In the recent linkage map collated by Coe the order and map position
in the distal part of 10L is given as follows:
The map positions enclosed in parentheses indicate tentative assignments. Our data suggest that some revision be considered. First, l2 is not beyond sr2. The evidence for this statement comes from our studies with Df K10(H) and (K). Seedlings homozygous for either of these chromosomes are green; later they become green-white striped due to the deficiency of Sr2 but this phenotype is not expressed until the plants approach maturity. Homozygous deficient plants should manifest a mutant phenotype, similar to that produced by a recessive allele, for all loci included in the deficiency. For example, Df K10(F) is deficient for the segment containing W2 and Sr2. Homozygous deficient seedlings were white as are hemizygous w2/Df and w2/w2 seedlings. However, seedlings homozygous for Df K10(H) or for Df K10(K) are not white, virescent, glossy, luteus, or dwarf indicating that no dominant alleles of these seedling traits are in the segment of K10 distal to the Sr2 locus. The failure of the homozygous deficient plants to show the luteus phenotype demonstrates that the L2 locus is not distal to Sr2, at least in the K10 chromosome. The data also indicate that Sr2 is situated near the K10 knob since no mutant effects have been observed in seedlings homozygous deficient for any euchromatin which may be distal to Sr2.
Second, since the l2 mutant has been lost, we suggest that the l13 mutant, which was accurately located by P. Mascia (1978 Maize News Letter) 4.5 map units to the left of Sr2 at map position 87, replace l2. Whether or not L13 and L2 are allelic cannot be ascertained since no stocks with l2 are extant.
The o7 locus is given in the above map as 7 crossover units distal to w2. This may be the correct order in N10 chromosomes but we have some reservations in accepting this placement. The o7 locus may be flanked by w2 and sr2 but this order is based on 2-point data from crosses of different stocks which could well differ in recombination frequency. We attempted to order o7 with respect to R and w2 using F2 data where all three loci were segregating, but modifiers affecting the o7 phenotype made accurate scoring impossible. In our 1980 News Letter article we stated that the o7 locus appeared to lie to the left of w2 since the dominant allele was retained by the Df K10(F) chromosome when the W2 and Sr2 loci were lost. After three backcrosses to the o7 tester to eliminate modifying genes which inhibited the expression of the opaque trait, we are convinced that the Df K10(F) chromosome, deficient for W2 and Sr2, does indeed possess the dominant allele of the o7 locus and that the linear order in the K10 chromosome is R O7 W2 Sr2. Either the accepted linear order in N10 is wrong or the w2 o7 segment has been inverted in the K10 chromosome. Studies in progress involving three point linkage tests in N10 should reveal which alternative is correct.
M. M. Rhoades and Ellen Dempsey
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