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Agronomy Day 2009

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Tour B

Genetic discoveries at Illinois continue to improve sweet corn

Snook Pataky
Snook Pataky
Professor of Plant Pathology
Department of Crop Sciences
217-333-6606
j-pataky@illinois.edu
Marty Williams
Marty Williams
USDA ARS Weed Ecologist
Department of Crop Sciences
217-244-5476
mmwillms@illinois.edu

Discoveries at the University of Illinois have contributed greatly to the sweetness, quality, and ease of  production of sweet corn.  Professor John Laughnan’s discovery in the 1950s of the high sugar characteristic of shrunken-2 corn lead to the development of supersweet sweet corn.  In addition to having higher levels of kernel sugars, shrunken-2 varieties are unique in their ability to maintain a sweet flavor over an extended period.  Sweet corn quality also was improved as a result of Professor A. M. “Dusty” Rhodes’ discovery in the 1970s of the sugary enhancer trait.  Although not as sweet as supersweet varieties, sugary enhanced varieties have increased levels of sugar compared to normal sugary sweet corn.  Sugary enhanced varieties also are extremely tender due to a thin pericarp and have a creamy sweet corn texture as a result of kernel polysaccharides.  In the past decade, commercial sweet corn breeders have combined the quality traits conveyed by Laughnan’s and Rhodes’ endopserm types to develop ‘Xtra Tender’, ‘Mirai’, and augmented-types of sweet corn with a combination of tenderness and long-lasting sweetness previously unknown. Several other genetic discoveries at Illinois have been important in the improvement of sweet corn production.  

Common rust, caused by the fungus Puccinia sorghi, has been a consistent, yield-limiting problem in sweet corn production since the 1970s, especially among many high quality shrunken-2 varieties.  Over 25 rust resistance genes (i.e., Rp genes) were discovered in the 1960s at Illinois by Professor A.L. Hooker.  From the mid-1980s until 1999, a single Rp gene (Rp1-D) was used effectively throughout North America to control rust in sweet corn.  In 1999, when a new race of rust overcame the Rp1D gene, commercial sweet corn breeders turned to sweet corn germplasm available through the UI to incorporate several of the other Rp genes into their hybrids.  Presently, more than half of the 600 sweet corn hybrids available commercially carry one or more Rp gene for resistance to common rust.  
 
Commercial sweet corn breeders also have used germplasm developed at Illinois to solve production problems caused by maize viruses.  Maize dwarf mosaic (MDM) is caused by maize dwarf mosaic and sugarcane mosaic viruses which are vectored by aphids.  Yield is significantly reduced when sweet corn is infection by these viruses at early growth stages.  Germplasm developed in the 1980s by Rhodes and his student, Mark Mikel, have been a major source of MDM resistance in the sweet corn industry.  About 20% of all commercial sweet corn varieties carry the Mdm1 virus-resistance gene and modifier genes.  
 
Similar to the Xtra Tender and Mirai-types of corn which combine the favorable attributes of Laughnan’s and Rhodes’ discoveries to produce exceptional quality, sweet corn hybrids with resistance to multiple diseases, such as rust, MDM, northern leaf blight, and Stewart’s wilt, have been developed largely through cooperative efforts of breeder/pathologists in industry and at the UI.  Hybrids with resistance to multiple diseases have improved yields and/or reduced costs of production when grown in areas where these diseases are prevalent.   

During the past decade, researchers at Illinois have discovered the genetic basis of increased sensitivity in sweet corn to certain post-emergence herbicides. A mutation of single gene affecting cytochrome P450 metabolism of herbicides causes sweet corn and field corn lines to be sensitive to several herbicides from different chemical families with different modes of action, including compounds such as:  nicosulfuron, foramsulfuron, halosulfuron, bentazon, mesotrione, tembotrione, carfentrazone and diflufenzopyr.  Hybrids which are homozygous for the mutation (i.e., receiving mutant alleles from both inbred parents) can be killed or severely injured by these herbicides.  Hybrids which are heterozygous for the mutation (i.e., receiving a mutant allele from one inbred parent) have an intermediate level of P450 metabolism that results in varied responses to these herbicides under different environmental conditions.  Hybrids which are homozygous for functional P450 alleles are not injured when the herbicides are used according to the instructions on their labels.  The mutant allele has been identified in about 20% of all sugary, sugary enhanced, and shrunken-2 sweet corn grown for processing and fresh market; and it occurs in hybrids sold by every major sweet corn seed company.  Based on the information from research at Illinois, commercial sweet corn breeders are now cognizant of this genetic basis of herbicide sensitivity in sweet corn; and the mutant allele that is rendering germplasm sensitive to these herbicides is being eliminated from breeding populations, inbreds, and commercially-available hybrids.  Formulation of herbicides with safeners that enhance the activity of P450 enzymes is another method to reduce potential injury to hybrids that carry a mutant P450 allele.

Response of a sweet corn hybrid heterozygous for P450 alleles affecting metabolism of an ALS-inhibiting herbicide: left – ears from a non-treated control; right – ears from plants treated at the 5- to 7-leaf stage with an ALS-inhibiting herbicide.Figure 1. Response of a sweet corn hybrid heterozygous for P450 alleles affecting metabolism of an ALS-inhibiting herbicide:  left – ears from a non-treated control; right – ears from plants treated at the 5- to 7-leaf stage with an ALS-inhibiting herbicide.
Response of a sweet corn hybrid heterozygous for P450 alleles affecting metabolism of an ALS-inhibiting herbicide: left – ears from a non-treated control; right – ears from plants treated at the 5- to 7-leaf stage with an ALS-inhibiting herbicide.Figure 2. Response of a sweet corn hybrid heterozygous for P450 alleles affecting metabolism of an ALS-inhibiting herbicide:  left – ears from a non-treated control; right – ears from plants treated at the 5- to 7-leaf stage with an ALS-inhibiting herbicide.
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