Abstract
The objective of this study was to map quantitative trait loci (QTL) for the vernalization response in perennial ryegrass (Lolium perenne L.). The mapping population consisted of 184 F2 genotypes produced from a cross between one genotype of a synthetic perennial ryegrass variety “Veyo” and one genotype from the perennial ryegrass ecotype “Falster”. Veyo and Falster were chosen among four different populations because of their contrasting vernalization requirements. In total, five QTL for the vernalization response, measured as days to heading, were identified and mapped to linkage groups (LG) LG2, LG4, LG6 and LG7. Individually, these QTL explained between 5.4 and 28.0% of the total phenotypic variation. The overall contribution of these five QTL was 80% of the total phenotypic variation. A putative orthologue of Triticum monococcum VRN1 was amplified from genomic DNA from perennial ryegrass. PCR fragments covering the proximal part of the promoter and the 5′ end of the orthologue were subsequently PCR-amplified from both parents of the mapping population and shown to possess 95% DNA sequence identity to VRN1. Several polymorphisms were identified between Veyo and Falster in this fragment of the putative VRN1 orthologue. A CAPS marker, vrn-1, was developed and found to co-segregate with a major QTL on LG4 for the vernalization response. This indicates that the CAPS marker vrn-1 could be located in an orthologous gene of the wheat VRN1.
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Acknowledgements
The authors thank The Danish Directorate for Food, Fisheries and Agribusiness for financial support. We would like to thank Dr. Birte Boelt from DIAS for her advice regarding the development and phenotyping of the mapping population. Ann Johansen and Sanne Seval are thanked for excellent technical assistance, and Ole Braad Hansen for taking optimal care of the plants.
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Jensen, L.B., Andersen, J.R., Frei, U. et al. QTL mapping of vernalization response in perennial ryegrass (Lolium perenne L.) reveals co-location with an orthologue of wheat VRN1 . Theor Appl Genet 110, 527–536 (2005). https://doi.org/10.1007/s00122-004-1865-8
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DOI: https://doi.org/10.1007/s00122-004-1865-8