Dr. Bruce Aronow

The ScienceDaily article Evolution Of Human Genome’s “Guardian” Gives People Unique Protections From DNA Damage said

Human evolution has created enhancements in key genes connected to the p53 regulatory network — the so-called guardian of the genome — by creating additional safeguards in human genes to boost the network’s ability to guard against DNA damage that could cause cancer or a variety of genetic diseases, an international team of scientists led by Cincinnati Children’s Hospital Medical Center discovered.
 
“The fact that DNA metabolism and repair genes have undergone this kind of evolution in humans may reflect an increased need for coordinated control of molecular repair activities during DNA replication to allow for the maintenance of genomic integrity during complex differentiation, growth, and aging,” said Bruce Aronow, Ph.D., co-director of Computational Medicine at Cincinnati Children’s and a study coauthor.
 
“That different strategies to guard our chromosome structures and DNA sequences against damage are subject to evolutionary adaptation is also suggested by other knowledge we have,” Dr. Aronow explained. “For example, compared to rodents humans have much shorter telomeres, which are regions of highly repetitive DNA at the end of chromosomes that help shield against damage. Shorter telomeres can make people more susceptible to chromosomal damage and increase our risk of developing malignant tumors. When genes replicate, the process does not copy the very ends of the gene, so telomeres act like caps on the ends of shoelaces, helping preserve DNA structure and preventing genetic unraveling and loss of genetic information.”

Bruce Aronow, Ph.D. is Professor and Co-director, Computational Medicine Center, Cincinnati Children’s Hospital Medical Center.
 
Bruce’s research lab is devoted to unraveling both the role and mechanism by which the functional capabilities of the human genome shape human health and our ability to adapt to stressful challenges. His lab is using a wide variety of available structural and functional genomic and biological systems descriptive data to form models of how biological systems assemble, adapt and become impaired in disease. The lab’s overall hypothesis is that by interconnecting as much experimental and observational information as possible, they can gain new insights into the mechanisms by which different biological systems can achieve health or healthy adaptation, or undergo disease processes.
 
More specifically, his lab is identifying genetic features that control gene expression including cis-elements, trans factors and microRNAs, which normally work together in extended cell, tissue, organ and systems networks to enable development and homeostasis. Alterations of these features can alter phenotypes and increase or decrease disease. Some of the lab’s work includes the identification of conserved, diverged and evolved cis-element clusters that are acted on by transcription and chromatin proteins. The lab has developed a web-based tool called GenomeTraFaC that at present allows discovery of shared cis-elements in conserved non-coding sequences of mice and humans. GenomeTraFaC identifies the cis-elements in phylogenetic footprints, or non-coding DNA regions of six or more base pairs having almost 100 percent similarity and conserved across several species separated by several million years of evolution.
 
Extending the scope of GenomeTraFaC, the lab has developed CisMols, a tool that identifies compositionally similar cis-regulatory element clusters that occur in groups of co-regulated genes. These computationally predicted cis-clusters could serve as valuable probes for genome-wide identification of regulatory regions.
 
Another area of the lab’s research is the integration of SNP information with the protein structure and protein functional domains. The lab is using all available gene-to-disease and gene-to-pathway association data to study the effects of non-synonymous SNPs and other important polymorphisms that occur in functional domains of proteins in specific diseases and biological processes. The lab has developed another web-based tool, PolyDoms, to aid in this effort.
 
Bruce coedited Genomics in Endocrinology: DNA Microarray Analysis in Endocrine Health and Disease, and coauthored Design and implementation of microarray gene expression markup language (MAGE-ML), Mitochondrial death protein Nix is induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy, Clusterin contributes to caspase-3-independent brain injury following neonatal hypoxia-ischemia, Divergent transcriptional responses to independent genetic causes of cardiac hypertrophy, Detection and Visualization of Compositionally Similar cis-Regulatory Element Clusters in Orthologous and Coordinately Controlled Genes, and A Genome — Phenome Integrated Approach for Mining Disease-Causal Genes using Semantic Web. Read the full list of his publications!
 
Bruce earned his BS in Chemistry at Stanford University in 1976 and his PhD in Biochemistry at the University of Kentucky in 1986. He completed his Research Fellowship at the Division of Basic Science Research, Cincinnati Children’s Research Foundation from 1986 to 1989. His patents include CFTR modifier genes and expressed polypeptides useful in treating cystic fibrosis and methods and products for detecting and/or identifying same and Altered gene expression profiles in stable versus acute childhood asthma.
 
Read Researchers First To Map Gene That Regulates Adult Stem Cell Growth.