Lomeli Shull
University of New Mexico, NM·Biology·Early-career
The bones of the face and jaw first form as cartilage, a template laid down by cells called chondrocytes that come from the cranial neural crest, a group of embryonic cells that migrate into the head. These cells must condense, line up, grow and mature on a precise schedule before bone replaces the cartilage.
- Fields
Biology
Genetics
Biochemistry
- Topics
craniofacial development
cartilage
chondrocytes
- Grants
- 2 known grants, through Jun 2028
What they work on
- 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.
- Test whether Prdm3 and Prdm16 control chondrocyte polarity and differentiation through Wnt/β-catenin in the mouse craniofacial skeleton, checking whether functions seen in zebrafish are conserved in mammals.
- Assess the activity of Wnt/β-catenin enhancers, DNA switch regions regulated by Prdm3 and Prdm16 and conserved across vertebrates, in the craniofacial mesenchyme.
- Analyze mouse Prdm3;Prdm16 combinatorial mutants made with Wnt1-Cre across developmental time by histology and transcriptomics, and map direct gene targets with CUT&RUN to explain loss of Meckel's cartilage in the jaw.
- Use dTAG/BromoTag degradation systems to precisely tune PRDM3 and PRDM16 protein levels in a cultured cranial neural crest model and test whether dosage refines Wnt/β-catenin activity.
More about the research
When the genes guiding this process go wrong, babies can be born with birth defects such as cleft lip or palate, an undersized lower jaw, or prematurely fused skull bones. The research asks how two chromatin modifiers, PRDM3 and PRDM16, enzymes that add chemical marks to histone proteins to switch genes on or off, control facial cartilage formation. A shared hypothesis links both projects: these factors act upstream of Wnt/β-catenin, a signaling pathway that controls cell fate, to balance chondrocyte behavior.
Why it matters
Craniofacial birth defects such as cleft lip with or without cleft palate, micrognathia (small jaw), mandibular hypoplasia and craniosynostosis affect many newborns. By showing how PRDM3 and PRDM16 levels shape cartilage through Wnt/β-catenin signaling, this work could explain how losing these factors contributes to such disorders and deepen understanding of the causes of congenital facial malformations.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Kristin Artinger
University of Minnesota, MN·Biology
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.
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 New Mexico: 27 labs on PI Pages, $355M a year on research, 182 research doctorates a year.
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