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Plant Cell, Vol. 10, 209-218, Copyright © 1998, American Society of Plant Physiologists
The Self-Incompatibility Phenotype in Brassica Is Altered by the Transformation of a Mutant S Locus Receptor Kinase
Richard J. Stahla,
MaryAnne Arnoldob,
Tracy L. Glavina,
Daphne R. Goringc, and
Steven J. Rothsteina
a Department of Molecular Biology and Genetics, University of Guelph, Guelph, Ontario N1G 2W1, Canada
b Pioneer Hi-Bred Production Limited, Canola Research Station, 12111 Mississauga Road, Georgetown, Ontario L7G 4S7, Canada
c Biology Department, York University, 4700 Keele Avenue, North York, Ontario M3J 1P3, Canada
Correspondence to:
Steven J. Rothstein, srothste{at}uoguelph.ca (E-mail), 519-837-2075 (fax).
The self-incompatible (SI) Brassica napus line W1, which carries the 910 S allele, was transformed with an inactive copy of the 910 S locus receptor kinase (SRK) gene. Two transformed lines were analyzed based on their heritable ability to set self-seed. The first line was virtually completely self-compatible (SC), and reciprocal pollinations with the original W1 line demonstrated that only the stigma side of the SI phenotype was altered. An analysis of the expression of endogenous SRK-910 demonstrated that the mechanism of transgene action is via gene suppression. Furthermore, the expression of the S locus glycoprotein gene present in the 910 allele (SLG-910), SLG-A10, which is derived from a nonfunctional S allele, and an S locus–related gene were also suppressed. When the transgene was crossed into another SI line carrying the A14 S allele, it was also capable of suppressing the expression of the endogenous genes and of making this line SC. The second transgenic line studied was only partly SC. In this case as well, only the stigma phenotype was affected, although no gene suppression was detected for endogenous SRK-910 or SLG-910. In this line, the expression of the transgene most likely was causing the change in phenotype, and no effect was observed when this transgene was crossed into the other SI line. Therefore, this work reinforces the hypothesis that the SRK gene is required, but only for the stigma side of the SI phenotype, and that a single transgene can alter the SI phenotype of more than one S allele.
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