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CELL BIOLOGY AND SIGNAL TRANSDUCTION

A Mitogen-Activated Protein Kinase Signals to Programmed Cell Death Induced by Self-Incompatibility in Papaver Pollen^1,[OA]

Shutian Li², Jozef amaj and Vernonica E. Franklin-Tong^*

School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom (S.L., V.E.F.-T.); Institute of Cellular and Molecular Botany, University of Bonn, 53115 Bonn, Germany (J..); and Institute of Plant Genetics and Biotechnology, Slovak Academy of Sciences, 950 07 Nitra, Slovak Republic (J..)

Self-incompatibility (SI) in higher plants is an important mechanism to prevent inbreeding and involves specific rejection of incompatible ("self") pollen. In field poppy (Papaver rhoeas), S proteins encoded by the stigma component of the S-locus interact with incompatible pollen, resulting in cessation of tip growth. This "self" interaction triggers a Ca²⁺-dependent signaling network, involving programmed cell death (PCD). We previously identified p56, a mitogen-activated protein kinase (MAPK) that is activated during the SI response in incompatible pollen. Here, we show that p56 cross-reacts with AtMPK3, but not with AtMPK4 or salicylic acid-induced protein kinase antibodies. We provide good evidence that a MAPK is involved in initiation of SI-induced PCD in incompatible pollen. SI rapidly reduces pollen viability and the MAPK cascade inhibitor U0126, which prevents the SI-induced activation of p56 in incompatible pollen, "rescues" incompatible pollen, while its negative analog, U0124, does not. This strongly implicates the involvement of a MAPK in SI-mediated loss of pollen viability and cell death. SI also stimulates caspase-3-like (DEVDase) activity and later DNA fragmentation. Both these markers of PCD are significantly reduced by pretreatment with U0126, implicating the involvement of a MAPK in signaling during early PCD. As p56 appears to be the only MAPK activated by SI, our studies imply that p56 could be the MAPK involved in mediating SI-induced PCD.

² Present address: Department of Molecular Plant Genetics, Max Planck Institute for Plant Breeding Research, Carl-von-Linné-Weg 10, 50829 Cologne, Germany.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Vernonica E. Franklin-Tong (v.e.franklin-tong{at}bham.ac.uk).

^[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.107.101741

^* Corresponding author; e-mail v.e.franklin-tong{at}bham.ac.uk.

Received May 9, 2007; accepted July 17, 2007; published July 27, 2007.

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