Davis M W, Somerville D, Lee R Y, Lockery S, Avery L, Fambrough D M
Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas 75235-9038, USA.
J Neurosci. 1995 Dec;15(12):8408-18. doi: 10.1523/JNEUROSCI.15-12-08408.1995.
We have cloned a Na,K-ATPase alpha-subunit gene from Caenorhabditis elegans and discovered that it is identical to the gene eat-6, eat-6 mutations cause feeble contractions and slow, delayed relaxations of pharyngeal muscle. The resting membrane potential of eat-6 mutant pharynxes is consistently depolarized compared to wild-type. The action potentials are smaller, and the return to resting potential is slower. To explain these abnormalities, we propose that a reduction of Na,K-ATPase activity in eat-6 mutants leads to a reduction of the ion concentration gradients that power membrane potential changes.
我们从秀丽隐杆线虫中克隆了一个钠钾ATP酶α亚基基因，发现它与eat-6基因相同，eat-6突变会导致咽部肌肉收缩无力以及缓慢、延迟的松弛。与野生型相比，eat-6突变型咽部的静息膜电位持续去极化。动作电位较小，恢复到静息电位的速度较慢。为了解释这些异常现象，我们提出eat-6突变体中钠钾ATP酶活性的降低导致了驱动膜电位变化的离子浓度梯度的降低。
