This thesis examines how octopuses respond to climate change at a molecular level, focusing on ocean acidification and RNA editing. Rising temperatures harm octopus reproduction, growth, and survival, while acidification produces mixed effects—some species show stress, yet others demonstrate resilience. Cephalopods overall appear more tolerant of acidification than fish, raising questions about the mechanisms behind this adaptability. Thousands of acidification-responsive edits disproportionately affect C2H2 zinc finger regulators, altering predicted binding targets, including nuclear pore components implicated in stress responses.

This research investigates HMGN proteins, which organize the genome and help cells access the correct genes. By mapping their activity and removing them with CRISPR, the study shows that HMGNs act as DNA “librarians.” Their dysfunction leads to gene misregulation linked to many diseases.

Pain-sensing neurons require the gene PRDM12 not only to develop, but also to maintain their identity in adulthood. Removing PRDM12 causes neurons to express mixed identities, disrupting function. Understanding how neuron identity is preserved may enable regeneration of pain-sensing neurons and lead to new, non-addictive pain treatments.

Cleft lip formation may result from broken DNA enhancers—switches that control facial development genes. Scanning the genomes of 130 African children with clefts, this research identified harmful enhancer variants and confirmed their effects in mouse models. The disrupted enhancer likely regulates BMP2, offering new insight into cleft biology and future prevention.