ms23 and ms35 are alleles of the same gene that maps to chromosome 8

--Trimnell, MR, Fox, TW, Albertsen, MC

As we reported in MNL 76:37-38, ms23 and ms35 were found to be allelic, although their reported map locations indicated they were not on the same chromosome (see MNL 62:71 and MNL 69:126–128). In our 1999 Hawaii winter nursery, a family segregating for the ms35-6011 mutation was sampled for SSR mapping (described in MNL 76:38) to confirm the mutant’s reported map location on 9L (MNL 69:126–128). Results of our SSR mapping showed linkage with two markers, both of which map to chromosome 8. To verify this linkage, the segregating ms35 family was replanted in a subsequent nursery and re-sampled for mapping. Again, the same two chromosome 8 markers showed linkage. Below is the composite data for these two mapping experiments.

Marker Recomb. Alleles Mutant Plants % Recombination
umc1075 19 44 21.6
bnlg1194 29 38 26.3


These data show that, although not tightly linked to the SSR markers in this population, the ms35 mutation maps on chromosome 8, not the long arm of chromosome 9 as previously reported. To confirm this map position, a family segregating for the ms23 mutant (allelic to ms35-6011) also was sampled for SSR mapping. As shown below, the same two chromosome 8 markers with linkage to the ms35-6011 allele also were linked to the ms23 allele. The differences in % recombination result from a smaller sample size and from the two alleles being in different mapping populations. The key point is that two independent populations show linkage of a male sterile allele with the same two SSR markers on chromosome 8.

Marker Recomb. Alleles Mutant Plants % Recombination
umc1075 3 23 6.5
bnlg1194 4 24 8.3


Independently, but concurrently with the ms23 and ms35-6011 mapping studies, we mapped a previously unmapped male-sterile mutant, ms*-6059 (described by the late Dr. Earl Patterson in MNL 69:126–128), to chromosome 8. It showed linkage with the umc1075 SSR marker (% Recombination = 16.7). This mutant was testcrossed with ms23 in our 2001 Hawaii winter nursery. The progeny were grown in our 2002 Johnston nursery, and the mutants were found to be allelic (data shown below). In each testcross, the female parent was homozygous recessive for the indicated allele, and the male parent was heterozygous.

Female Male Progeny   χ2(1:1, P>0.050=3.84)
ms*-6059 ms23 37 Fertiles 40 Steriles 0.12
ms23 ms*-6059 21 Fertiles 12 Steriles 2.45


We conclude that ms*-6059 is allelic to ms23, and that its proper allelic designation is ms23-6059. We also conclude that results of the allelism tests with ms23, ms23-6059, and ms35-6011, coupled with the mapping of these mutations in three different mapping populations that show linkage to the same markers on the same chromosome, indicate that ms23, ms23-6059, and ms35-6011 are alleles of the same gene that maps to chromosome 8. We propose that subsequent gene lists show ms23 = ms35. The following male-sterile alleles currently represent the same gene family: ms23; ms23-6059; ms35-6011; ms35-6018; ms35-6027; ms35-6031.

The question remains as to how two different sets of A-B interchanges could have led to an error in the chromosome placement of two different alleles. One answer would involve analyzing these interchange stocks with SSR’s to determine the actual chromosome composition of the interchanged chromosomes, if these stocks were still available. This would reveal whether there had been additional rearrangements that might have involved chromosome 8 and that previously had been undetected. If this were true, then perhaps the ms23 alleles are located in such a region. Otherwise, this points out the caution that should be applied to mapping data obtained without independent corroboration.