Nature Genetics

doi: 10.1038/75946pmid: 10835616

Aparicio, Samuel A J R

doi: 10.1038/75949pmid: 10835617

Mombaerts, Peter

doi: 10.1038/75952pmid: 10835618

Wedding genetics with genomics, two groups 1,2,3 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.

Klein, Hannah L

doi: 10.1038/75957pmid: 10835619

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

Serup, Palle

doi: 10.1038/75960pmid: 10835620

Thanks to their much-lauded potential in treating a variety of debilitating diseases, and their recent isolation, human embryonic stem (ES) cells 1 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.

Walport, Mark J

doi: 10.1038/75963pmid: 10835621

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.

doi: 10.1038/75968pmid: 10835622

Rodríguez, Carolyn I.; Buchholz, Frank; Galloway, Jenna; Sequerra, Reynaldo; Kasper, Jocelyn; Ayala, Ramses; Stewart, A. Francis; Dymecki, Susan M.

doi: 10.1038/75973pmid: 10835623

Chavanas, Stéphane; Bodemer, Christine; Rochat, Ariane; Hamel-Teillac, Dominique; Ali, Mohsin; Irvine, Alan D.; Bonafé, Jean-Louis; Wilkinson, John; Taïeb, Alain; Barrandon, Yann; Harper, John I.; de Prost, Yves; Hovnanian, Alain

Watnick, Terry; He, Ning; Wang, Kairong; Liang, Yan; Parfrey, Patrick; Hefferton, Donna; St George-Hyslop, Peter; Germino, Gregory; Pei, York

doi: 10.1038/75981pmid: 10835625

Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 and PKD2. The products of these genes associate to form heteromeric complexes. Several models have been proposed to explain the mechanism of cyst formation. Here we find somatic mutations of PKD2 in 71% of ADPKD2 cysts analysed. Clonal somatic mutations of PKD1 were identified in a subset of cysts that lacked PKD2 mutations.