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EMBO Rep. 2002 Oct;3(10):962-6. Epub 2002 Sep 13.

A CaMK cascade activates CRE-mediated transcription in neurons of Caenorhabditis elegans.

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1
Department of Functional Genomics, Medical Research Institute, Tokyo Medical and Dental University, Japan.

Abstract

Calcium (Ca2+) signals regulate a diverse set of cellular responses, from proliferation to muscular contraction and neuro-endocrine secretion. The ubiquitous Ca2+ sensor, calmodulin (CaM), translates changes in local intracellular Ca2+ concentrations into changes in enzyme activities. Among its targets, the Ca2+/CaM-dependent protein kinases I and IV (CaMKs) are capable of transducing intraneuronal signals, and these kinases are implicated in neuronal gene regulation that mediates synaptic plasticity in mammals. Recently, the cyclic AMP response element binding protein (CREB) has been proposed as a target for a CaMK cascade involving not only CaMKI or CaMKIV, but also an upstream kinase kinase that is also CaM regulated (CaMKK). Here, we report that all components of this pathway are coexpressed in head neurons of Caenorhabditis elegans. Utilizing a transgenic approach to visualize CREB-dependent transcription in vivo, we show that this CaMK cascade regulates CRE-mediated transcription in a subset of head neurons in living nematodes.

PMID:
12231504
PMCID:
PMC1307624
DOI:
10.1093/embo-reports/kvf191
[Indexed for MEDLINE]
Free PMC Article
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