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.
Wedding genetics with genomics, two groups1,2,3 have independently identified in mammals a multigene family encoding seven-transmembrane proteins that probably represent the hitherto elusive taste receptors. Functional expression in heterologous cells confers responsiveness to bitter tastants in several cases. This discovery may lead to the design of bitter antagonists—and perhaps better butter for Betty Botter.
The Saccharomyces cerevisiae gene SGS1 encodes a protein related to the human DNA helicases defective in Werner syndrome, Bloom syndrome and Rothmund-Thomson syndrome. Yeast cells lacking the Sgs1 helicase and a related helicase, Srs2, are inviable or grow extremely poorly. The growth defect can be rescued by crippling the homologous recombination repair pathway, indicating that the essential function of these genes is related to recombination
Thanks to their much-lauded potential in treating a variety of debilitating diseases, and their recent isolation, human embryonic stem (ES) cells1 have been the focus of a great deal of attention over the past several months. And yet we are startlingly ignorant of the biology of stem cells and their differentiation; an intimate appreciation of these is required to realize therapeutic aspirations. A timely meeting* in mid-April brought together investigators with expertise in stem cell biology and developmental biology of the pancreas as a first step to harness stem cells in the treatment of diabetes.
Apoptotic and necrotic cells are strong candidates as sources of the autoantigens that drive the autoantibody response in systemic lupus erythematosus (SLE). Defects in the physiological mechanisms for the clearance of dying cells may promote disease susceptibility to SLE. Ablation of the mouse gene Dnase1 results in the development of anti-chromatin autoimmunity and glomerulonephritis, indicating that the enzyme protects against autoimmunity by digesting extracellular chromatin.
