Benjamin L. Emert

The paper shows that gene proximity to nuclear speckles increases spliceosome binding and co-transcriptional splicing efficiency, highlighting the role of 3D genome organization in mRNA splicing.

The paper identifies molecular factors that mark pluripotency potential in rare somatic cells by analyzing fibroblast reprogramming efficiency.

The paper develops a method to quantify gene expression memory and identify regulators of cell state transitions, showing that modulating PI3K and TGF-β pathways can reduce drug resistance in melanoma.

The paper shows that dimerization networks can perform diverse computations with varying inputs and are versatile across cell types, especially when large enough.

The paper investigates cell type determination during cardiac differentiation of hiPS cells, finding that cell type specification begins shortly after seeding and is cell-autonomous.

The paper shows that resistant fates in cancer cells are predetermined by intrinsic molecular differences, not microenvironmental factors, and can be influenced by drug type and dose.

The paper analyzes how gene transcription responds to two signals in human cells, finding that combined responses are mostly additive or multiplicative, with some associations between chromatin accessibility and transcriptional outcomes.

The paper introduces MemorySeq, a method to identify gene expression fluctuations persisting across cell divisions, revealing non-genetic, heritable cellular behaviors in cancer cell lines.

The paper shows that transcriptional bursting in gene networks can produce rare coordinated high expression states in cancer cells, which are linked to drug resistance.

The paper identifies rare cell states in melanoma that contribute to drug resistance by analyzing single-cell gene expression and signaling dynamics.