PIPages
Labs

Xin Jie Chen

Upstate Medical University, NY·Biology

Two compartments inside cells tend to fail together in aging and in diseases such as Parkinson's disease and amyotrophic lateral sclerosis (ALS). Mitochondria are the cell's power plants, and they also help control stress responses and cell death.

Fields

Biology

Biochemistry

Genetics

Topics

mitochondria

lysosome

vacuole

Grants
1 known grant, through Apr 2028

What they work on

  1. Test in yeast whether specific mitochondrial stresses cause severe protein-handling damage to the vacuole, the yeast lysosome. Use genetic screens to find genes that suppress this signaling and may extend lifespan.
  2. Validate the mitochondria-to-lysosome stress pathway in cultured mammalian cells. Determine whether mitochondrial precursor overaccumulation stress (mPOS) also damages lysosomes in these cells.
  3. Test whether mitochondrial stress damages lysosomes and disrupts tissue health in a newly developed mouse model. Determine how this damage arises in non-dividing tissues.

More about the research

Lysosomes are the cell's recycling centers; in yeast the equivalent is called the vacuole. They break down proteins, control acidity and nutrient levels, and carry out autophagy (self-digestion of worn-out parts). This project asks whether mitochondrial damage directly harms lysosomes, and whether this chain of events weakens and kills aging cells.

Why it matters

Mitochondrial and lysosomal defects are both hallmarks of aging and of diseases such as Parkinson's disease and ALS. Uncovering a stress signal running from mitochondria to lysosomes could explain why cells die when both organelles fail. This basic understanding could eventually inform how researchers study and target aging-associated degenerative diseases.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

A novel mitochondria-to-lysosome stress signaling pathway in degenerative disease and aging

NIH · Aug 2023 – Apr 2028

Closest labs

John Buchan

University of Arizona, AZ·Biochemistry

Define how much each reported clearance route contributes to removing stress granules and P-bodies under disease-relevant stress, and how the routes cooperate. Use genetic, biochemical and cell biology assays in yeast and human cells.

Jeroen Roelofs

University of Kansas, KS·Biochemistry

Determine how proteasome-associated assembly factors, including Pba1-Pba2/PAC1-PAC2, Fub1/PI31, and Blm10/PA200, contribute to sequential versus parallel pathways during the early assembly of new proteasome complexes.

Jingjing Liang

University of Arizona, AZ·Neuroscience

Test how Aggregatin, a protein encoded by the Alzheimer's-linked gene FAM222A, controls TDP-43 clumping and toxicity in neurons, using Aggregatin knockout models.

The school

Upstate Medical University: 7 labs on PI Pages, $59M a year on research, 23 research doctorates a year.

More about Upstate Medical University

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