MITOCHONDRIAL DYNAMICS IN THE INTEGRATION OF NEURONAL AND INNATE IMMUNE SIGNALING

Mitochondria are increasingly recognized as dynamic signaling platforms that integrate metabolic state, redox homeostasis, and cellular stress responses. Beyond their classical bioenergetic functions, mitochondria play a central role in innate immune signaling, acting as both sources and targets of signaling events that regulate transcriptional responses. In parallel, monoaminergic neurotransmission, particularly dopaminergic signaling, places substantial metabolic and oxidative demands on mitochondria, suggesting a mechanistic intersection between neuronal signaling pathways and mitochondrial immune functions.
In this project, we investigate a possible role of mitochondria in dopaminergic signaling and innate immune pathways in neuronal model systems. We are studying the impact of mitochondrial dynamics and function on receptor-dependent signaling cascades.
Preliminary observations indicate that both dopaminergic receptor activation and IFNα stimulation induce dynamic changes in transcription factor localization that coincide with pronounced mitochondrial repositioning toward the perinuclear region. This spatial reorganization suggests that mitochondrial mobility contributes to efficient signal propagation and transcriptional activation. Disruption of intracellular transport further implicates mitochondrial dynamics as a functional component of these signaling pathways.
Together, this work explores mitochondria as a shared signaling hub linking monoaminergic neurotransmission and innate immune activation. By integrating neuronal and immune signaling within a mitochondrial framework, the project aims to elucidate how subcellular organization and mitochondrial dynamics contribute to neuro-immune communication. Ongoing studies will further address the molecular mechanisms underlying mitochondrial involvement in innate immune signaling and its relevance to monoaminergic systems in health and disease.