THE SELF-INCOMPATIBILITY PHENOTYPE IN BRASSICA IS ALTERED BY THE TRANSFORMATION OF A MUTANT S-LOCUS RECEPTOR KINASE

Citation
Rj. Stahl et al., THE SELF-INCOMPATIBILITY PHENOTYPE IN BRASSICA IS ALTERED BY THE TRANSFORMATION OF A MUTANT S-LOCUS RECEPTOR KINASE, The Plant cell, 10(2), 1998, pp. 209-218
Citations number
33
Categorie Soggetti
Plant Sciences",Biology,"Cell Biology
Journal title
ISSN journal
10404651
Volume
10
Issue
2
Year of publication
1998
Pages
209 - 218
Database
ISI
SICI code
1040-4651(1998)10:2<209:TSPIBI>2.0.ZU;2-P
Abstract
The self-incompatible (SI) Brassica napus line W1, which carries the 9 10 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 virtua lly 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 s uppression. Furthermore, the expression of the S locus glycoprotein ge ne 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 suppr essed. When the transgene was crossed into another SI line carrying th e A14 S allele, it was also capable of suppressing the expression of t he 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 tr ansgene 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 re quired, but only for the stigma side of the SI phenotype, and that a s ingle transgene can alter the SI phenotype of more than one S allele.