Lloyd and Priyadarshi Basu, Ph.D., lead investigator at VCU, and the research team compared mice that were missing the gene for KLF2 to normal mice. They found that the KLF2-deficient mice produced embryonic red blood cells that appeared abnormal, were more likely to undergo cell death, and produced significantly lower amounts of globin mRNA than those found in normal mice. Globin mRNA is a key player in gene expression that helps translate the DNA's genetic code.
Lloyd and her colleagues identified that the role of KLF2 for the embryonic epsilon-globin genes is analogous to that of a protein called EKLF. EKLF plays a central role in the developmental regulation of the adult beta-globin gene, and is essential for the maturation and stability of adult red blood cells. Researchers believe that the roles of EKLF and KLF2 may partially overlap in controlling human embryonic and fetal globin gene expression.
This research was supported by a grant from the National Institutes of Health.
Lloyd collaborated with colleagues in the VCU Department of Human Genetics, and the VCU Department of Anatomy and Neurobiology; the Department of Molecular Genetics, Biochemistry and Microbiology at the University of Cincinnati; and the Department of Medicine at the University of California-San Francisco.