Kristin Artinger
University of Minnesota, MN·Biology
Early in the embryo, a group of cells called the neural crest leaves its birthplace near the developing spinal cord. These cells travel through the body and turn into many different tissues, including the bones and cartilage of the face.
- Fields
Biology
Genetics
- Topics
neural crest
cell migration
mRNA localization
- Grants
- 2 known grants, through Jun 2027
What they work on
- Identify the RNAs and proteins concentrated in the thin protrusions of migrating neural crest cells, by profiling their transcriptome and proteome, and test whether these molecules are required for directed cell movement.
- Test whether "zipcode" sequences in the untranslated regions (UTRs) of protrusion-enriched mRNAs, the non-coding ends of these gene messages, are needed to deliver the RNAs to protrusions and for normal neural crest migration.
- Test whether PRDM proteins, a family of gene-regulating factors, act inside cranial neural crest cells upstream of Wnt signaling to control when these cells become cartilage-forming chondrocytes.
- Determine whether the related regulators Prdm3 and Prdm16 genetically interact to control gene expression and chromatin accessibility at neural crest and Wnt target genes.
- Test whether loss of Prdm3 changes where Prdm16 binds across the genome, altering chromatin state at progenitor genes and the timing of cartilage differentiation.
More about the research
When they move to the wrong place or mature at the wrong time, babies can be born with conditions such as cleft lip and palate, Treacher-Collins syndrome, DiGeorge syndrome or Hirschsprung's disease. This research asks two linked questions. How do neural crest cells (NCCs) find their way? And once they arrive, what controls when they become cartilage and bone?
Why it matters
Many common birth defects of the face and head, including cleft lip with or without palate, Treacher-Collins syndrome, DiGeorge syndrome and Hirschsprung's disease, arise when neural crest cells migrate or mature abnormally. Knowing how these cells are guided and timed could help explain why such defects occur. It may also help explain why people with the same genetic change can be affected differently. That knowledge could provide a foundation for future treatment strategies. The work on cell migration may also inform how cancer cells spread.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Lomeli Shull
University of New Mexico, NM·Biology·Early-career
Define how Prdm3 and Prdm16 regulate Wnt/β-catenin signaling, a pathway that steers cell fate, in cartilage cells during zebrafish craniofacial development using molecular, genetic and epigenetic tools.
Soma Dash
University at Albany, NY·Genetics·Early-career
Identify the mechanism behind craniofacial defects in mice lacking Med23, a Mediator complex subunit, in neural crest cells, by analyzing transcriptomic changes and mapping Med23's DNA and protein binding partners.
Mark Grimes
University of Montana, MT·Biomedical Engineering
Test whether seeding human neural crest stem cells in 3D hydrogel scaffolds with extracellular matrix components identified in organoids makes craniofacial cartilage faster and more reproducibly than self-organizing organoids.
The school
University of Minnesota: 88 labs on PI Pages, $1.4B a year on research, 722 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.