Mutating Mice and Other Genetics News

Researchers from the University of Utah and the Howard Hughes Medical Institute have developed a quicker and less expensive way of creating mutant mice--to test the effect of mutations in non-gene DNA.

The new method for mutating large, non-gene stretches of DNA is outlined in this week’s online edition of Nature Genetics. Capecchi and Wu conducted the research with two other University of Utah human geneticists: Guoxin Ying, a postdoctoral fellow, and Qiang Wu, an assistant professor (and no relation to Sen Wu).

In the journal paper, the University of Utah scientists report:

* They found a way to delete or duplicate moderately long to very long pieces of DNA and make those mutations happen much more frequently than other methods can. That makes it easier to find out what defects or diseases arise due to such mutations, and thus what the DNA does normally.

* They devised a much more efficient method for mixing and recombining pieces of two chromosomes, making it easier to breed mice with human cancers. Such mice are needed to develop new treatments.

Read more at the Source

In this study, researchers at the University of Chicago the genetic basis of phenotype differences between chimps and humans. They discovered that much of the difference between gene expression in ten genes in humans and chimps, was due to differences in promoter activity. In other words, even with almost the same genes, differences in gene regulation achieves significant phenotype differences.

Berkeley Lab researchers are discovering more of the importance of "junk DNA" for cell organisation and survival.

Researchers at the University of Virginia Health System discovered yet another interesting determinant of gene expression. It seems that the chromatin packaging of genes (how tightly the genes are wrapped on histones) can determine how quickly, and at what level, the gene will be expressed. This is particularly important in development and cell differentiation.

A collaborative study published in Nature offers more information about the relationship of "junk DNA" and disease causation.

And Yale researchers are using advanced gene sequencing technology to identify HIV strains that are resistant to standard therapy. These particular strains were not detectable using available hospital lab testing.

Gene expression is far more complex than originally thought. The gene regulating effect of "junk DNA" may explain a great deal of disease etiology and progression that has been a mystery up until now. Phenotypic differences between species with similar genomes are becoming easier to explain as the larger picture of gene regulation is elucidated.

We are literally only just beginning to open the book of genetics.