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Inheritance of Bentazon Susceptibility in a Corn (Zea mays) Line

Published online by Cambridge University Press:  12 June 2017

Laura D. Bradshaw
Affiliation:
Dep. Agron., Univ. Kentucky, Lexington, KY 40546-0091
Michael Barrett
Affiliation:
Dep. Agron., Univ. Kentucky, Lexington, KY 40546-0091
Charles G. Poneleit
Affiliation:
Dep. Agron., Univ. Kentucky, Lexington, KY 40546-0091

Abstract

Greenhouse experiments were conducted to determine if the inheritance of bentazon susceptibility in the corn inbred ‘GA209’ is a recessive single gene trait Bentazon was applied at 4.4 kg ai ha-1 plus 1% by vol crop oil concentrate in all experiments. This treatment caused 96 and 30% visual injury and 86 and 50% dry weight loss for corn inbreds GA209 and ‘Ky226,’ respectively. Corn inbreds ‘B73,’ ‘T61,’ Mo17,’ ‘Pa91,’ and ‘CI66’ showed less than 18% injury and 10% dry weight loss and were considered tolerant of bentazon. Single crosses and reciprocal single crosses of GA209 with the other inbreds were considered bentazon tolerant with approximately 10% stunting and tissue necrosis and 20% dry weight reduction resulting from bentazon. Bentazon susceptibility was not maternally inherited. Apparent single recessive gene control of bentazon susceptibility of GA209 was observed for F2 and backcross segregations. However, subsequent analyses of F3 and selfed-backcross populations indicated that two genes, probably located on the same chromosome, controlled the bentazon susceptibility. Duplicate dominant epistasis provided the best fit for injury and dry weight reduction segregations in populations derived from the cross of inbreds GA209 and B73.

Type
Special Topics
Copyright
Copyright © 1994 by the Weed Science Society of America 

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References

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