Abstract
Previously, an interspecific cross between Fusarium circinatum and Fusarium subglutinans was used to generate a genetic linkage map. A ca. 55 % of genotyped markers displayed transmission ratio distortion (TRD) that demonstrated a genome-wide distribution. The working hypothesis for this study was that TRD would be non-randomly distributed throughout the genetic linkage map. This would indicate the presence of distorting loci. Using a genome-wide threshold of α = 0.01, 79 markers displaying TRD were distributed on all 12 linkage groups (LGs). Eleven putative transmission ratio distortion loci (TRDLs), spanning eight LGs, were identified in regions containing three or more adjacent markers displaying distortion. No epistatic interactions were observed between these TRDLs. Thus, it is uncertain whether the genome-wide TRD was due to linkage between markers and genomic regions causing distortion. The parental origins of markers followed a non-random distribution throughout the linkage map, with LGs containing stretches of markers originating from only one parent. Thus, due to the nature of the interspecific cross, the current hypothesis to explain these observations is that the observed genome-wide segregation was caused by the high level of genomic divergence between the parental isolates. Therefore, homologous chromosomes do not align properly during meiosis, resulting in aberrant transmission of markers. This also explains previous observations of the preferential transmission of F. subglutinans alleles to the F1 progeny.
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Acknowledgments
This work was supported by the National Research Foundation (NRF), University of Pretoria, Forestry and Agricultural Biotechnology Institute (FABI), the DST/NRF Center of Excellence in Tree Health Biotechnology (CTHB), members of the Tree Protection Co-operative Programme (TPCP), and the Andrew Mellon Foundation.
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De Vos, L., van der Merwe, N.A., Wingfield, M.J. et al. Transmission ratio distortion in an interspecific cross between Fusarium circinatum and Fusarium subglutinans . Genes Genom 35, 177–183 (2013). https://doi.org/10.1007/s13258-013-0066-8
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DOI: https://doi.org/10.1007/s13258-013-0066-8