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This article in CS

  1. Vol. 46 No. 4, p. 1456-1461
    Received: July 22, 2004

    * Corresponding author(s): Jijun.Zou@pioneer.com
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SSR Markers Exhibit Trisomic Segregation Distortion in Soybean

  1. J. J. Zou *a,
  2. R. J. Singhd,
  3. J. Leec,
  4. S. J. Xub and
  5. T. Hymowitzd
  1. a Pioneer Hi-Bred International, Inc., Johnston, IA 50131
    d Department of Crop Sciences, University of Illinois, Urbana, IL 61801
    c Genetic Resources Division, National Institute of Agricultural Biotechnology, Suweon, 441-701, South Korea
    b USDA-ARS, Northern Crop Science Laboratory, Fargo, ND 58105


A primary trisomic (2n = 2x + 1) is an excellent cytogenetic tool to locate genes and associate linkage groups to their respective chromosomes in diploid plant species. In soybean [Glycine max (L.) Merr.], 11 molecular linkage groups (MLGs) were previously assigned to their respective chromosomes using simple sequence repeat (SSR) markers and primary trisomics. The chromosome location of the SSR markers was determined by altered segregation ratios from a disomic (1:2:1) to a trisomic genotypic ratio (6:11:1) in the F2 offspring derived from the crosses of soybean primary trisomics and G. soja Siebold & Zucc. In this study, we established the association between soybean Triplo 4 and MLG C1 based on trisomic segregation ratio (6:11:1) and cytological analysis. In addition, we identified four SSR markers that exhibited trisomic segregation distortion on three soybean chromosomes. Those SSR markers, including Satt565 and SOYGPATR on chromosome 4 (MLG C1), Satt193 on chromosome 13 (MLG F), and Satt226 on chromosome 17 (MLG D2) segregated in a 1:11:6 ratio, which is the reverse of the standard trisomic genotypic ratio. This is the first report of trisomic segregation distortion in soybean. Since G. max and G. soja usually differ either by a reciprocal translocation or by a paracentric inversion, we hypothesize that the genomic divergence between the two species and the numerically unbalanced genome in the trisomics might contribute to the distorted trisomic ratios. Genome instability may have been triggered in F1 primary trisomics causing unexpected trisomic inheritance in F2 Our results indicate that both normal and distorted trisomic segregation ratios should be considered when analyzing the association between chromosomes and linkage groups using primary trisomic analysis.

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