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Published on July 27, 2007; 10.1104/pp.107.101741

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Received May 9, 2007
Accepted July 17, 2007

A MAPK Signals to Programmed Cell Death Induced by Self-Incompatibility in Papaver Pollen

Shutian Li , Jozef Samaj , and Vernonica E. Franklin-Tong *

School of Biosciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, U.K; Institute of Cellular and Molecular Botany, University of Bonn, Kirschallee 1, 53115 Bonn, Germany; Institute of Plant Genetics and Biotechnology, Slovak Academy of Sciences, Akademicka 2, 950 07 Nitra, Slovak Republic

* Corresponding author; email: V.E.Franklin-Tong{at}bham.ac.uk.

Self-incompatibility (SI) in higher plants is an important mechanism to prevent inbreeding and involves specific rejection of incompatible ("self") pollen. In 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 crossreacts with AtMPK3, but not with AtMPK4 or SIPK 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 the 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 a 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.




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