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Sweet Corn
HORT410 - Vegetable Crops

Sweet Corn - Notes

  • Common name: sweet corn.
  • Latin name: Zea mays L. [some refer to sweet corn as a separate variety of corn: Zea mays L. var. rugosa (or saccharata].
  • Family name: Gramineae (Poaceae) [Poaceae Images].
  • Annual.
  • Monocotyledon.
  • Diploid (2n = 20).
  • Harvested organ: immature fruit [typically harvested 18 to 21 days after pollinating (DAP)].
  • Sweet corn history (TAMU).
  • Monoecious, with separate male and female flowers.
  • Warm season, frost-sensitive.
  • Differs from other corn types primarily for gene(s) that affect starch synthesis in the endosperm:
      • sugary (su) allele [strictly sugary1 (su1)] (located on chromosome 4S): elevates the level of the water-soluble polysaccharide (WSP), phytoglycogen, and decreases starch. Phytoglycogen is a highly branched polysaccharide and gives the endosperm of su1 varieties a smooth creamy texture (Tracy, 1993). The wild-type Su1 allele encodes starch debranching enzyme I. Dry kernels are wrinkled in appearance.
      • sugary enhancer (se) [strictly sugary enhancer 1 (se1)]: when in combination with the homozygous su1 allele results in increased sugar levels and WSP levels similar to unmodified su1, resulting in a high quality, sweet, creamy endosperm (Tracy, 1993). The se1 gene product is not yet known.
      • sugary2 (su2) (located on chromosome 6L) is thought to encode a starch branching enzyme. The recessive su2 allele causes a sugary, translucent kernel with a glassy, opaque endosperm (Tracy, 1993; Coe et al., 1988). The kernel is sometimes wrinkled like su1 (Coe et al., 1988).
      • shrunken2 (sh2) [supersweet] (located on chromosome 3L). The gene product of the wild-type Sh2 allele is ADP-glucose pyrophosphorylase, a key enzyme of starch synthesis (Coe et al., 1988). The shrunken2 (sh2) mutation causes accumulation of sugars at the expense of starch. Kernels have greatly decreased total carbohydrates at the mature seed stage (Tracy, 1993). Failure to make ADP-glucose pyrophosphorylase causes accumulation of sucrose and lipids instead of WSP and starch (Coe et al., 1988). sh2 kernels are large, plump and translucent, crisp and very sweet at the milk stage, but collapse on drying, becoming angular and brittle (Coe et al., 1988). They germinate poorly to produce smaller but otherwise normal plants (Tracy, 1993).

    The shrunken2 mutation causes a block in starch synthesis

  • In su1 endosperm sugars are rapidly converted to phytoglycogen both preharvest and postharvest, resulting in a continuous decrease in sugar content from the maximum attained around 18-20 days after pollination (DAP) (Tracy, 1993). When kept at room temperature standard su1 sweet corn will lose 50% or more of its sugar in 24 hours (Tracy, 1993). Rate of sugar loss can be reduced by cooling harvested corn (Tracy, 1993). Even when kept at 5 - 10 C, up to two-thirds of the sucrose of su1 kernels will be lost over a 3-day period (Tracy, 1993).
  • In sh2, the rate of sugar loss is much slower than in the sugary and sugar-enhanced varieties (Tracy, 1993). After 48 h at 27 C a sh2 hybrid has double the sucrose content of a freshly-picked near-isogenic su1 hybrid (Tracy, 1993). When the sh2 hybrid is stored at 4 C, there is no change in sucrose levels after 96 h (Tracy, 1993). Because of the extended shelf-life of these hybrids these are now the preferred type for the long-distance shipping trade (Tracy, 1993).
  • Because all the above genes are recessive, sweet corn must be isolated from field corn pollen by either a distance of 250 feet, or by a tasseling date of 14 days.
  • Supersweets (sh2) must be isolated from standard sugary (su) and sugar-enhanced (se) types by a distance of 250 feet, or by a tasseling date of 14 days. Failure to isolate these types will result in kernels which will be starchy instead of sweet. Isolation of sugar-enhanced (se) types from sugary (su) sweet corns is not essential, but will allow maximum expression of the sugar-enhanced traits.
  • Other simply inherited traits that are important in sweet corn improvement include kernel, cob and plant color (Tracy, 1993):
      • Commercial sweet corn varieties must have white cobs and clear pericarps, and most inbreds are homozygous for the allele P-ww at the pericarp-cob color locus (Tracy, 1993).
      • Sweet corn lines often carry the C1-I allele, which inhibits anthocyanin development in the aleurone (Tracy, 1993). Many sh2 varieties carry the a allele, which inhibits anthocyanin development in the entire plant and is tightly linked to sh2 (Tracy, 1993).
      • The color of the endosperm is also important with three main types of varieties: yellow, white and bicolor (25% white and 75% yellow on the same ear) (Tracy, 1993). Yellow versus white endosperm is controlled by the Y locus, and white is recessive to yellow (Tracy, 1993). Bicolor hybrids are produced by crossing a yellow inbred (YY) with a white inbred (yy) (Tracy, 1993). Most corn for processing is yellow, and yellow corn is predominant in the fresh market (bicolors are particularly important in the northeastern U.S. and Japan) (Tracy, 1993). White endosperm is preferred from the mid-Atlantic region through the southern U.S. (Tracy, 1993). Although the Y allele is required for yellow endosperm, modifying genes have an effect on the shade of yellow, with a bright, glossy yellow being the desired type (Tracy, 1993).
      • Isolation is required when pure white sweet corns are to be grown. Because white is recessive to yellow, pollen from yellow or bicolor varieties will produce some yellow kernels on the white ears if not isolated (Tracy, 1993).
  • Major insect pests of sweet corn in the Midwest:
  • Minor insect pests of sweet corn in the Midwest:

