Assistant Professor and Cluster Coordinator
Department: Biological Sciences; Biochemistry and Microbiology
Research Cluster: Neuroscience and Developmental Biology
Office: Science Building 361-B
Phone: (304) 696-6111 or 4673 | Fax: (304) 696-7136
Personal website: http://www.science.marshall.edu/collierp/
Genetic control of cell polarity in development and disease
The Collier lab uses both invertebrate (Drosophila) and vertebrate (cell culture) model systems to investigate the importance of planar cell polarity in development and disease. Planar cell polarity (PCP) refers to the orientation of a cell within the plane of an epithelial cell layer, and the precise control of PCP during development is critical for normal tissue function. For example, loss of normal PCP disrupts neural tube closure in vertebrates and is responsible for cases of familial spina bifida in humans.
Research in the Collier lab focuses upon how epithelial cells become polarized, and what signals determine the direction of cell polarity within a tissue. Projects in the lab involve a wide range of molecular (protein, DNA, RNA), cellular and genetic (Drosophila) techniques, and also employ a variety of imaging techniques including confocal and electron microscopy.
- Directional control of Planar Cell Polarity by Prickle protein variants. Mutations in the human Prickle1 gene cause progressive myoclonus epilepsy-ataxia syndrome, an inherited form of epilepsy. Drosophila prickle gene mutations also cause seizures, implying that prickle function is conserved between vertebrates and invertebrates. The Prickle gene product is required for normal PCP, and the Collier lab has shown that the direction of PCP in Drosophila depends upon which variant (isoform) of the Prickle protein is active within the tissue. This project aims to characterize the activities of the different Prickle protein isoforms using molecular and genetic approaches.
- Function of the PCP Effector proteins Fritz and Fuzzy. The PCP Effector proteins, Fritz and Fuzzy, were first identified in the Collier lab, and are required for normal PCP in both vertebrates and invertebrates. In vertebrates, Fritz and Fuzzy control cilia formation, and mutations in the human fritz gene are associated with the ciliopathic diseases, Meckel-Gruber syndrome and Bardet-Biedl syndrome. This project aims to further characterize the activity of the human Fritz and Fuzzy proteins using Drosophila and vertebrate cell culture systems.
Neff D, Hogan J, Collier S (2012) Cuticle Refraction Microscopy (CRM); a rapid and simple method for imaging Drosophila wing topography, an alternative readout of wing Planar Cell Polarity. Methods in Molecular Biology; 839:43-52.
Hogan J, Valentine M, Cox C, Doyle K, Collier S (2011) Two Frizzled planar cell polarity signals in the Drosophila wing are differentially organized by the Fat/Dachsous pathway. PLoS Genet. Feb;7(2):e1001305.
Valentine M, Collier S (2011) Extra View: Planar Cell Polarity and Tissue Design. Fly (Austin) 5(4).
Hirano M, Neff D and Collier S (2009) Cell shape and epithelial patterning in the Drosophila embryonic epidermis. Fly (Austin) 3(3).
Doyle K, Hogan J, Lester M, and Collier S (2008) The Frizzled Planar Cell Polarity signaling pathway controls Drosophila wing topography. Developmental Biology 317(1): 354-67.