Dionna Kasper
Dartmouth College, NH·Biology
How does a cell decide what kind of cell to become? Getting this choice wrong can disrupt tissue formation and lead to disease.
- Fields
Biology
Genetics
Biochemistry
- Topics
glycosylation
glycans
glycoproteins
- Grants
- 1 known grant, through Jul 2029
What they work on
- Test how five N-glycoproteins control the transformation of arterial endothelial cells into hematopoietic stem/progenitor cells, using loss-of-function zebrafish and live imaging of transparent embryos.
- Determine whether sugar attachment itself is required for these proteins' fate-setting roles by creating missense mutations that block glycan attachment at specific glycosylation sites.
- Identify the glycosylation enzymes and glycan repertoire needed for vein endothelial cells to become lymphatic progenitors, using a cell fate mutant, genetics and glycomic profiling.
- Compare glycosylation in the two fate decisions to separate universal from cell-specific rules by which glycan composition sets endothelial cell identity.
More about the research
Knowing the rules could also help scientists make specific cell types to repair damaged tissues. Earlier work by the PI identified glycosylation, the attachment of sugar chains (glycans) to proteins, as an unexplored regulator of cell fate. The lab uses endothelial cells, which line blood and lymph vessels and can change identity, to learn how sugar tags shape a cell's identity.
Why it matters
Learning how sugar tags on proteins direct cell identity could reveal general rules for how cells become arteries, veins, lymphatic vessels or blood stem cells. That knowledge could eventually inform glycoengineering approaches, which alter these sugar tags, to reprogram cells and produce clinically useful cell types for repairing damaged or diseased tissues.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Pamela Wenzel
University of Texas Health Science Center at Houston, TX·Biology
Test how interrupting mitochondrial maturation affects commitment of hemogenic endothelium (blood-forming vessel cells) to blood fate, using drugs, in vitro vessel-mimicking platforms and cardiac mutant mice.
Teresa V Bowman
Albert Einstein College of Medicine, NY·Genetics
Test whether DDX41 insufficiency cooperates with age-associated activity of cGAS, an inflammation-triggering DNA sensor, to impair blood stem and progenitor cells in germline ddx41 heterozygous zebrafish that develop MDS-like disease.
Nancy Speck
University of Pennsylvania, PA·Biology
Determine which components of the TGFβ/BMP signaling pathways must be inhibited, and at what time, to improve maturation of SMAD7-deficient pre-HSCs into HSCs, using a quantitative ex vivo culture system with mouse embryo cells.
The school
Dartmouth College: 16 labs on PI Pages, $418M a year on research, 104 research doctorates a year.
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