Haley Fortin, BS, MB(ASCP)

Genetic variation between individuals in a population promotes distinct physical, behavioral, and molecular phenotypes. The molecular mechanisms by which genetic variation allows for differences in regulation of gene expression, remain poorly understood. Previous work from the Baker laboratory demonstrated genetic variation in mouse embryonic stem cells (mESCs), from C57BL/6J (B6) and DBA/2J (D2), impacts cell state transitions through chromatin regulation. Quantitative trait locus (QTL) mapping identified several trans-acting loci that co-regulate chromatin accessibility and gene expression. Currently, the role trans-regulation has on three-dimensional (3D) interactions as a mediator of this coordinated regulation is unknown. By leveraging the power of molecular techniques and genomics alongside genetically diverse biological samples, I am investigating how trans-regulation of chromatin impacts 3D interactions in development. Furthermore, I will expand on these observations to gain novel insight into understanding whether repressive factors, like KZFPs, can alter 3D genome contacts, how 3D interactions are regulated in trans, and the relationship between chromatin accessibility and 3D contacts.

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Haley Fortin on ORCID