Abstract:
Escape from X chromosome inactivation allows a subset of genes on the inactive X chromosome to remain expressed. This process varies between genes, cell types, and genetic backgrounds, but the contribution of three-dimensional chromosome organization remains unclear.
We are investigating this question using female mouse neural progenitor cell clones in which the inactive X chromosome can be identified. We combine chromosome imaging with allele specific RNA measurements to compare the physical organization of the inactive and active X chromosomes and relate these measurements to gene escape behavior. Our analyses examine chromosome compaction, local chromatin organization, contacts between escape genes, spatial relationships to Xist, and variation in chromosome structure between individual cells.
This work asks whether escape genes share a common structural environment or whether escape is controlled primarily by local, gene specific mechanisms. Understanding this relationship will help clarify how chromosome architecture and gene regulation interact during X chromosome inactivation.

Bio:
Abrar Aljahani’s research aims to understand the regulatory code of the human genome. Her work focuses on the fundamental principles that link the genome's three-dimensional structure to the precise regulation of gene expression, a relationship that represents a major unsolved challenge in modern biology. During her PhD with Marieke Oudelaar at the Max Planck Institute for Multidisciplinary Sciences, she developed an ultra-high-resolution method to map enhancer-promoter interactions, revealing how fine-scale chromatin architecture controls gene regulation. As a postdoctoral fellow in Alistair Boettiger’s lab at Stanford, she now combines multiplexed super-resolution imaging, spatial transcriptomics and epigenomics with biophysical modeling to derive the general rules governing genome folding. Her ultimate goal is to construct a predictive model of the genome’s regulatory code, providing a new framework for understanding how structure dictates function in both health and disease.