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Allelic mutations in acetyl-coenzyme A carboxylase confer herbicide tolerance in maize (1992)

Marshall, L. C. ; Somers, D. A. ; Dotray, P. D. ; [et al.]

Springer

Theoretical and applied genetics 83 (1992), S. 435-442

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ISSN: 1432-2242

Keywords: Tissue culture mutant selection ; Herbicide tolerance ; Fatty acid biosynthesis ; Acetyl-CoA carboxylase ; maize

Source: Springer Online Journal Archives 1860-2000

Topics: Biology

Notes: Summary The genetic relationship between acetyl-coenzyme A carboxylase (ACCase; EC 6.4.1.2.) activity and herbicide tolerance was determined for five maize (Zea mays L.) mutants regenerated from tissue cultures selected for tolerance to the ACCase-inhibiting herbicides, sethoxydim and haloxyfop. Herbicide tolerance in each mutant was inherited as a partially dominant, nuclear mutation. Allelism tests indicated that the five mutations were allelic. Three distinguishable herbicide tolerance phenotypes were differentiated among the five mutants. Seedling tolerance to herbicide treatments cosegregated with reduced inhibition of seedling leaf ACCase activity by sethoxydim and haloxyfop demonstrating that alterations of ACCase conferred herbicide tolerance. Therefore, we propose that at least three, and possible five, new alleles of the maize ACCase structural gene (Acc1) were identified based on their differential response to sethoxydim and haloxyfop. The group represented by Acc1-S1, Acc1-S2 and Acc1-S3 alleles, which had similar phenotypes, exhibited tolerance to high rates of sethoxydim and haloxyfop. The Acc1-H1 allele lacked sethoxydim tolerance but was tolerant to haloxyfop, whereas the Acc1-H2 allele had intermediate tolerance to sethoxydim but was tolerant to haloxyfop. Differences in tolerance to the two herbicides among mutants homozygous for different Acc1 alleles suggested that sites on ACCase that interact with the different herbicides do not completely overlap. These mutations in maize ACCase should prove useful in characterization of the regulatory role of ACCase in fatty acid biosynthesis and in development of herbicide-tolerant maize germplasm.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00226531

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Preliminary studies on phospholipase A2-induced mouse paw edema as a model to evaluate antiinflammatory agents (1989)

Marshall, L. A. ; Chang, J. Y. ; Calhoun, W. ; [et al.]

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 40 (1989), S. 147-155

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ISSN: 0730-2312

Keywords: platelet-activating factor ; prostaglandins ; D-49 snake venom PLA2 ; inflammation ; leukotrienes ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: Phospholipase A2 (PLA2) is a key component of the inflammatory process because of its role in the generation of eicosanoids and platelet-activating factor (PAF). Manipulation of PLA2 activity offers a novel therapeutic approach for the development of antiinflammatory agents; however, there is a need for a suitable in vivo model. Injection of 1 μg of snake venom PLA2 (A. piscivorus piscivorus, D-49) into the mouse hind footpad produced a significant three- to four-fold rise in paw edema within 10 min, compared to the saline control. Edema formation depended on enzyme concentration and appeared specific for PLA2 since edema was negated by enzyme pretreatment with p-bromophenacyl bromide, a nonspecific PLA2 inhibitor. Moreover, injection of a protein such as bovine serum albumin did not result in significant edema. Coinjection of phenidone (lipoxygenase inhibitor, 50 μg), indomethacin (cyclooxygenase inhibitor, 50 μg), cyproheptadine (antihistamine/antiserotonin, 50 μg), aristolochic acid (putative PLA2 inhibitor, 100 μg), or kadsurenone (PAF antagonist, 50μg) with PLA2 (1 μg/paw) resulted in partial reduction (44.5, 34.2, 54.7, 64, and 50% inhibition, respectively) of edema formation. Oral administration of cyproheptadine (10 mg/kg), indomethacin (10 mg/kg), BW 755c (100 mg/kg), or dexamethasone (1 mg/kg) 1-3 h before challenge also decreased PLA2-induced edema (63.0, 30.1, 47.8, or 62.5% inhibition, respectively). The data suggest that mouse paw edema resulting from PLA2 injection is a multicomponent event, influenced by both autacoids and lipid mediators of inflammation.

Additional Material: 4 Ill.