Piya Ghose
University of Texas at Arlington, TX·Biology
Cells die on purpose throughout normal development, and the debris must be cleared promptly. Faulty programmed cell death is linked to cancer therapy resistance.
- Fields
Biology
Genetics
Neuroscience
- Topics
programmed cell death
apoptosis
cell clearance
- Grants
- 1 known grant, through May 2027
What they work on
- Determine how mitochondrial trafficking, the transport of the cell's energy-producing organelles, influences elimination of cell processes during Compartmentalized Cell Elimination of the C. elegans tail-spike cell.
- Identify new genes that govern Compartmentalized Cell Elimination of the tail-spike cell, including compartment-specific killing and clearance, using genetic and cell biological analysis in living worms.
- Identify new genes that regulate Compartmentalized Cell Elimination in other complex cells, such as a set of sex-specific neurons in C. elegans.
More about the research
Poor clearance of dead cells can lead to inflammation and autoimmune disease. Most textbook models of cell death treat the cell as a simple unit. Many real cells, however, are elaborately shaped, and their different parts sit in very different surroundings. Some cells die as a whole, while others lose only certain extensions. Neurons, for example, prune branches to wire the brain correctly. The central question here is how such morphologically complex cells are taken apart.
Why it matters
Programmed cell death and debris clearance go wrong in cancer, neurodegeneration, autoimmune and developmental disorders. Identifying new genes that control how complex cells and neuron branches are dismantled could reveal targets for therapies against tumor formation and immune dysfunction. It could also help explain brain development, injury and disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Chenshu Liu
Lehigh University, PA·Genetics
Determine how the force-sensing ion channel Piezo works at the oocyte nuclear envelope to relay a signal that triggers cell death after synapsis fails in the C. elegans germline.
E. Jane Hubbard
New York University, NY·Biology
Identify the molecular mechanisms by which insulin/IGF-like signaling acts from other tissues to drive age-related decline of the one-cell germline stem cell niche in C. elegans.
Jennifer Watts
Washington State University, WA·Genetics
Identify genes and pathways that control ferroptosis triggered by dietary polyunsaturated fatty acids in C. elegans germ cells, using genetic, dietary and biochemical approaches.
The school
University of Texas at Arlington: 11 labs on PI Pages, $154M a year on research, 177 research doctorates a year.
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