  • Diseases of sweet corn:
      • Common corn rust (Puccinia sorghi); resistance genes available; Rp1 and Rp3.
      • Northern corn leaf blight (Helminthosporium turcicum).
      • Stewart's wilt, caused by the bacterium Erwinia (Xanthomonas) stewartii; spread by the corn flea beetle (Tracy, 1993). The disease is a problem anywhere the insect overwinters. Overwintering of the flea beetle is severely limited when the sum of the mean temperatures for Dec., Jan. and Feb. is 32 C or below (Tracy, 1993). If this sum is >37 C, Stewart's wilt can be a serious problem (Tracy, 1993). Resistance to Stewart's wilt is controlled by a few genes; resistant hybrids are available (Tracy, 1993).
      • Common smut (Ustilago maydis) is widely-distributed in the corn growing regions of the U.S. and can cause serious economic damage on susceptible hybrids; resistant hybrids are available (Tracy, 1993)
      • Head smut (Sphacelotheca reilana) can result in economic damage in Idaho, Washington, Oregon and California (Tracy, 1993). Its presence in the sweet corn growing region of Idaho is of particular concern because it can be seed-borne (Tracy, 1993). Resistant hybrids are available (Tracy, 1993).
      • Maize dwarf mosaic virus (MDMV) is the most serious virus disease of sweet corn in the U.S., and production of sweet corn has been limited in areas where the virus overwinters (Tracy, 1993). The virus does not overwinter in the northern tier of states but may cause serious losses in late-planted corn in this region (Tracy, 1993). MDMV is transmitted by aphids, but is also seed-transmitted (Tracy, 1993). Resistant hybrids are available (Tracy, 1993).
      • Sweet corn is harvested around 20 DAP, well before the seed matures and the plants begin to senesence (Tracy, 1993). Thus, stalk, kernel and ear rots are usually not a problem in sweet corn production (Tracy, 1993). However, these diseases cause serious economic losses in the production of sweet corn seed (Tracy, 1993). The kernel and ear rots caused by Fusarium, Diplodia and Gibberella are the main reason why the seed industry is located in the desert climate of southwestern Idaho (Tracy, 1993). With the introduction of high-sugar corns the problem has intensified, and kernel rots have even appeared on sweet corn grown for processing (Tracy, 1993). Growers have reported Fusarium kernel rots on high-sugar sweet corn harvested later than normal (25 - 30 DAP) (Tracy, 1993). Fusarium kernel rot is often associated with insect damage (Tracy, 1993).
    (see: ID-56: Midwest Vegetable Production Guide for Commercial Growers 2008 - Sweet Corn (PURDUE) for information on sweet corn varieties, isolation requirements, spacing, seeding, fertilizing, and specific sweet corn disease, weed and insect control recommendations for the Midwest)

    Sources of information:

  • Tracy, W.F. Sweet corn, Zea mays L. In "Genetic Improvement of Vegetable Crops", (ed. G. Kalloo, B.O. Bergh), Pergamon Press, Oxford, UK, pp. 777-807 (1993).
  • Nonnecke, I.L. "Vegetable Production", Van Nostrand Reinhold, NY (1989).
  • Flood, B., Foster, R., Hutchinson, B. Sweet corn. In "Vegetable Insect Management With Emphasis on the Midwest", (ed. R. Foster, B. Flood), Meister Publishing Co., Willoughby, Ohio, pp. 19-40 (1995).
  • Midwest Vegetable Production Guide for Commercial Growers, ID-56, eds. R. Foster, D. Egel, E. Maynard, R. Weinzierl, H. Taber, L.W. Jett, B. Hutchinson, Purdue University Cooperative Extension Service, 2003.
  • Coe, E.H.Jr., Neuffer, M.G., Hoisington, D.A. The genetics of corn. In "Corn and Corn Improvement" Third Edition, (ed. G.F. Sprague, J.W. Dudley), American Society of Agronomy, Madison, WI, pp. 81-258 (1988).

    Additional reading:

  • Tracy, W.F. Sweet corn. In "Specialty Corns", (ed. A.R. Hallauer), CRC Press, Boca Raton, FL, pp. 147-187 (1994).
  • Smith, D.R., White, D.G. Diseases of corn. In "Corn and Corn Improvement" Third Edition, (ed. G.F. Sprague, J.W. Dudley), American Society of Agronomy, Madison, WI, pp. 687-766 (1988).
  • Dicke, F.F., Guthrie, W.D. The most important corn insects. In "Corn and Corn Improvement" Third Edition, (ed. G.F. Sprague, J.W. Dudley), American Society of Agronomy, Madison, WI, pp. 767-867 (1988).
  • Phillips, R., Rix, M. "The Random House Book of Vegetables", Random House, NY (1993).
  • Ghorpade, V.M., Hanna, M.A., Jadhav, S.J. In "Handbook of Vegetable Science and Technology: Production, Composition, Storage, and Processing", (ed. D.K. Salunkhe, S.S. Kadam), Marcel Dekker, Inc., NY, pp. 609-646 (1998).

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  • David Rhodes
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    Last Update: 01/21/09