Published online 21 June 2006
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited.
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RNA helicases and abiotic stress
Department of Biological Sciences, University of Alberta Edmonton, Alberta, Canada T6G 2E9
*Tel: +1 780 492 1803; Fax: +1 780 492 9234; Email: g.owttrim{at}ualberta.ca
Received March 27, 2006. Revised May 15, 2006. Accepted May 17, 2006.
RNA helicases function as molecular motors that rearrange RNA secondary structure, potentially performing roles in any cellular process involving RNA metabolism. Although RNA helicase association with a range of cellular functions is well documented, their importance in response to abiotic stress is only beginning to emerge. This review summarizes the available data on the expression, biochemistry and physiological function(s) of RNA helicases regulated by abiotic stress. Examples originate primarily from non-mammalian organisms while instances from mammalian sources are restricted to post-translational regulation of helicase biochemical activity. Common emerging themes include the requirement of a cold-induced helicase in non-homeothermic organisms, association and regulation of helicase activity by stress-induced phosphorylation cascades, altered nuclearcytoplasmic shuttling in eukaryotes, association with the transcriptional apparatus and the diversity of biochemical activities catalyzed by a subgroup of stress-induced helicases. The data are placed in the context of a mechanism for RNA helicase involvement in cellular response to abiotic stress. It is proposed that stress-regulated helicases can catalyze a nonlinear, reversible sequence of RNA secondary structure rearrangements which function in RNA maturation or RNA proofreading, providing a mechanism by which helicase activity alters the activation state of target RNAs through regulation of the reaction equilibrium.
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