ABSTRACT
Technologies that probe genomic responses to chemical exposure are expected to improve our understanding of molecular mechanisms of toxicity. Accelerated by advances in high-throughput DNA sequencing, a number of animals that are important as models of human disease (e.g., yeast, worm, fruit fly) have been completely sequenced. A draft of the human genome released in February 2001 and a draft of the mouse genome released in December 2002 have provided a wealth of genetic information much sooner than initially anticipated (1-3). A high-quality draft covering more than 90% of the Brown Norway rat genome has also been recently reported (4). The availability of genomic sequences has provided revolutionary opportunities to monitor gene expression changes across an entire genome. This flood of genomic data has also led to the identification and quantitation of sequence differences between individual humans or between animal strains in the form of deletions, insertions, and single nucleotide polymorphisms. Dual sources of information about global gene expression and genetic differences will facilitate an understanding of the molecular basis of disease in general and, in particular, how chemicals interact with genes, proteins, and other biological components to cause adverse or beneficial effects.
