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Reversion of Male-Sterile T-Cytoplasm Maize to Male Fertility in Tissue Culture¹

This study was conducted to determine the inheritance of altered traits in plants regenerated from Texas male-sterile cytoplasm (T) maize (Zea mays L.) tissue cultures. Plants were regenerated from AlSSTcms (rflrf1;Rf2Rf2) tissue cultures grown on control media or on media containing different levels of streptomycin. Of 169 regenerated plants, eight expressed unexpected changes to male fertility and/or resistance to Helminthosporium maydis pathotoxin even though the cultures had not been selected for pathotoxin resistance. The male fertility and disease resistance traits had a cytoplasmic mode of inheritance. Two regenerated plants were male fertile and toxin susceptible, but their first generation progeny were either male fertile and resistant or male sterile and susceptible. Some regenerated plants apparently were chimeric for two cytoplasm conditions, one causing male fertility and toxin resistance and the other causing male sterility and toxin susceptibility. Mitochondrial DNA (mtDNA) was extracted from six variant lines and analyzed by restriction enzyme digestion and agarose gel electrophoresis. Five of the six variants were distinguishable from control A188Tcms (rflrfl;Rf2Rf2) by virtue of an alteration(s) in a mtDNA sequence of about 6,600 base pairs (6.6 Kb). A 6.6 Kb fragment characteristic of A188Tcms (rflrfl-Rf2Rf2) mtDNA was not detected in the five variant lines when mtDNA was digested with the restriction enzyme Xhol; however, no difference could be detected between the sixth variant line and A188Tcms (rflrfl-Rf2Rf2). A possible relationship between the mtDNA changes and the cytoplasmically controlled changes to male fertility and toxin resistance is proposed.

Key Words: Corn • Zea mays L. • Southern corn leaf blight resistance • Mitochondrial DNA

² Formerly graduate research assistant (now research associate, Dep. of Plant and Soil Science, Univ. of Tennessee, Knoxville, TN 37996) and professor.

Received for publication April 26, 1982.

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