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Blindness and auditory impairment caused by loss of the sodium bicarbonate cotransporter NBC3 总被引:7,自引:0,他引:7
Bok D Galbraith G Lopez I Woodruff M Nusinowitz S BeltrandelRio H Huang W Zhao S Geske R Montgomery C Van Sligtenhorst I Friddle C Platt K Sparks MJ Pushkin A Abuladze N Ishiyama A Dukkipati R Liu W Kurtz I 《Nature genetics》2003,34(3):313-319
Normal sensory transduction requires the efficient disposal of acid (H+) generated by neuronal and sensory receptor activity. Multiple highly sensitive transport mechanisms have evolved in prokaryotic and eukaryotic organisms to maintain acidity within strict limits. It is currently assumed that the multiplicity of these processes provides a biological robustness. Here we report that the visual and auditory systems have a specific requirement for H+ disposal mediated by the sodium bicarbonate cotransporter NBC3 (refs. 7,8). Mice lacking NBC3 develop blindness and auditory impairment because of degeneration of sensory receptors in the eye and inner ear as in Usher syndrome. Our results indicate that in certain sensory organs, in which the requirement to transduce specific environmental signals with speed, sensitivity and reliability is paramount, the choice of the H+ disposal mechanism used is limited. 相似文献
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M. N. Galbraith D. H. S. Horn E. J. Middleton J. N. Kaplanis M. J. Thompson 《Cellular and molecular life sciences : CMLS》1973,29(7):782-782
Résumé Le Podecdysone C, un stérol extrait de l'écorce de l'arbrePodocarpus elatus R. Br. et qui fonctionne comme hormone de mue est identique au THE-III (26-hydroxy--ecdysone, II) extrait du ver du tabacManduca sexta. 相似文献
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M. N. Galbraith D. H. S. Horn E. J. Middleton J. A. Thomson 《Cellular and molecular life sciences : CMLS》1973,29(1):19-19
Résumé L'activité biologique de la 2, 22, 25-trideoxy--ecdysone chezCalliphora est plus élevéc que celle de toutes les substances analogues examinées. 相似文献
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Galbraith ED Jaccard SL Pedersen TF Sigman DM Haug GH Cook M Southon JR Francois R 《Nature》2007,449(7164):890-893
Atmospheric carbon dioxide concentrations were significantly lower during glacial periods than during intervening interglacial periods, but the mechanisms responsible for this difference remain uncertain. Many recent explanations call on greater carbon storage in a poorly ventilated deep ocean during glacial periods, but direct evidence regarding the ventilation and respired carbon content of the glacial deep ocean is sparse and often equivocal. Here we present sedimentary geochemical records from sites spanning the deep subarctic Pacific that--together with previously published results--show that a poorly ventilated water mass containing a high concentration of respired carbon dioxide occupied the North Pacific abyss during the Last Glacial Maximum. Despite an inferred increase in deep Southern Ocean ventilation during the first step of the deglaciation (18,000-15,000 years ago), we find no evidence for improved ventilation in the abyssal subarctic Pacific until a rapid transition approximately 14,600 years ago: this change was accompanied by an acceleration of export production from the surface waters above but only a small increase in atmospheric carbon dioxide concentration. We speculate that these changes were mechanistically linked to a roughly coeval increase in deep water formation in the North Atlantic, which flushed respired carbon dioxide from northern abyssal waters, but also increased the supply of nutrients to the upper ocean, leading to greater carbon dioxide sequestration at mid-depths and stalling the rise of atmospheric carbon dioxide concentrations. Our findings are qualitatively consistent with hypotheses invoking a deglacial flushing of respired carbon dioxide from an isolated, deep ocean reservoir, but suggest that the reservoir may have been released in stages, as vigorous deep water ventilation switched between North Atlantic and Southern Ocean source regions. 相似文献