ENOK
Our genome wide RNAi screen identified Enok as a trithorax group regulator, extending the set of factors involved in keeping target genes active.
Read the research ↗How are cell fates established, maintained, and changed?
Every cell in an organism shares the same genome, yet a neuron is fundamentally different from a muscle cell. How do cells establish and maintain these distinct identities?
The answer lies in epigenetic cell memory, a crucial mechanism ensuring cells "remember" who they are across successive divisions. This cellular identity relies on inheriting specific gene expression patterns, which are tightly regulated by two evolutionarily conserved protein families: the Polycomb group (PcG) for gene repression, and the trithorax group (trxG) for gene activation. Our lab investigates how these opposing systems preserve transcriptional memory throughout development.
Utilizing Drosophila melanogaster, alongside cell-based reporter assays, functional genomics, and molecular genetics, we aim to identify the core factors shaping this memory and explore how cell signaling pathways modulate them.
How do trxG proteins and their partners keep developmental genes active through successive cell divisions?
How do PcG and trxG systems interact and prevent each other from maintaining activation or repression, respectively?
Which cell signaling pathways modulate the chromatin regulators that maintain cell fate?
The genesis of this research traces back to 2011, when our first BS senior project student, Zain Umer, and our first postdoctoral fellow, Dr. Saima Anwar, successfully developed a novel cell-based reporter for PcG and trxG proteins. Utilizing this foundational system, we subsequently conducted robust ex vivo kinome-wide and genome-wide RNAi screens in the lab of Prof. Dr. Michael Boutros at DKFZ, Heidelberg. Ongoing follow-up studies on the identified candidates have since established their critical roles in epigenetic gene regulation.
Our genome wide RNAi screen identified Enok as a trithorax group regulator, extending the set of factors involved in keeping target genes active.
Read the research ↗A kinome wide screen identified Ballchen as a factor in trxG mediated gene activation. Later work connected BALL and CBP to H3K27 acetylation at active genes.
Read the research ↗Research on the chaperonin subunit CCT7 revealed an interaction with Polycomb that contributes to the maintenance of gene silencing in flies.
Read the research ↗Mask exhibits trxG like behavior and associates with H3K27ac marked chromatin, pointing to a link between gene activation and a protein also known for signaling roles.
Read the research ↗