Studies of CaMKIV, CaMKII and CaMKK in knockout mice show that these genes are critical for learning and memory. Curiously, CaMKI, a widely expressed CaMK has received little attention on its role in learning and memory. Our objective was to test the hypothesis that cmk-1 (homologous to CaMKI) is necessary for learning and/or memory. Because cmk-1 is highly homologous (and perhaps ancestral) to CaMKIV, and is widely expressed in the nervous system we predicted that animals with mutations in cmk-1 would show deficiencies in learning and/or memory. Worms strains with mutations in cmk-1, and ckk-1 (homologous to CaMKK and a known activator of cmk-1; Kimura et al. 2001) were tested for deficits in learning, short-term and long-term memory. Worms were habituated to mechanical stimuli (taps to the side of the Petri dish) using different stimulation protocols known to induce short-term, and long-term habituation. Worms with mutations in cmk-1 habituate normally when stimuli are presented at a 10s interstimulus interval (ISI), but do not habituate as deeply as wild-type animals when stimuli are presented at a 60s ISI, and cannot form long-term memory. No deficits in either short or long-term habituation were found in animals with a mutation in ckk-1. These results are similar to those of Satterlee et al. (2004) who also found that cmk-1, but not ckk-1 regulated gene expression, morphology, and functions of the AFD thermosensory neurons. This evidence suggests that a novel kinase may play the role of activating cmk-1 in the context of short-term habituation and long-term memory of habituation. To investigate whether the long-term memory deficit of the cmk-1 mutants is a result of the animals short-term habituation deficit or whether it is independently involved in both processes we created a strain that expresses the cmk-1 gene without the nuclear localization signal (NLS), restricting its expression to the cytoplasm (CaMKIV, and perhaps cmk-1 in some animals, are thought to participate in the induction of long-term memory by phosphorylating the transcription factor CREB in the nucleus). We predict that cmk-1 without the NLS will rescue the short-term habituation deficit but will be incapable of rescuing the long-term memory deficit, demonstrating that cmk-1 acts in independently in these two processes. In these studies we show, for the first time, that cmk-1 is critical for learning and memory. We also present data that support the hypothesis that cmk-1 is ancestral to mammalian CaMKIV and suggest that in species where CaMKIV does not exist, cmk-1 may function in its place.