Abstract

Phloem transport of D,L-[(14)C]glufosinate, D-[(14)C]glufosinate, and acetyl-L-[(14)C]glufosinate was examined in the susceptible Brassica napus cv Excel and a glufosinate-resistant genotype (HCN27) derived by transformation of cv Excel with the phosphinothricin-N-acetyltransferase (pat) gene. Considerably more (14)C was exported from an expanded leaf in HCN27 than in cv Excel following application of D,L-[(14)C]glufosinate (25% versus 6.3% of applied, respectively, 72 h after treatment). The inactive isomer, D-glufosinate, was much more phloem mobile in cv Excel than racemic D,L-glufosinate. Foliar or root supplementation with 1 mM glutamine increased D,L-[(14)C]glufosinate translocation in cv Excel but only transiently, suggesting that glutamine depletion is not the major cause of the limited phloem transport. Acetyl-L-[(14)C]glufosinate (applied as such or derived from L-glufosinate in pat transformants) was translocated extensively in the phloem of both genotypes. Acetyl-L-[(14)C]glufosinate was readily transported into the floral buds and flowers, and accumulated in the anthers in both genotypes. These results suggest that phloem transport of D,L-glufosinate is limited by rapid physiological effects of the L-isomer in source leaf tissue. The accumulation of acetyl-L-glufosinate in the anthers indicates that it is sufficiently phloem mobile to act as a foliar-applied chemical inducer of male sterility in plants expressing a deacetylase gene in the tapetum, generating toxic concentrations of L-glufosinate in pollen-producing tissues.

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