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Professor of Biochemistry
Primary Office: 3136 MERFIowa City, IA 52242
Email: email@example.comWeb: Wallrath Laboratory
BS, Microbiology, Michigan State UniversityPhD, Genetics, Michigan State University
Post Doctorate, Chromatin Structure and Gene Expression, Washington University in St. Louis
Department of Biochemistry PhDInterdisciplinary Graduate Program in GeneticsInterdisciplinary Graduate Program in Molecular and Cellular BiologyInterdisciplinary Graduate Program in Translational BiomedicineMedical Scientist Training Program
Research in the Wallrath laboratory is focused the role of chromatin packaging, gene expression and nuclear organization, with respect to human disease. The three dimensional organization of the genome within the nucleus is important for proper gene regulation. Lamins are intermediate filament proteins that line the inner side of the nuclear envelope providing structural support for the nucleus and regulating gene expression through connections made with chromatin. Mutations in lamins cause a collection of diseases called laminopathies that include musculear dystrophy, cardiomyopathy and early onset aging. It is unclear how mutant lamins cause disease. To address this issue, the laboratory has generated a Drosophila (fruit fly) model for muscle laminopathies. Flies expressing mutant lamins exhibit muscular dystrophy and die due to loss of muscle function. This model is currently being used to understand how mutant lamins misregulate genes and cause altered signaling in biological pathways.
Eukaryotic genomes are packaged with histones and non-histone chromosomal proteins that collectively regulate gene expression. Heterochromatin Protein 1 (HP1) is a non-histone protein that collaboratorates with DNA methyltransferase I (DNMT1) to silence tumor suppressor genes. In collaboration with the laboratories of Charles Brenner (Biochemistry) and Kai Tan (Internal Medicine), experiments are underway to determine the effects of novel DNMT1 inhibitors on the re-activation of tumor suppressor genes in human breast cancer cells.
Using Drosophila for Studies of Intermediate Filaments..
Methods in enzymology.
2016 January 1. 568:707-26.
A Drosophila Model of Epidermolysis Bullosa Simplex..
The Journal of investigative dermatology.
2015 August 1. 135(8):2031-9.
Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway..
2015 May 1. 11(5):e1005231.
Human heterochromatin protein 1α promotes nucleosome associations that drive chromatin condensation.
J Biol Chem.
Laccaic Acid A is a Direct, DNA-Competitive Inhibitor of DNA Methyltransferase 1.
The Journal of biological chemistry.
Myopathic lamin mutations impair nuclear stability in cells and tissue and disrupt nucleo-cytoskeletal coupling.
Human molecular genetics.
2013 June. 22(12):2335-49.
Enforcing silencing: dynamic HP1 complexes in Neurospora.
Nature structural & molecular biology.
2012 May. 19(5):465-7.
LMNA variants cause cytoplasmic distribution of nuclear pore proteins in Drosophila and human muscle.
Human molecular genetics.
2012 April. 21(7):1544-56.
Nuclear organization: taking a position on gene expression.
Current opinion in cell biology.
2011 June. 23(3):354-9.
Date Last Modified: 04/12/2016 -
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