In the globin gene family (shown in the below diagram), which pair of genes would exhibit a higher level of sequence similarity, the human δ-globin and human β-globin genes or the human β-globin and chimpanzee β-globin genes? Can you explain your answer in terms of the timing of gene duplications?

Researchers have compared candidate loci in humans and rats in search of loci in the human genome that are likely to contribute to the constellation of factors leading to hypertension [Stoll, M., et al. (2000). Genome Res. 10:473–482]. Through this research, they identified 26 chromosomal regions that they consider likely to contain hypertension genes. How can comparative genomics aid in the identification of genes responsible for such a complex human disease? The researchers state that comparisons of rat and human candidate loci to those in the mouse may help validate their studies. Why might this be so?

Homology can be defined as the presence of common structures because of shared ancestry. Homology can involve genes, proteins, or anatomical structures. As a result of 'descent with modification,' many homologous structures have adapted different purposes.

Under what circumstances might one expect proteins of similar function to not share homology? Would you expect such proteins to be homologous at the level of DNA sequences?

Homology can be defined as the presence of common structures because of shared ancestry. Homology can involve genes, proteins, or anatomical structures. As a result of 'descent with modification,' many homologous structures have adapted different purposes.

Is it likely that homologous proteins from different species have the same or similar functions? Explain.

Homology can be defined as the presence of common structures because of shared ancestry. Homology can involve genes, proteins, or anatomical structures. As a result of 'descent with modification,' many homologous structures have adapted different purposes.

List three anatomical structures in vertebrates that are homologous but have different functions.

Comparisons between human and chimpanzee genomes indicate that a gene that may function as a wild-type or normal gene in one primate may function as a disease-causing gene in another [The Chimpanzee Sequencing and Analysis Consortium (2005). Nature 437:69–87]. For instance, the PPARG locus (regulator of adipocyte differentiation) is a wild-type allele in chimps but is clearly associated with Type 2 diabetes in humans. What factors might cause this apparent contradiction? Would you consider such apparent contradictions to be rare or common? What impact might such findings have on the use of comparative genomics to identify and design therapies for disease-causing genes in humans?

Yeager, M., et al. [(2007) Nature Genetics 39:645–649] and Sladek, R., et al. [(2007) Nature 445:881–885] have used single-nucleotide polymorphisms (SNPs) in genome-wide association studies (GWAS) to identify novel risk loci for prostate cancer and Type 2 diabetes, respectively. Each study suggests that disease-risk genes can be identified that significantly contribute to the disease state. Given your understanding of such complex diseases, what would you determine as reasonable factors to consider when interpreting the results of GWAS?

You are studying similarities and differences in how organisms respond to high salt concentrations and high temperatures. You begin your investigation by using microarrays to compare gene expression patterns of S. cerevisiae in normal growth conditions, in high salt concentrations, and at high temperatures. The results are shown here, with the values of red and green representing the extent of increase and decrease, respectively, of expression for genes a–s in the experimental conditions versus the control (normal growth) conditions. What is the first step you will take to analyze your data?

Dominguez et al. (2004) suggest that by studying genes that determine growth and tissue specification in the eye of Drosophila, much can be learned about human eye development.

What evidence indicates that the eyeless gene is part of a developmental network?