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Roger Pauley. Earl Mack. Sonny Prince. This high-density assembly at super-enhancers was found to exhibit sharp transitions of formation and dissolution, forming as the consequence of a single nucleation event and collapsing when concentrated factors are depleted from chromatin or when nucleation sites are deleted.
These properties of super-enhancers led to our proposal that the high-density assembly of biomolecules at active super-enhancers is due to phase separation of enriched factors at these genetic elements Hnisz et al.
We recently provided experimental evidence that super-enhancers and their components do form phase-separated condensates Sabari et al. Our current studies focus on the mechanisms that have evolved to regulate the behaviors of these nuclear condensates.
Whyte, W. Master transcription factors and mediator establish super-enhancers at key cell identity genes. Hnisz, D.
A phase separation model for transcriptional control. Sabari, B. Coactivator condensation at super-enhancers links phase separation and gene control.
Boija, A. H, Taatjes, D. Transcription factors activate genes through the phase separation capacity of their activation domains.
Cell Guo, Y. K, Zamudio, A. I, Sharp, P. Pol II phosphorylation regulates a switch between transcriptional and splicing condensates. Nature Our studies of super-enhancers and their associated biomolecular condensates have led to new approaches to anti-cancer drugs.
These oncogenic super-enhancers can encompass exceptionally large domains, sometimes spanning more than kb, and are highly vulnerable to transcriptional inhibitors that target BRD4 and CDK7.
Normal cells appear to be relatively insensitive to inhibitors that target BRD4 and CDK7, suggesting that transcriptional inhibitors of this type may be useful for cancer therapy Bradner et al.
The vulnerability of large oncogenic super-enhancers may be due to the selective concentration of drugs in super-enhancer condensates at oncogenes Klein et al.
We are now investigating how specific functional groups in small molecules provide drugs with the ability to concentrate within specific compartments in cells.
Selective inhibition of tumor oncogenes by disruption of super-enhancers. Kwiatkowski, N. Targeting transcription regulation in cancer with a covalent CDK7 inhibitor.
Bradner, J. Transcriptional addiction in cancer. Klein, I. Partitioning of cancer therapeutics in nuclear condensates. Science — PMID: Postdocs Isaac Klein and Ann Boija discuss their discovery that cancer therapeutics selectively partition in nuclear condensates.
Our studies have revealed roles for specific chromosome structures in regulation of gene expression in healthy cells and in cancer.
We found that DNA loops between the enhancers and core promoters of active genes are formed and maintained by Mediator and cohesin in mammalian cells Kagey et al.
In cancer, disruption of these regulatory chromosome structures occurs at driver oncogenes and contributes to their dysregulation Hnisz et al. We also discovered that the transcription factor YY1 contributes to enhancer-promoter interactions by forming multimers analogous to the CTCF-CTCF interactions that contribute to chromosome neighborhoods Weintraub et al.
These studies provide a foundation for our current studies of the relationships between chromosome structure and gene control in development and disease.
Kagey, M. J, Bilodeau, S. Mediator and cohesin connect gene expression and chromatin architecture. Dowen, J. Control of cell identity genes occurs in insulated neighborhoods in mammalian chromosomes.
S, Day, D. P, Sigova, A. Activation of proto-oncogenes by disruption of chromosome neighborhoods. Weintraub, A. YY1 is a structural regulator of enhancer-promoter loops.
MeCP2 methyl CpG binding protein 2 is a key component of constitutive heterochromatin, which plays important roles in chromosome maintenance and transcriptional silencing.
Mutations in MeCP2 cause Rett syndrome RTT , a postnatal progressive neurodevelopmental disorder associated with severe mental disability and autism-like symptoms that manifests in girls during early childhood.
We found that MeCP2 is a dynamic component of heterochromatin condensates in cells and that both its DNA-binding domain and its C-terminal intrinsically disordered domain contribute to condensate formation Li et al.
MeCP2 manifests physicochemical properties that selectively concentrate heterochromatin cofactors compared to components of transcriptionally active condensates, and when altered by RTT-causing mutations, is disrupted in its ability to form condensates.
We are now studying the properties of nuclear condensate-promoting proteins such as MeCP2 to determine if their physicochemical properties contribute to the separation of euchromatic and heterochromatic condensates, and thereby ensure transcriptional silencing of heterochromatin.
Li, C. MeCP2 links heterochromatin condensates and neurodevelopmental disease. We are scientists with diverse backgrounds and affiliations that bring rich experience to our laboratory and community.
Our collective training is in basic biology, chemistry, physics, computing and medicine. We strive to contribute to our community and advance a new generation of scientific leaders.
Victoria is a senior neurosurgery resident physician at MGH. She is currently performing a research fellowship in the Young lab characterizing the epigenomic drivers of meningioma formation, with the goal of identifying novel medical treatments for patients with brain tumors.
My goal is to identify altered nuclear condensate properties in disease, including cancer and type 2 diabetes. I am a cellular and molecular biologist with an emphasis on human genetics, gene regulation, and the genetic basis of human disease.
My current research goals are to identify the master gene regulatory pathways that control human glial cell identity and state, and to use this information to produce superior stem cell-based models of human glia to study neurodegenerative disease.
I am a stem cell and molecular biologist exploring how RNA regulates biomolecular condensates and gene expression in both native and disease states.
I am interested in quantifying the chemical features and properties underlying the complex thermodynamic and kinetic phenomenon of condensate molecular grammar.
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