We hypothesize that Miwi2 inhibits red blood cell development by targeting Setdb1 to erythroid genes, where it methylates H3K9 to inhibit the expression of key genes involved in red blood cell development. The goal of this project is to inhibit the expression of Miwi2 and Setdb1 and determine whether the loss H3K9 methylation results in red blood cell differentiation. We hope to understand how mutations could potentially stimulate pathways related to erythropoiesis and cellular differentiation.
Analysis of the role of Miwi2 dependent regulation of histone modifications in stress erythropoiesis
by Kathryn Elizabeth Luteran
Immunology and Infectious Disease
Health and Life Sciences