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This article in CS

  1. Vol. 28 No. 5, p. 792-795
    Received: Oct 28, 1987

    * Corresponding author(s):
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Mitomycin C- and Streptomycin-Induced Male Sterility in Cultivated Sunflower

  1. C. C. Jan  and
  2. J. N. Rutger
  1. U SDA-ARS, Dep. of Agronomy, North Dakota State Univ., Fargo, ND 58105
    U SDA-ARS, Dep. of Agronomy and Range Science, Univ. of California, Davis, CA 95616



Worldwide hybrid sunflower (Helianthus annuus L.) production depends on a single source of cytoplasmic male sterility (CMS). Additional CMS sources would reduce the genetic vulnerability associated with the use of a single cytoplasm. The objectives of these studies were to evaluate the effectiveness of mitomycin C and streptomycin in inducing CMS in cultivated sunflower, and to evaluate fertility restoration relationships of induced CMS mutants with various restoration lines. Seeds of inbred maintainer line HA 89 were treated with mitomycin C and streptomycin. Induced male sterility was classified in M, heads as sectorial, semisterile or complete and further verified by observing open-pollinated M2 heads in progeny rows. Untreated HA 89 produced no CMS mutants. 5, 50, and 500 mg L‒1 mitomycin C treatments resulted in four total confirmed CMS mutants and the 5, 50, 500, and 5 000 mg L‒1 streptomycin treatments produced 18 total confirmed CMS mutants. Progeny of the 22 induced CMS mutants and CMS HA 89 crossed with fertility restorers RHA 266, RHA 274, RHA 280, and RHA 296 were all fertile. Seven nuclear gene controlled male-sterile (NMS) mutants with monogenic recessive inheritance were also verified. Streptomycin was a more effective mutagen than mitomycin C for inducing CMS mutations in sunflower. The induced CMS mutants can be used readily for hybrid seed production without altering current fertility restoration systems, and could provide alternative male-sterile cytoplasm for sunflower hybrid production.

Contribution from USDA-ARS in cooperation with Dep. of Agronomy, Agric. Exp. Stn., North Dakota State Univ., Journal Article no. 1623.

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