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Genetics of distyly and homostyly in a self-compatible Primula.
- Source :
-
Heredity [Heredity (Edinb)] 2019 Jan; Vol. 122 (1), pp. 110-119. Date of Electronic Publication: 2018 May 04. - Publication Year :
- 2019
-
Abstract
- The transition from outcrossing to selfing through the breakdown of distyly to homostyly has occurred repeatedly among families of flowering plants. Homostyles can originate by major gene changes at the S-locus linkage group, or by unlinked polygenic modifiers. Here, we investigate the inheritance of distyly and homostyly in Primula oreodoxa, a subalpine herb endemic to Sichuan, China. Controlled self- and cross-pollinations confirmed that P. oreodoxa unlike most heterostylous species is fully self-compatible. Segregation patterns indicated that the inheritance of distyly is governed by a single Mendelian locus with the short-styled morph carrying at least one dominant S-allele (S-) and long-styled plants homozygous recessive (ss). Crossing data were consistent with a model in which homostyly results from genetic changes at the distylous linkage group, with the homostylous allele (S <superscript>h</superscript> ) dominant to the long-styled allele (s), but recessive to the short-styled allele (S). Progeny tests of open-pollinated seed families revealed high rates of intermorph mating in the L-morph but considerable selfing and possibly intramorph mating in the S-morph and in homostyles. S-morph plants homozygous at the S-locus (SS) occurred in several populations but may experience viability selection. The crossing data from distylous and homostylous plants are consistent with either recombination at the S-locus governing distyly, or mutation at gene(s) controlling sex-organ height; both models predict the same patterns of segregation. Recent studies on the molecular genetics of distyly in Primula demonstrating the hemizygous nature of genes at the S-locus make it more likely that homostyles have resulted from mutation rather than recombination.
Details
- Language :
- English
- ISSN :
- 1365-2540
- Volume :
- 122
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Heredity
- Publication Type :
- Academic Journal
- Accession number :
- 29728676
- Full Text :
- https://doi.org/10.1038/s41437-018-0081-2