Yi Kuang

A Drosophila Su(H) Model of Adams-Oliver Syndrome Reveals Notch Cofactor Titration as a Mechanism Underlying Developmental Defects

This study uses a Drosophila Su(H) model to show that AOS-linked RBPJ variants cause developmental defects by sequestering Notch cofactors, leading to dysregulated target gene expression.

Enhancers with cooperative Notch binding sites are more resistant to regulation by the Hairless co-repressor

The paper shows that enhancers with SPS sites are more resistant to repression by Hairless co-repressor compared to those with CSL sites.

Enhancer architecture sensitizes cell specific responses to Notch gene dose via a bind and discard mechanism

The paper shows that an enhancer with specific binding sites can induce Notch haploinsufficiency phenotypes in Drosophila with wild-type Notch gene dose by promoting rapid Notch turnover through a bind and discard mechanism.

Exposure to Mites Sensitizes Intestinal Stem Cell Maintenance, Splenic Marginal Zone B Cell Homeostasis, And Heart Development to Notch Dosage and Cooperativity.

This study shows that Notch dimerization is critical for intestinal homeostasis and immune responses, with mite infestation worsening related phenotypes and triggering lymphoma in mutant mice.