Mutator-tagged defective kernel mutants as putative QTL for kernel size

--M.Lee, L.Veldboom, M.Scanlon, A.Myers, M.James and D.Robertson

Mutator-induced defective kernel mutants are being pursued in order to investigate their role in kernel growth and development and to test an hypothesis regarding the relationship between qualitative and quantitative genetic variation (see D. Robertson, J. Theor. Biol. 117:1-10, 1985; T. Helentjaris and D. Shattuck-Eidens, MNL. 61:88-89, 1987). In this note, we describe initial results of the test of the possible contribution of dek mutants to quantitative genetic variation for kernel size.

Briefly, Robertson's hypothesis states that a locus may contribute to quantitative or qualitative variation for a trait depending upon the allelic forms at the locus. For example, null alleles would presumably represent qualitative Mendelian variation while functional alleles of the same locus, perhaps coding for more or less effective or efficient gene products, contribute to quantitative genetic variation (quantitative trait loci, QTL) by differences in degree of trait expression. If true, the hypothesis further suggests the swiftest, surest routes to understanding the genetic basis of many polygenic traits, identifying and characterizing key genetic factors, may be created through studies of genetically well-defined, easily characterized mutants. While the basis of the hypothesis may seem obvious, and perhaps trivial, obtaining physical and genetic evidence has been difficult. With the advent of maize RFLP mapping and more routine transposon tagging coupled with decades of maize genetic research, such evidence may be within reach.

To test the hypothesis, Mutator-induced dek mutants will be tagged and cloned. The clones will be used as probes, mapped relative to known, previously placed RFLP probes and evaluated for their contribution to kernel size in RFLP analysis of an F2 population created by crossing inbreds with relatively large differences for kernel size (Mo17 and H99; 95 and 50 grams per 300 kernels, respectively). To date, two dek mutants have been tagged, dek*-807 and dek*-1047, and co-segregating genomic clones have been obtained.

The deks have been mapped genetically through RFLP mapping and physically using B-A translocations. RFLP mapping with MAPMAKER located dek*-807 to chromosome 5, 8 cM distal to UMC51 and 12 cM proximal to UMC68. dek*-1047 was placed to chromosome 2, 9 cM distal to PIO1012 and 14 cM proximal to UMC131. Chromosome placement of dek*-1047 was in agreement with the physical location revealed by the translocations (see note by M. Scanlon et al. - this issue). Molecular and biological characterizations of dek*-807 and dek*-1047 are in progress.

The chromosome regions defined by the dek clones and other adjacent RFLP loci will be evaluated for their contribution to genetic variation for kernel size among 150 F3 families derived from the Mo17/H99 F2 population. Initial analysis indicated the dek clones may be identifying loci or chromosome regions affecting kernel size. Comparison of average kernel weight (gms/300k) for the three genotypic classes (H99/H99, Mo17/H99, Mo17/Mo17) revealed the following: 76, 77, and 79gms/300k for dek*-807 and 75, 78, and 79 gms/300k for the dek*-1047 probe. While these differences are clearly very small, the trend is in agreement with the hypothesis. Additional statistical analyses of traits possibly affecting kernel size and of RFLP probes in regions linked and unlinked to dek*-807 and dek*-1047 are in progress. The dek clones will be evaluated in other populations. Also, other dek mutants are being tagged and cloned. The availability of Mutator-induced mutants for other traits, such as plant height, may allow us to extend our investigation of the molecular and biological basis of the relationship between qualitative and quantitative genetic variation.


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