epigenetic controls that govern cell cycle progression and mammalian differentiation. Using muscle differentiation as a model, we are attempting to unravel mechanisms that underlie the transition between growth and terminal differentiation. Using stem cells as muscle precursors, we are also attempting to reveal the epigenetic controls that determine whether a cell will adopt one mesodermal fate versus another.
Understanding the Biochemical Mechanisms that Underlie Centrosome Duplication and Assembly of Primary Cilia
We focus on understanding the molecular controls that promote ciliogenesis and centrosome duplication, which play a pivotal role in cell cycle progression and mitosis. The primary cilium is a key signaling organelle that plays a key role in regulating cell growth and differentiation, and defects in this structure are associated with many human diseases. Yet the switching mechanisms that convert centrosomes that organize the mitotic spindle to a primary cilium from which it is derived are not known. We are interested in understanding the proteins that regulate centrosome dynamics, structure, and function, with particular emphasis on the proteins that promote the conversion of a centriole to primary cilium, a key crossroads for cell cycle exit and differentiation. We are interested in how defects in centrosomal and ciliary proteins promote human disease.