As corn got dispersed from its origin in Mexico it was eventually realized that some plants would delay the synthesis of starch in kernels leaving them with a creamy texture and a sweet taste. This was caused by a recessive gene mutation that resulted in a sweet tasting substance, phytoglycogen. This was used by natives before the Europeans arrived in America. This recessive gene is known as su. In the 1970’s another recessive gene mutant was found that makes more sweetness, and tends to be associated with more easily digested pericarp. This sweetness enhanced gene (se) gives sweeter corn when combined with su gene but will also eventually become starchy. Another recessive gene (sh2) was discovered in the 1950’s to have higher sugar content and a much longer shelf life before producing starch. As a consequence, the shrunken gene (sh2), the kernels do not become plump and with lack of starch reserve, may be vulnerable to poor emergence if planted too deep.
Endosperm genetics, being affected by the genetics of the pollen producer, and the sweetness genes being recessive requires isolation from field corn to express the sweetness. Sweet corn hybrids tend to have large amounts of pollen, reducing the threat from other pollen but isolation in the seed production is imperative to assure that the seed is homozygous for the recessive gene(s). The best and purest sweet corn is produced with some distance away from field corn.
About Corn Journal
The purpose of this blog is to share perspectives of the biology of corn, its seed and diseases in a mix of technical and not so technical terms with all who are interested in this major crop. With more technical references to any of the topics easily available on the web with a search of key words, the blog will rarely cite references but will attempt to be accurate. Comments are welcome but will be screened before publishing. Comments and questions directed to the author by emails are encouraged.