Abstract
Nitric oxide (NO) emerged as one of the major signaling molecules operating during plant development and plant responses to its environment. Beyond the identification of the direct molecular targets of NO, a series of studies considered its interplay with other actors of signal transduction and the integration of NO into complex signaling networks. Beside the close relationships between NO and calcium or phosphatidic acid signaling pathways that are now well-established, recent reports paved the way for interplays between NO and sphingolipids (SLs). This mini-review summarizes our current knowledge of the influence NO and SLs might exert on each other in plant physiology. Based on comparisons with examples from the animal field, it further indicates that, although SL–NO interplays are common features in signaling networks of eukaryotic cells, the underlying mechanisms and molecular targets significantly differ.
Highlights
Nitric oxide (NO) is a pleiotropic actor of signaling cascades in eukaryotes (Baudouin, 2011; Martínez-Ruiz et al, 2011)
For instance long chain bases (LCB) and Cer participate in the induction and/or control of plant cell death as illustrated by several studies in which LCB/Cer content was modified by exogenous treatments or the disruption of key genes of SL metabolism (Liang et al, 2003; Lachaud et al, 2010; Saucedo-Garcia et al, 2011; Ternes et al, 2011)
phospholipase Dα1 (PLDα1) is a target for LCB-P that stimulate PtdOH synthesis (Guo and Wang, 2012). This apparent simplicity turns to complexity when considering that (i) PtdOH generated by PLDα1 interacts with and further stimulates the LCB kinase sphingosine kinase 1 (SPHK1) (Guo et al, 2012) and (ii) that a abscisic acid (ABA)-triggered NO production is required for the activation of Phospholipase Dδ and PtdOH synthesis (Distéfano et al, 2012)
Summary
Nitric oxide (NO) is a pleiotropic actor of signaling cascades in eukaryotes (Baudouin, 2011; Martínez-Ruiz et al, 2011). Best documented are signaling functions for the precursors of complex SL, i.e., LCB and Cer. For instance LCB and Cer participate in the induction and/or control of plant cell death as illustrated by several studies in which LCB/Cer content was modified by exogenous treatments or the disruption of key genes of SL metabolism (Liang et al, 2003; Lachaud et al, 2010; Saucedo-Garcia et al, 2011; Ternes et al, 2011). Noteworthy complex membrane-located SL participate in pathogen-triggered cell death (Wang et al, 2008).
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