Description and purpose
The project analyzed bulk RNA-seq and ChIP-seq data from murine liver organoids treated with oleic acid to model non-alcoholic fatty liver disease (NAFLD), aiming to assess how nuclear compression affects nuclear mechanics and chromatin regulation.
Purpose
To evaluate transcriptomic and chromatin alterations induced by oleic acid, identifying biological processes, signaling pathways, and molecular regulators linked to NAFLD and nuclear mechanics.
Expected results
Activation of NAFLD-associated genes and pathways, validation of oleic acid-treated organoids as a relevant disease model, detection of potential changes in H3K9me3 profiles reflecting chromatin remodeling between conditions, and insights into molecular mechanisms driving nuclear alterations.
Achieved results
Bulk RNA-seq analysis with specific tools revealed enrichment in nuclear and chromatin-related processes, in addition to metabolic genes. Pathway and upstream regulator analysis validated the organoid model. Comparison with public datasets confirmed NAFLD disease features. ChIP-seq analysis of H3K9me3 showed no major differences between conditions, suggesting stable levels, but further work is needed to investigate possible histone mark changes at transposable elements.
