Cation channels in the DEG/ENaC family are proposed to detect cutaneous stimuli in mammals. We localized one such channel, DRASIC, in several different specialized sensory nerve endings of skin, suggesting it might participate in mechanosensation and/or acid-evoked nociception. Disrupting the mouse DRASIC gene altered sensory transduction in specific and distinct ways. Loss of DRASIC increased the sensitivity of mechanoreceptors detecting light touch, but it reduced the sensitivity of a mechanoreceptor responding to noxious pinch and decreased the response of acid- and noxious heat-sensitive nociceptors. The data suggest that DRASIC subunits participate in heteromultimeric channel complexes in sensory neurons. Moreover, in different cellular contexts, DRASIC may respond to mechanical stimuli or to low pH to mediate normal touch and pain sensation.

In the article by Price et al. (Neuron 32, 1071-1083 [December 20, 2001]), the x axis for stimulus response functions shown in Figures 3A-3F were incorrectly labeled and should read 50, 100, 200, and 400 m instead of 5, 10, 20, 40 m, as indicated in the original article. This error does not alter any of the conclusions made in the manuscript.

The epithelial Na ؉ channel (ENaC) is composed of three homologous subunits: ␣, ␤ and ␥. We used gene targeting to disrupt the ␤ subunit gene of ENaC in mice. The ␤ENaC-deficient mice showed normal prenatal development but died within 2 days after birth, most likely of hyperkalemia. In the ؊͞؊ mice, we found an increased urine Na ؉ concentration despite hyponatremia and a decreased urine K ؉ concentration despite hyperkalemia. Moreover, serum aldosterone levels were increased. In contrast to ␣ENaC-deficient mice, which die because of defective lung liquid clearance, neonatal ␤ENaC deficient mice did not die of respiratory failure and showed only a small increase in wet lung weight that had little, if any, adverse physiologic consequence. The results indicate that, in vivo, the ␤ subunit is required for ENaC function in the renal collecting duct, but, in contrast to the ␣ subunit, the ␤ subunit is not required for the transition from a liquid-filled to an air-filled lung. The phenotype of the ␤ENaC-deficient mice is similar to that of humans with pseudohypoaldosteronism type 1 and may provide a useful model to study the pathogenesis and treatment of this disorder.

Background: Plant resistance (R) gene products recognize pathogen effector molecules. Many R genes code for proteins containing nucleotide binding site (NBS) and C-terminal leucine-rich repeat (LRR) domains. NBS-LRR proteins can be divided into two groups, TIR-NBS-LRR and non-TIR-NBS-LRR, based on the structure of the N-terminal domain. Although both classes are clearly present in gymnosperms and eudicots, only non-TIR sequences have been found consistently in monocots. Since most studies in monocots have been limited to agriculturally important grasses, it is difficult to draw conclusions. The purpose of our study was to look for evidence of these sequences in additional monocot orders.

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