Student Major/Year in School
Medical Biochemistry, First Year
Faculty Mentor Information
Jocelyn A. McDonald, Department of Biology, College of Arts and Sciences
Abstract
Cells can migrate collectively in tightly or loosely-associated groups during tissue and organ formation, during embryonic development, in tumor metastases, and in wound healing. Drosophilaborder cellsserve as an excellent genetic model of collective cell migration inside a developing tissue. During ovarian development, 6-8 cells form the border cell cluster and migrate together as a cohesive group to reach the large oocyte. Previous experiments have shown that Nuclear inhibitor of Protein Serine Threonine Phosphatase 1 (NiPP1) causes border cells to separate into single cells, rather than stay in a group, and limits their ability to migrate. NiPP1 inhibits the activity of the Protein Phosphatase 1 (PP1) enzyme. Therefore, overexpressing NiPP1, though a modifier screen, will allows us identify genes that work with PP1 to promote the adhesion and collective migration of border cells. To carry out this genetic screen, females expressing NiPP1 in border cells are crossed to a collection of mutant strains, called deficiencies, that remove a number of genes. Ovaries from the resulting progeny are assayed for cohesion and migration of the border cell cluster by fluorescent microscopy. In this project, larger deficiencies have been shown to suppress (“revert to wild type”), or enhance (“make worse”) the mutant phenotype. The goal is to identify the exact gene required for this suppression or enhancement, using smaller deficiency mutant strains that delete only a few genes. Such mutant deficiencies represent candidate NiPP1 modifying genes. The candidate genes will be knocked out by RNAi one by one to definitively determine the genes required for PP1 function in cell-to-cell adhesion and collective migration. Because many Drosophilagenes have human homologs, these studies of PP1 have implications for collective cell migration in humans.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License
Recommended Citation
Del Real, Carmen F.; Chen, Yujun; Komp, Marissa; and McDonald, Jocelyn A. (2019). "A Screen for Genetic Modifiers of Protein Phosphatase 1 Function in Drosophila Collective Cell Cohesion and Migration," Kansas State University Undergraduate Research Conference. https://newprairiepress.org/ksuugradresearch/2019/posters/9
A Screen for Genetic Modifiers of Protein Phosphatase 1 Function in Drosophila Collective Cell Cohesion and Migration
Cells can migrate collectively in tightly or loosely-associated groups during tissue and organ formation, during embryonic development, in tumor metastases, and in wound healing. Drosophilaborder cellsserve as an excellent genetic model of collective cell migration inside a developing tissue. During ovarian development, 6-8 cells form the border cell cluster and migrate together as a cohesive group to reach the large oocyte. Previous experiments have shown that Nuclear inhibitor of Protein Serine Threonine Phosphatase 1 (NiPP1) causes border cells to separate into single cells, rather than stay in a group, and limits their ability to migrate. NiPP1 inhibits the activity of the Protein Phosphatase 1 (PP1) enzyme. Therefore, overexpressing NiPP1, though a modifier screen, will allows us identify genes that work with PP1 to promote the adhesion and collective migration of border cells. To carry out this genetic screen, females expressing NiPP1 in border cells are crossed to a collection of mutant strains, called deficiencies, that remove a number of genes. Ovaries from the resulting progeny are assayed for cohesion and migration of the border cell cluster by fluorescent microscopy. In this project, larger deficiencies have been shown to suppress (“revert to wild type”), or enhance (“make worse”) the mutant phenotype. The goal is to identify the exact gene required for this suppression or enhancement, using smaller deficiency mutant strains that delete only a few genes. Such mutant deficiencies represent candidate NiPP1 modifying genes. The candidate genes will be knocked out by RNAi one by one to definitively determine the genes required for PP1 function in cell-to-cell adhesion and collective migration. Because many Drosophilagenes have human homologs, these studies of PP1 have implications for collective cell migration in humans.
