Abstract

Segregation distortion has been reported repeatedly in soybean (Glycine max [L.] Merr.) inbred line populations segregating for the soybean cyst nematode (SCN) (Heterodera glycines Ichinohe) resistance gene rhg1. In each reported case, the frequency of the SCN resistance allele at the rhg1 locus was lower than expected. Segregation distortion was studied in 51 F4 populations by counting the number of plants predicted to be homozygous resistant, susceptible, and heterozygous for rhg1 based on the genetic markers Satt309, CTA, or TMA5. Significant (P<0.05) segregation distortion was observed in 44 out of the 51 F4 populations. When the heterozygotes were ignored, there were significantly fewer homozygous-resistant plants than expected in 33 populations. To study whether differential field emergence was a cause of the segregation distortion, three near isogenic line (NIL) populations segregating at the rhg1 locus for SCN resistance from plant introduction 88788 were tested. Population sizes ranged from 32 to 44 NILs and emergence was determined in field experiments in three environments. In each population, SCN-resistant NILs had significantly (P<0.05) less field emergence than susceptible NILs. In the population with the greatest effect, field emergence of resistant NILs was 6% less than susceptible NILs, with the entire population having an average emergence rate of 46%. Equations were derived to describe the effect of selection on segregation ratios over generations of population development and the observed emergence rates were transformed into fitness factors. Depending on assumptions of gene action, it was predicted from these fitness factors that segregation distortions were in the range of those reported previously for the rhg1 locus and were similar to what was observed on average across the 51 F4 populations. While other factors might also be involved, the results suggest that reduced field emergence associated with the SCN resistance allele contributes to previously reported segregation distortion at the rhg1 locus.

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