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Dep. of Agronomy, Univ. of Wisconsin-Madison, 53706
Dep. of Plant, Soil, and Insect Sciences, Univ. of Wyoming, Laramie, WY 82071
AgResearch Grasslands, New Zealand Pastoral Agriculture Research Inst., Palmerston North, New Zealand
* Corresponding author.
Greater complementary gene interaction in autotetraploid alfalfa (Medicago sativa L., 2n = 4x = 32) may explain differences in vigor and breeding behavior between diploids and autotetraploids. Complementary gene interaction is nonallelic gene interaction or epistasis where dominant alleles at heterozygous loci may complement each other by masking recessive alleles at respective loci. This paper describes how tetrasomic segregations of linkage blocks in linkage disequilibrium produce tetraploid individuals and populations with greater complementary gene interaction than is possible at the diploid level. This finding helps explain autotetraploid superiority and unique breeding behavior. Research on gene action in autotetraploid alfalfa has demonstrated that favorable alleles in linkage blocks underpin population improvement and increased heterosis. The individual favorable alleles with additive effects also contribute to non-additive complementary gene interactions in linkage blocks. Apparent multiple allelic interaction (overdominance) effects discussed in earlier studies inbreeding depression and progressive heterosis in alfalfa are due mainly to linkage disequilibrium, which agrees with findings in maize. The severe inbreeding depression in autotetraploids is due mainly to the rapid loss of complementary gene interactions in the first few generations of inbreeding. Correspondingly, the progressive heterosis of autotetraploids is due mainly to a progressive increase in complementary gene interactions. Greater complementary gene interactions in tetraploid alfalfa also helps explain recent DNA research indicating that yield in tetraploids is more responsive to genetic diversity than in diploids. Many differences between diploid and autotetraploid alfalfa reported in earlier studies now may be explained by inherent differences in the levels of complementary gene interactions.
Received for publication July 12, 1993.
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