--Albertsen, MC; Fox, TW and Trimnell, MR
I was fortunate to have met and visited in 1987 with the well known maize geneticist and plant breeder, Prof. C. H. Li (now deceased), from the Peoples Republic of China. He was another of those individuals who had an incredible wealth of knowledge about maize. Our conversation eventually came around to the subject of maize male sterility. I mentioned to him that I was interested in receiving as many male-sterile mutations as I could so as to better understand the process of pollen development in maize. A year or so later he sent me a few seeds of a new male-sterile mutant he had found. He attached the following note, originally written in his handwriting.
"This new male sterile gene was first found in 1978 and proved to be nonallelic to ms2, ms10, and ms1. By using a T4-9(5657) stock which has breakpoints at 4L.33 and 9S.35 and the su1 in the linkage test, I obtained 5-6% crossover between su--T and 8-13% between T--ms(L) from different sets of the tested material. From the su-seeds I provided herewith, you will get mostly male steriles as non-crossovers, and from Su-kernel(s) mostly heterozygote translocations, t/T, which are to be readily identified from pollen examination. The identification of ms t/T genotype (any crossovers) can be made by the seed set only (semi-steriles)..."
I do not know the origin of the material, other than that it was from a 1987 source. Of the Su kernels that we planted, we obtained eight male fertiles and four male steriles. From the su kernels, we obtained one male fertile and 10 male steriles. The mutant segregated as a single recessive allele on chromosome 4. We knew that there were no recessive male sterile mutants currently described on chromosome 4 and that this was likely a new genetic male sterile. To verify and to further develop bulk segregant analysis, we crossed this mutant (our designation ms*-LI89) with A632 and selfed the progeny. Equal amounts of DNA from 20 male-fertile plants and DNA from 20 male-sterile plants from the self were pooled according to fertility classification. Each pool was digested with BamHI, EcoRV, and HindIII, run on a gel, and southern blotted. Initially, two RFLP markers on each arm of chromosome 4 were used to screen the southern blots. Both probes from 4L, bnl7.65 and php20608, gave polymorphisms with at least one enzyme. Two additional probes from 4L, umc15 and umc19, also gave polymorphisms. To confirm and narrow down the map location, blots were made using DNA from the individuals that comprised each bulk. The data indicated that the allele responsible for male sterility is between RFLP markers umc158 and umc15 on chromosome 4L.
Based on Prof Li's genetic tests and our molecular work, we normally would propose a new ms-designation for this mutant. There are, however, two dominant male-sterile mutations on chromosome 4, Ms41 and Ms44. They originally were distinguished from each other by virtue of the ability of Ms41 to shed a small amount of pollen in certain environments, and this pollen being used to conduct an allelism test with Ms44 (Albertsen and Neuffer, MNL 64:52, 1990). The suggested location of ms*-LI89 by our molecular analysis placed it provocatively close to Ms44. Although there is no instance to date of a dominant male-sterile mutant and a recessive male-sterile mutant being allelic, we did not want to make a definite call until we conducted further linkage tests. Suggestions as to how to proceed are welcomed.
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