Mark Deehan, Phd Email & Phone Number

Boston, Ma, Us

Boston, Ma, Us

A newly identified mutation in the gene NACC1 causes severe neurodevelopmental delay. NACC1's function in brain remains poorly characterized and how this mutation causes the NACC1 disorder is unknown. To date I have extensively collaborated to characterize the first mouse model of the NACC1 disorder that we generated. Mice display behavioral and electrophysiological phenotypes that mimic patient phenotypes. RNA and protein quantification support synaptic dysfunction as a strong molecular signature underlying the disorder.We have generated knock-in isogenic human embryonic stem cell lines and leveraged small molecule and transcription factor based neuronal differentiations to study early developmental phenotypes that may underly the NACC1 disorder. This approach allows us to compare datasets with our mouse model to identify conserved phenotypes across models and human specific phenotypes. This work is currently being finalized into a manuscript. Additional projects include investigating the function of normal and mutant NACC1 in the brain to decipher an underlying mechanism driving postnatal phenotypes which could be targeted for therapeutic intervention.

Boston, Ma, Us

My research focused on two biological systems: (1) stem cell identification and development and (2) host innate immunity and metabolic reprogramming in response to intracellular bacterial infection. (1) Mosquito's require a blood meal to produce eggs, but this requirement drives the spread of disease making them one of the deadliest animals to humans. My research identified germline and somatic stem cells necessary to allow for unlimited egg laying capacity, which could drive repeated blood feeding. I utilized confocal and electron microscopy, antibody screening and developed in vivo and ex vivo cell tracing assays to identify and characterize stem cells and their early developmental kinetics. (2) An intracellular bacterium is required to subvert host defenses and compete for host resources to ensure survival. I discovered the cellular and molecular mechanisms by which autophagy, a host cell degradation pathway, can regulate intracellular bacteria in an opposite manner dependent on cell-type. Specifically, autophagy can target bacteria for degradation in certain cell types but provide nutrients for bacterial replication in other cell types in Drosophila melanogaster (fruit fly). Furthermore, I identified bacterial proteins which can modulate infectivity. A collaborative interdisciplinary approach including quantitative confocal microscopy, global metabolomics, molecular techniques, and genetic mutants helped elucidate the mechanisms of host-bacteria interactions.

Boston, Ma, Us

I have extensive teaching experience having taught 20 courses and approximately 600 students across both lab and discussion formats. I have aided in laboratory design to facilitate a better learning experience.

My research characterized how several different strains of the intracellular bacteria Wolbachia affects germline stem cell division and cell death of developing eggs in Drosophila melanogaster. I utilized in vivo and ex vivo culturing, confocal microscopy, and cell death assays to confirm specific strains of Wolbachia drive higher developmental cell death.

Doctor Of Philosophy (Ph.D.), Cellular And Molecular Biology

Bachelor Of Science (Bs), Biology, General