Characterizing the Interaction Between Mesotrione and Atrazine
Broadleaf weeds such as waterhemp and kochia have evolved resistance to many different classes of herbicides, with some biotypes having 'multiple resistance', meaning resistance to more than one class of herbicides in the same plant. HPPD-inhibiting herbicides, such as Callisto (mesotrione) and Balance Pro (isoxaflutole), are relatively new herbicides with excellent activity on these problem broadleaf weeds. Since these herbicides have only been used in corn for a few years, weed resistance to HPPD inhibitors has not developed so far. Callisto is often tank-mixed with a low amount of atrazine, a photosystem II inhibitor, and displays synergistic herbicidal activity on waterhemp and pigweeds when applied postemergence. In addition to improving weed control with the Callisto plus atrazine tank mix, this weed management strategy may also aid in preventing or delaying the development of weed resistance to Callisto through the combination of herbicides having two distinct target sites and modes of action. Interestingly, the synergism between Callisto and atrazine has also been documented in atrazine-resistant waterhemp and pigweed biotypes. Ongoing greenhouse and laboratory studies are aimed at determining the underlying physiological basis for this interaction.
Soybean Injury from Plant Growth Regulator (PGR) Herbicides
Several auxin-like herbicides (dicamba, clopyralid, 2,4-D) commonly used in corn for postemergence weed control can injure soybeans at extremely low rates. These plant growth regulator (PGR) herbicides can drift onto nearby soybean fields, or can be directly applied at very low rates if spray tanks are not thoroughly cleaned before spraying soybeans. These herbicides can cause severe injury to newly emerging soybean leaves, and also delayed maturity and decreased yield. Injury symptoms include leaf cupping, strapping, parallel veination, and puckering.
We are working on developing a laboratory assay to detect the presence of these PGR herbicides in soybean leaves, based on their effects on gene expression levels and expression patterns. Using molecular techniques such as RT-PCR and differential display of mRNA, we can fingerprint the expression of one or many genes in soybean leaves that have been treated with very low levels of the PGR herbicides. We hope to find a gene (or genes) that is only expressed in PGR-treated soybean leaves, and will then use the expression of this gene as a molecular marker to diagnose the presence of the herbicide. We have already found an auxin-regulated gene that is only expressed in soybean leaves treated with each of the three PGR herbicides listed above. We also hope to find specific genes that can be used to distinguish among dicamba, clopyralid, and 2,4-D.
Characterization of Glutathione S-Transferases (GSTs) in Triticum tauschii
We have cloned and sequenced three GST genes from Triticum tauschii, which is a wild progenitor of cultivated wheat, Triticum aestivum. We are utilizing T. tauschii as a model plant system to study the regulation of GST gene expression by herbicide safeners. Reasons for using T. tauschii as a model system are that it is diploid, contains the D genome found in cultivated wheat (ABD genomes), and also responds to safeners in a similar manner as cultivated wheat.
Herbicide safeners protect grass crops from herbicide injury by increasing the activity of herbicide detoxification enzymes, such as GSTs and cytochrome P-450s. The precise reason and molecular mechanism for this induction of GST activity is not known. One theory is that safeners cause a stress response in the plant that leads to transcriptional activation of defense genes, such as GSTs. We hope to gain insight into safener mode of action by understanding the mechanism for activation of GST gene expression in response to safeners and various plant hormones. Currently, we are examining the promoters of the GST genes from T. tauschii for regulatory elements that might be involved with transcriptional activation and increased expression following herbicide safener treatment.
Previous research mapped homoeologous copies of the GST genes to the short arms of chromosomes 6A, 6B, and 6D in cultivated wheat. Recent research findings show that only the GST genes on chromosome 6D are expressed in safener-treated wheat shoots. We plan to compare the promoters of the GST genes from 6A, 6B, and 6D to help identify critical regulatory elements involved in the safener response that might be missing from the promoters of non-responsive GST genes on chromosomes 6A and 6B.