Faithful inheritance of chromatin states is essential for preserving gene expression patterns and genome integrity. I am interested in understanding the molecular mechanisms of how chromatin maintains its epigenetic information during essential biological processes, including chromosomal duplication, transcription, and other large-scale chromatin remodeling events.

My Ph.D. thesis work uncovered a novel function of replication checkpoint factor Mrc1/CLASPIN in epigenetic inheritance by distributing parental histones to both daughter DNA strands. Mechanistically, Mrc1/CLASPIN contains a conserved histone H3-H4 tetramer binding domain that anchors at the center of the replication fork. Together with other replisome-associated histone chaperones, his thesis work suggests that the replisome contains multiple intermediate sites for parental histone recycling. (Yu et al., PMID: 39094570, 2024).

Adult stem cells undergo asymmetric cell division to generate a self-renewing stem cell and a differentiating cell. A fundamental unsolved question is how two daughter cells can adopt distinct cell fates during this process.

During asymmetric divisions of the Drosophila male germline stem cell, sister chromatids undergo non-random segregation. This observation suggests that two genetically identical sister chromatids are created differently, potentially priming for cell fate decisions. However, it remains unclear how the differences between sister chromatids are established and recognized by germline stem cells. My postdoc work aims to understand the molecular basis underlying non-random sister chromatid segregation (NRSS) and its role in cell fate specification and differentiation.