Explore Research Innovation at the David Geffen School of Medicine
Jeffrey H. Miller, PhDProfessor, Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine at UCLA
Member, Molecular Biology Institute at UCLA
Dr. Jeffrey H. Miller studies how microorganism cells repair and mutate to maximize survival. He explores how we might leverage those processes to treat human disease.
After pinpointing mechanisms that activate, inhibit, or influence DNA repair and mutation in microorganisms, Dr. Miller searches for human counterparts to these processes. This investigative technique led to the discovery of a gene-induced cellular repair mechanism that prevents colon cancer.
Dr. Miller hopes to find additional ways his research can help predict, influence, and treat human disease.
The Miller Lab studies how microorganism cells repair themselves, how they avoid mutation, and how they react to antibiotics. The team questions each finding to determine if it reveals anything significant about human disease.
Dr. Miller and his team have defined genes with a clinically significant effect on antibiotics. Using this knowledge, researchers can mitigate antibiotic resistance and even design drugs to reduce negative antibiotic side effects. Read more in Deoxycytidine Deaminase-Deficient Escherichia coli Strains Display Acute Sensitivity to Cytidine, Adenosine, and Guanosine and Increased Sensitivity to a Range of Antibiotics, Including Vancomycin, published in the Journal of Bacteriology.
Photo from UCLA College Report 2011
Preventing and Repairing DNA Damage
The Miller Lab isolated genes that cause spontaneous mutations in Escherichia coli. Further study could elucidate techniques to prevent and repair DNA damage and even correct errors in DNA replication. Read more in Polynucleotide Phosphorylase Plays an Important Role in the Generation of Spontaneous Mutations in Escherichia coli, published in the Journal of Bacteriology.
After determining the genes driving a mechanism Escherichia coli uses for cell repair, Dr. Miller conducted a murine study and determined the same mechanism could play a role in preventing cancer. Subsequent human studies associated a lack of the gene with an increased risk of colon cancer. Read more in Deficiencies in Mouse Myh and Ogg1 Result in Tumor Predisposition and G to T Mutations in Codon 12 of the K-Ras Oncogene in Lung Tumors, published in Cancer Research.
When it comes to studying the interplay of DNA and disease, Dr. Miller believes he has only skimmed the surface of knowledge we might adapt to repair damaged cells, maximize antibiotic effectiveness, and prevent disease.
If a bacterial repair gene can help prevent human cancer, then equally significant discoveries could be on the horizon.
Help Dr. Miller discover more genes critical to health by supporting immunology research >
Jeffrey H. Miller Lab