Ryan Insolera
Wayne State University, MI·Biology
Mitochondria are the compartments that generate a cell's energy, and the very work they do leaves them prone to damage. Damaged mitochondria that pile up are a shared feature of many human diseases, including metabolic and neurodegenerative conditions.
- Fields
Biology
Genetics
Neuroscience
- Topics
mitophagy
mitochondria
autophagy
- Grants
- 1 known grant, through Nov 2029
What they work on
- Engineer the genes encoding mitophagy adapter and receptor proteins in Drosophila melanogaster to create tools that can switch each known form of mitophagy on or off in a living animal.
- Determine the physiological role of ubiquitin-dependent mitophagy, in which a small protein tag marks damaged mitochondria for degradation, in maintaining fly tissue function.
- Determine the physiological role of receptor-dependent mitophagy, in which proteins on the mitochondrial surface directly recruit the degradation machinery, in fly tissues.
- Probe how the ubiquitin-dependent and receptor-dependent routes interact to maintain tissue health, building on the finding that disrupting the ataxia-associated gene Vps13D stalls mitochondria before degradation.
More about the research
Cells defend themselves with mitophagy, a cleanup process that singles out broken mitochondria and digests them. Almost everything known about mitophagy comes from cells grown in dishes, so it is unclear how its different mechanisms actually keep tissues healthy in a whole animal.
Why it matters
Buildup of damaged mitochondria is proposed to underlie aging, neurodegenerative diseases, metabolic diseases and cardiovascular disease. Establishing how the different forms of mitophagy work in an intact animal would provide the foundational knowledge needed to pursue mitophagy-targeting therapies for conditions such as Parkinson's disease, diabetes and injury from blocked and restored blood flow.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Erin Barnhart
Columbia University, NY·Neuroscience
Compare calcium signals in the cytosol and in the endoplasmic reticulum, the neuron's main calcium store, across defined Drosophila motion vision cell types, using simultaneous in vivo imaging in living flies.
Andrew Pickering
University of Texas Health Science Center at Houston, TX·Biology
Determine whether the mitochondrial uncoupling protein UCP4b, which lets mitochondria release energy as heat, is required and sufficient for cold-induced lifespan extension and redox balance in Drosophila, using genetic manipulation.
Shermali Gunawardena
University at Buffalo, NY·Neuroscience
Test whether the N-terminal region of α-synuclein, the Parkinson's-linked protein, controls how mitochondria break into smaller pieces, using transgenic Drosophila carrying N-terminal deletions.
The school
Wayne State University: 21 labs on PI Pages, $292M a year on research, 194 research doctorates a year.
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