Self-incompatibility signalling networks and identification of the pollen S-determinant: PrpS
Prof. Vernonica Franklin-Tong University of Birmingham Sponsored by VH BIO
Self-incompatibility (SI) is an important mechanism used by many higher plant species to prevent inbreeding. It is controlled by a multi-allelic S locus that allows discrimination between “self” (incompatible) pollen from “non-self” (compatible) pollen, which is allowed to fertilize the plant by interaction of pollen and pistil S locus components. In Papaver rhoeas, the pistil S locus product is a small ligand (S protein) which interacts with incompatible pollen. This triggers a Ca2+-dependent signalling network, resulting in pollen inhibition and programmed cell death (PCD), providing a neat way to get rid of unwanted incompatible pollen. I will review recent progress in elucidating mechanisms involved in mediating SI, which involves rapid depolymerization of the actin and microtubule cytoskeleton, phosphorylation of a soluble inorganic pyrophosphatase, Pr-p26.1, activation of a MAPK, p56, and PCD involving a DEVDase/caspase-3-like activity. I will describe important new data on our recent cloning and identification of PrpS, the Papaver pollen S locus determinant. PrpS is tightly linked to the pistil S gene and displays the polymorphism expected of an S locus component. PrpS encodes a ~20 kDa protein with three predicted transmembrane domains. Sequence analysis reveals that it represents a novel class of receptor, as it has no homology to proteins in existing databases. PrpS is associated with the plasma membrane, suggesting that it is likely to be a transmembrane receptor. Importantly, we have obtained evidence that PrpS is functionally involved in SI using PrpS antisense oligonucleotides to alleviate inhibition of incompatible pollen in an S-specific manner. Our identification of PrpS as the Papaver pollen S locus determinant represents a major advance in our understanding of SI and strongly supports our hypothesis that Papaver SI is triggered by a receptor-ligand interaction. Recent publications: 1. Poulter, N. S., Vatovec, S. and Franklin-Tong VE. (2008). Microtubules Are a Target for Self-Incompatibility Signaling in Papaver Pollen. Plant Physiol. 146, 1358-1367. 2. V. E. Franklin-Tong and C. W. Gourlay (2008). A role for actin in regulating apoptosis/programmed cell death -evidence spanning yeast, plants and animals. Biochemical Journal 413, 389-404. (publ. online 15 Jul 2008; cover date 01 Aug 2008). 3. M. Bosch, N. Poulter, S. Vatovec, S. Li & V. E. Franklin-Tong. (2008). Programmed Cell Death in self-incompatibility: suicide of “self” pollen involves several caspase-like activities. Molecular Plant: special issue on Plant Cell Biology. 4. Bosch M. & Franklin-Tong VE. (2007). Temporal and spatial activation of caspase-like enzymes induced by self-incompatibility in Papaver pollen. Proc. Natl. Acad. Sci. USA. 104 (46) 18327-18332. 5. S. Li, J. Samaj & V. E. Franklin-Tong. (2007). A MAP kinase signals to Programmed Cell Death induced by Self-Incompatibility in Papaver pollen. Plant Physiol 145, 236–245. 6. B.H.J. de Graaf, J.J. Rudd, M. J. Wheeler, R.M. Perry, E. M. Bell, K. Osman, F. C.H. Franklin & V. E. Franklin-Tong (2006). Self-incompatibility in Papaver targets soluble inorganic pyrophosphatases in pollen. Nature 444, 490-493. Selected for “Editor’s Choice” in Nature. 7. Thomas, S. Huang , S. Li, C.J. Staiger and V.E. Franklin-Tong. (2006). Actin depolymerization is sufficient to induce programmed cell death in self-incompatible pollen. S.G. Journal of Cell Biology 174, 221-229. **This article was selected for a highlight JCB “In This Issue” section and by Cell in a “Leading Edge” (Aug 11th 2006 issue of Cell). 8. Thomas, S.G. & Franklin-Tong, VE. (2004) Programmed Cell Death is triggered by self-incompatibility in Papaver pollen. Nature 429, 305-309. (Selected for Nature News & Views). Website link- http://www.biosciences.bham.ac.uk/About/staff_profiles_Research.htm?ID=16
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