Neuroendocrine Coordination of Mitochondrial Stress Signaling and Proteostasis
Description: PROJECT NARRATIVE Our fundamental direction as a research team remain the same in striving to uncover the basic mechanisms that drive neuroendocrine stress signaling of mitochondria. With our current understanding, we propose to extend our findings of non-autonomous signaling into other neural populations. This proposal ties all of what we have previously identified together into a proposal aiming to understand the communication between specific neural subtypes (various neuronal and glial subtypes) and mapping the complex circuitry involved in mitochondrial stress signaling. Moreover, we will directly test both the impact of changes to chromatin state that 1) directly impact the ability of neurons and glia to elicit a signal, and 2) impact how distal tissue can properly receive – and respond – to the mitochondrial stress signals from neural cells. Finally, we will address how these widespread changes to chromatin architecture downstream of neural signals directly impact organelle physiology (mitochondrial form and function, including import capacity), and how these factors all coalesce to drive organismal homeostasis and lifespan extension.
Funding type: research
Funder scheme: R01
Start date: 2012-03-01
End date: 2026-08-31
Investigator: ANDREW G DILLIN
Institution: UNIVERSITY OF CALIFORNIA BERKELEY
Subfield: Molecular Biology
Domain: Life Sciences
Funded outputs count: 38
Funder award ID: R01ES021667
OpenAlex ID: G8387104455