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Reference Report for IND21977166
Title:Recombination and linkage estimation between the k2 and Mdh1-n y20 loci in soybean.
Authors:Chen, X.F., Palmer, R.G.
Source:J. Hered. 1998, 89(6):488-494
Abstract:Tan saddle seed coat (k2), mitochondrial malate dehydrogenase 1 null (Mdh1-n), and yellow foliage (y20) are three mutant phenotypes in soybean [Glycine max (L.) Merr.] that are conditioned by three closely linked but distinct genetic loci-k2, Mdh1-n, and y20, respectively. In this report, genetic recombinations were examined between the k2 and the Mdh1-n y20 loci in repulsion phase and among the k2, Mdh1-n, and y20 loci in coupling phase. Reduced viability with the yellow foliage plants was evident in all F2 cross combinations in both coupling and repulsion phases. However, the segregation of the homozygous green to heterozygous green F2 plants fit a 1:2 ratio, suggesting that the putative deletion mutations at the k2, Mdh1-n, and y20 loci did not affect the transmissibility of the mutant chromosome. Recombination rates of approximately 55-60% between the k2 and Mdh1-n y20 loci were estimated by Kuspira and Bhambhani's (1984) square root approach in repulsion phase in F2 plants derived from crossing T323 (Mdh1-n y20), T324 (Mdh1-n y20), and T325 (Mdh1-n y20) with T239 (k2) and L67-3483 (k2). However, no recombination among the k2, Mdh1-n, and y20 loci was detected in coupling phase in the estimated total of 13,187 F2 plants. The excess of the recombinants in repulsion phase in F2 plants was considered to be the result of breakage at the k2 Mdh1 Y20 chromosomal region in T239 and L67-3483 when the Mdh1-n y20 loci were introduced into the T239 and L67-3483 genetic backgrounds. In contrast, no recombinants were identified in repulsion phase in 455 F2 yellow foliage plants derived from the crosses of T317 (Mdh1-n y20) with T239 (k2) and L67-3483 (k2). However, an approximately 3.04 +/- 0.48% recombination rate was estimated between the k2 and Mdh1-n y20 loci in a total of 677 F2:3 families with tan saddle seed coat derived from crossing T317 (Mdh1-n y20) with T239 (k2) and L67-3483 (k2). Our data suggests that the mutation in T317 is different from that in T323, T324, and T325.






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