CALMODULIN ACTIVATED CHANNELS AND MOLECULAR PHYSIOLOGY

钙调蛋白激活通道和分子生理学

基本信息

批准号：
2701519
负责人：
YOSHIRO SAIMI
金额：
$ 25.06万
依托单位：
UNIVERSITY OF WISCONSIN-MADISON
依托单位国家：
美国
项目类别：
财政年份：
1986
资助国家：
美国
起止时间：
1986-04-01 至 2000-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/2701519
关键词：
Paramecium behavioral genetics bioenergetics biological transport calcium channel calmodulin electrophysiology enzyme inhibitors ionophores membrane channels membrane permeability molecular cloning physiology polymerase chain reaction potassium channel site directed mutagenesis transport proteins voltage /patch clamp

项目摘要

Regulations by direct interaction between Ca2+-calmodulin and ion channels have now been found in many systems including the mammalian photoreceptor and olfactory receptor. We intend to continue to investigate this phenomenon using Paramecium where it was first explicitly demonstrated. We also found that in vivo mutations defective in the C-terminal lobe of calmodulin weaken Ca2+-calmodulin dependent K+ currents, while those in the N-lobe delete their Na+ currents. We will continue to examine whole- cell currents as well as single- channel currents to study this functional bipartition with existing and newly generated Paramecium mutants. We will try to extend this functional bipartition hypothesis to mammals by testing the effects of the two classes of mutant calmodulins on cNMP-dependent channels in olfactory neurons and ryanodine receptor/Ca2+-release channels. For our long-term project of Paramecium behavioral genetics, mutants and revertants will continue to be examined electrophysiologically. We also intend to make Paramecium an efficient system for reverse genetics, i.e. to generate live mutants each lacking a macronuclear gene that is homologous to a mammalian sequence. Genes of neurobiological interests will be tested first.

通过Ca2+-calmodulin和离子通道之间的直接相互作用进行法规现在已经在包括哺乳动物感光器在内的许多系统中发现和嗅觉受体。我们打算继续调查现象使用Pragemium首先被明确证明。我们还发现，体内突变在C末端叶中有缺陷钙调蛋白削弱了Ca2+ -calmodulin依赖K+电流，而在 N-LOBE删除其Na+电流。我们将继续研究整个细胞电流以及单个通道电流来研究此功能现有和新生成的甲丙基突变体的两部分。我们将尝试通过测试将此功能性两部分假设扩展到哺乳动物两类突变体钙调蛋白对CNMP依赖性的影响嗅觉神经元和ryanodine受体/Ca2+ - 释放的通道频道。对于我们的黑甲行遗传学长期项目，突变体和恢复物将继续检查电生理学。我们还打算使Pragecium有效反向遗传学的系统，即生成活突变体，每个突变体缺乏与哺乳动物序列同源的大核基因。基因神经生物学兴趣将首先进行测试。