Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The identification of hundreds of thousands of clusters of transcriptional start sites, many located within internal exons of protein-coding genes, indicates that promoter sites are common and that transcriptional organization is complex. This transcriptional architecture implies that most genomic regions serve multiple functions.
Two new studies evaluate the extent to which widely used SNP platforms capture common variation in different populations, and they present strategies for improving power in whole-genome association studies using fixed marker sets. Their results suggest that genome-wide association studies are finally ready to move from theory to practice.
The most recent National Academies Keck Futures Initiative Conference, entitled 'The Genomics Revolution: Implications for Treatment and Control of Infectious Disease', was held at the Arnold and Mabel Beckman Center in Irvine, California. It provided strategies and opportunities for interdisciplinary collaboration and incentives to innovate.
Aberrant methylation of a CpG island in cancer is thought to silence a single gene but not its neighbors. A new study in colon cancer shows that transcriptional silencing can also be unexpectedly diffuse, encompassing all the genes over the 4 Mb of chromosome band 2q14.2, marked by archipelagos of methylated islands and uniform heterochromatin modification.
It has long been suspected that phenotypic diversity results, in large part, from variation in DNA regulatory sequences. A new study now shows that adaptive changes in an upstream regulatory sequence of tb1 are responsible for major phenotypic changes associated with maize domestication.
Mutations in hemojuvelin disrupt its ability to stimulate expression of the iron regulatory peptide hepcidin and result in the severe iron loading disorder juvenile hemochromatosis. A new study shows that hemojuvelin acts through the multifunctional bone morphogenetic protein pathway to modulate hepcidin levels, providing new insights into communication within a key physiological pathway.
New studies indicate that damage to the mitochondrial genome (mtDNA) accumulates with age, specifically in the dopaminergic neurons of the substantia nigra implicated in Parkinson disease. These findings suggest that mtDNA damage is important in the decay of dopaminergic neurons in aging and in Parkinson disease, resulting in loss of mitochondrial function and, ultimately, neuronal death.
A new study shows that Slc26a6-null mice manifest calcium-oxalate nephrolithiasis accompanied by enhanced net intestinal oxalate absorption. These findings point to a critical role for Slc26a6 in gastrointestinal oxalate secretion and suggest a genetic explanation for a common form of renal stone disease in humans.
A new study elucidates a drug interaction network using a simple combination of theory and experiments, testing drug combinations on Escherichia coli. The results are elegant, uncovering drug interactions shared within drug classes and providing useful tools for functional classifications of drugs.
