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This article in CS

  1. Vol. 36 No. 5, p. 1153-1158
     
    Received: Nov 21, 1995


    * Corresponding author(s): j-harper@uiuc.edu
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doi:10.2135/cropsci1996.0011183X003600050015x

Genetic and Allelism Analyses of Hypernodulation Soybean Mutants from Two Genetic Backgrounds

  1. T. D. Vuong,
  2. C. D. Nickell and
  3. J. E. Harper 
  1. Dep. of Crop Sciences, Univ. of Illinois, Urbana, IL 61801
    Plant Physiology and Genetics Res. Unit, USDA-ARS and Dep. of Crop Sciences, Univ. of Illinois, 1201 W. Gregory Dr., Urbana IL 61801

Abstract

Abstract

Several chemically mutagenized lines of soybean [Glycine max (L.) Merr.] have shown enhanced nodulation and partial tolerance to high NO3 levels. Previous genetic analyses of hypernodulating or supernodulating soybean mutants indicated that they were genetically controlled by recessive monogenes following simple Mendelian principles. In the present study, we determined the genetic control of hypernodulating mutants selected from two soybean cultivars, Williams and Enrei, and analyzed the allelism of mutant genes controlling the hypernodulating phenotypes. Reciprocal crosses between four hypernodulating mutants (NOD1-3, NOD2-4, NOD4, and En6500) and two normally nodulated cultivars (Williams 82 and Harosoy 63) were made. The patterns of nodulation in F1s, F2s, and F2:3 progeny were visually evaluated at 14 d after planting in the greenhouse. Chi squares for each progeny and homogeneity tests for each cross were calculated. The results indicated that hypernodulation in the mutants studied was conditioned by single recessive genes. Three mutants (NOD1-3, NOD4, and En6500) were controlled by a single recessive allele rj7, although they were isolated from distinctly different genetic materials. The allelism study indicated that another non-allelic mutant gene was identified which was responsible for hypernodulation in mutant NOD2-4. This new gene has been tentatively designated rj8. With respect to genetic interaction between the two mutant genes identified, the segregation ratio in the F2 did not fit a classical pattern and therefore we speculated that these two genes interact to modify expression in an unknown fashion. Hence, additional genetic analysis is needed to clarify the genetic interaction between rj7 and the proposed rj8 gene.

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