Journal of Experimental Botany, Vol. 54, No. 380, pp. 141-148,
January 1, 2003
© 2003 Oxford University Press
Signals and targets of the self-incompatibility response in pollen of Papaver rhoeas
Received 12 April 2002; Accepted 14 June 2002
School of Biosciences, University of Birmingham, Edgbaston B15 2TT, UK
1 To whom correspondence should be addressed. fax: +44 (0)121 414 5925. E-mail: V.E.Franklin-Tong{at}bham.ac.uk
2 Present address: Institut für Pflanzenbiochemie, Weinberg 3, D-06120 Halle/Saale, Germany.
Self-incompatibility (SI) in Papaver rhoeas involves an allele-specific recognition between stigmatic S-proteins and pollen, resulting in inhibition of incompatible pollen. A picture of some of the signalling events and mechanisms involved in this specific inhibition of pollen tube growth is beginning to be built up. This highly specific response triggers a Ca2+-dependent signalling cascade in incompatible pollen when a stigmatic S-protein interacts with it. Rapid increases in cytosolic free Ca2+ concentration ([Ca2+]i) can now be attributed (at least in part) to Ca2+ influx. The rapid loss of the pollen apical Ca2+ gradient within 
1–2 min is accompanied by the inhibition of pollen tube tip growth. Concomitant with this time-frame, hyper-phosphorylation of p26, a soluble pollen phosphoprotein is detected. Characterization of p26 reveals that it is a soluble inorganic pyrophosphatase, which suggests a possible direct functional role in pollen tube growth. Slightly later, a putative MAP kinase (p52) is thought to be activated. Finally, preliminary evidence that programmed cell death (PCD) may be triggered in this response is described. A key target for these signals, the actin cytoskeleton, has also been identified. In this article the current understanding of some of the components of this signalling cascade and how they are beginning to throw some light on possible mechanisms involved in this SI-induced inhibition of pollen tube growth, is discussed.
Key words: Ca2+ signalling, MAPK, phosphorylation, pollen, programmed cell death (PCD), self-incompatibility (SI), signal transduction.
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