Jamy Peng Lab

Of all the different types of mechanisms that regulate chromatin structure, we concentrate on the modification of histone H3. This histone protein has a twenty-seventh residue, lysine (K), that can be methylated or acetylated. Our interest in H3K27 arises from the fact that, in pediatric cancers (blood, bone, brain, etc.), all the enzymes that modify H3K27 are either mutated or dysfunctional. 

To analyze the normal and diseased functions of these H3K27 modifiers, we try to identify new factors and potential regulators. We study how these new factors control the stem cell models to grow or give rise to specialized neuronal cells. New knowledge from these studies enables us to uncover molecular mechanisms that regulate H3K27 modifications, chromatin structure, as well as gene expression and stem cell behavior.

In our examination of the factors that interact with H3K27 modifiers, we find these factors regulate neural stem cell growth, survival, and differentiation. Without these factors, we characterize the brain to undergo massive cell death or excessive cell proliferation to the point that the cells do not differentiate. As we try to expand our understanding of these factors, we strive to define a pathway from transcription circuitry and signaling pathways to intrinsic mechanisms that alter chromatin structure, gene expression, and stem cell behaviors. To this end, we use increasingly advanced techniques—imaging, deep sequencing, and data analysis—to profile the effects of stem cell behavior on normal and disease development in brain organoids and pediatric cancer models.