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.
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