Submitted to: Journal of the American Society for Horticultural Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/20/1998
Publication Date: N/A
Interpretive Summary: Yellow nutsedge is the major weed pest of bell peppers in the United States. The primary control method at present is soil fumigation, but an alternative measure will be needed by the end of the decade because of the pending withdrawal of the leading fumigant (methyl bromide) from the U. S. market. Bentazon, a postemergence herbicide used to control yellow nutsedge in a number of agronomic crops, is an excellent candidate for use as a herbicide for postemergence control of the nutsedge in bell pepper. However, most bell pepper cultivars are severely injured by this herbicide, and tolerant cultivars need to be developed before the use of bentazon would be practical. This paper reports the results of a series of greenhouse and field studies conducted to develop the detailed genetic information needed to effectively use known sources of bentazon tolerance to develop bentazon-tolerant hybrid bell pepper cultivars. The results of these studies indicate that the bentazon tolerance gene in 'Santaka' is th "gene-of-choice" for use in bell pepper breeding programs. The development of an alternative control for yellow nutsedge will greatly decrease the dependence on methyl bromide by the bell pepper industry, which accounts for 11.9% of the U. S. methyl bromide use for preplant treatments.
Technical Abstract: A series of greenhouse and field studies was conducted to examine the type of gene action controlling bentazon tolerance in the pepper cv. Bohemian Chili (BC), to evaluate the importance of cytoplasmic factors in the expression of the tolerance, and to determine the genetic relationship between the bentazon tolerance trait exhibited by BC and the bentazon tolerance trait exhibited by the cv. Santaka (SK). Evaluation of parental F1, F2, and backcross populations of a cross between the susceptible cv. Sweet Banana (SB) and BC indicated that the bentazon tolerance trait in BC is conditioned by a factor with variable gene action. The tolerance is inherited as a dominant trait in some instances and as a recessive trait in other instances. Evaluations of the progeny populations in both BC and SB cytoplasm indicated that a chromosomal factor is responsible for the high level of bentazon tolerance exhibited by BC. Evaluation of parental and F2 2populations of the cross SK x BC indicated that the gene conditioning tolerance in BC is allelic to the Bzt gene that conditions tolerance in SK. The allele at the Bzt locus in BC is probably not the Bzt allele. Our results demonstrate that the BC tolerance allele utilized in the heterozygous condition is not sufficient to condition a high level of tolerance under all conditions.