515 Delaware Street SE
Minneapolis, MN 55455
Neural crest cells are transient migratory stem cells in vertebrate embryos that give rise to cell types as diverse as facial bones, heart muscle, and neurons. The Gammill lab combines genetics, cell biology, and proteomics using chicken embryos to study the post-translational regulation of neural crest cell formation and migration. In addition to phosphorylation and extracellular vesicles, we have implicated multiple methyltransferases in neural crest development and are currently characterizing the role of their non-histone targets in migratory neural crest cells.
Once an egg is fertilized, that single cell must divide repeatedly to become the myriad cell types that are properly positioned in a complex, multicellular organism. One way that cells arrange themselves in the developing embryo is by moving. The vertebrate neural crest is a striking example of developmental cell migration. Neural crest cells arise in the future brain and spinal cord, but become disconnected from their neighbors and migrate over long distances throughout the embryo to form surprisingly diverse derivatives, including the peripheral nervous system, outflow tract of the heart, and craniofacial skeleton. How do neural crest cells become different from their neighbors and migrate? How do they know where to go? The Gammill lab uses chick and mouse embryos to elucidate molecular mechanisms regulating neural crest cell formation, migration, and guidance. We combine embryological (explants, primary neural crest cell cultures) and molecular manipulations (electroporation of gain and loss of function reagents) of chick embryonic development with genomic analysis (ChIPseq and RNAseq) and proteomics (arrays, metabolic labelling, mass spectrometry), while relying on mouse mutants for robust genetic functional analyses. This combination of organisms and techniques allows us to integrate the advantages of each system toward a clearer understanding of early neural crest development.
Gustafson CM, Roffers-Agarwal J, Gammill LS (2022). Chick cranial neural crest cells release extracellular vesicles that are critical for their migration. J Cell Sci. 135(12):jcs260272.
Roffers-Agarwal J, Lidberg KA, Gammill LS (2021). The lysine methyltransferase SETD2 is a dynamically expressed regulator of early neural crest development. Genesis 59(10):e23448.
Jacques-Fricke BT, Roffers-Agarwal J, Hussein AO, Yoder KJ, Gearhart MD, Gammill LS (2021). Profiling NSD3-dependent neural crest gene expression reveals known and novel candidate regulatory factors. Dev Biol. 475:118-130.
Gammill, L., Cox, T., Moody, S., Taneyhill, L., Trainor, P., Marcucio, R. (2018) The Society for Craniofacial Genetics and Developmental Biology 40th Annual Meeting. Am. J. Med. Genet. A 176(5):1270-1273.
Fairchild, C.A., Conway, J.A., Schiffmacher, A., Taneyhill, L.A. and Gammill, L.S. (2014) FoxD3 regulates cranial neural crest EMT via downregulation of Tetraspanin18 independent of its functions during neural crest formation. Mech. Dev. 132:1-12.
Vermillion, K.A., Lidberg, K.A. and Gammill, L.S. (2014) Expression of actin binding proteins and requirement for actin depolymerizing factor in chick neural crest cells. Dev. Dyn. 243(5):730-8.
Vermillion, K.A., Lidberg, K.A. and Gammill, L.S. (2014) Cytoplasmic protein methylation regulates neural crest migration. J. Cell Biol. 204:95-109. Fairchild, C.A. and Gammill, L.S. (2013). Tetraspanin18 is a FoxD3-responsive antagonist of cranial neural crest epithelial to mesenchymal transition that maintains Cadherin6B protein. J. Cell Sci. 126:1464-76.
Jacques-Fricke, B.T., Roffers-Agarwal, J. and Gammill, L.S. (2012). DNA methyltransferase 3b is dispensable for mouse neural crest development. PLOS One 7(10):e47794.
Roffers-Agarwal, J., Hutt, K.J. and Gammill, L.S. (2012). Paladin is an antiphosphatase that regulates neural crest cell formation and migration. Dev. Biol. 371(2):180-90.
Kulesa PM, Gammill LS. (2010) Neural crest migration: patterns, phases and signals. Dev Biol. 344(2):566-8.