Our ongoing study of the genetic control of maysin synthesis in maize silks has included QTL analysis of four populations to date (see Byrne et al., Proc. Natl. Acad. Sci. USA 93:8820-8825, 1996, for details of methodology). The most striking consistency is the detection in each population of a region on chromosome 9S significantly associated with maysin concentration (Table 1). The position of peak significance varied somewhat, but always fell in bin 9.02, between bz1 and wx1. In each case, the QTL has displayed dominance to partial dominance for low maysin concentration. The homozygous recessive genotype in this region has given a sizable boost in maysin level over the homozygous dominant genotype, ranging from a 49% increase in (GE37 x FF8) F2:3 grown at Columbia, MO to a 111% increase in (GE37 x Mp464) F2 (Table 1). The high-maysin allele was detected in three inbred lines (GT119, NC7A, and GE37), suggesting that it is fairly common in Southern U.S. germplasm. We currently have three main hypotheses to explain the nature of the gene on 9S:
1) We have previously proposed (Byrne et al., Proc. Natl. Acad. Sci.
USA 93:8820-8825,1996), that the 9S locus is brown pericarp1, which
we hypothesized to be a structural gene in the pathway leading to 3-deoxyanthocyanins.
The homozygous recessive genotype blocks a step in that pathway, resulting
in a shunting of intermediates to the flavone (maysin) pathway.
2) The gene on 9S is a negative regulator (inhibitor) of p1 expression. In the homozygous recessive class, this inhibition is released, resulting in enhanced p1 expression and hence, an increase in p1-controlled structural genes.
3) The 9S locus is a transcription factor that competes with or inhibits P1 protein from binding or activating the structural genes required for flavone synthesis. An analogy for this may be the IN1 protein which has sequence similarity to MYC-class transcription activators and down-regulates many of the structural genes of the anthocyanin pathway (Burr et al., Plant Cell 8:1249-1259, 1996). In addition, the MYB-homologous zm38 gene has been shown to inhibit transcriptional activation of the a1 promoter in the presence of functional C1 protein in transient expression assays (Franken et al., Plant J. 6:21-30, 1994). Experiments to differentiate among these hypotheses are currently underway.
Based on the consistent expression of an apparently single QTL for enhanced maysin in all four populations examined, we wish to designate the corresponding genetic factor as rem1 (recessive enhancer of maysin1), pending allelism tests with verified brown pericarp1 stocks, if these become available.
Table 1. Genotype class means at chromosome 9S loci for silk maysin
concentration in four populations. All trials were grown in Columbia, MO,
except for population (GE37 x FF8) F2:3, which was grown both in Columbia,
MO and Tifton, GA.
|(GT114 x GT119) F2||% maysin (umc105a)*|
|(GT114 x NC7A) F2||% maysin (wx1)|
|(GE37 x Mp464) F2||% maysin (bz1)|
|(GE37 x FF8) F2:3||% maysin, MO (wx1)||% maysin, GA (wx1)|
|FF8||0.35 a||0.24 a|
|GE37/FF8||0.39 a||0.29 a|
|GE37||0.52 b||0.42 b|
*Loci in parentheses showed highest significance level. Indicated loci
are on chromosome 9S in the order bz1 - umc105a - wx1.
bz1 and wx1 ranges from 20 to 30 cM.
¶For a given population and trait, means followed by the same letter are not significantly different at P<0.05.<
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