Abstract

Herbicide safeners protect cereal crops from herbicide injury by inducing genes and proteins involved in detoxification reactions, such as glutathione S-transferases (GSTs) and cytochrome P450s (P450s). Only a few studies have characterized gene or protein expression profiles for investigating plant responses to safener treatment in cereal crops, and most transcriptome analyses in response to safener treatments have been conducted in dicot model species that are not protected by safener from herbicide injury. In this study, three different approaches were utilized in grain sorghum (Sorghum bicolor (L.) Moench) to investigate mechanisms involved in safener-regulated signaling pathways. An initial transcriptome analysis was performed to examine global gene expression in etiolated shoot tissues of hybrid grain sorghum following treatment with the sorghum safener, fluxofenim. Most upregulated transcripts encoded detoxification enzymes, including P450s, GSTs, and UDP-dependent glucosyltransferases (UGTs). Interestingly, several of these upregulated transcripts are similar to genes involved with the biosynthesis and recycling/catabolism of dhurrin, an important chemical defense compound, in these seedling tissues. Secondly, 761 diverse sorghum inbred lines were evaluated in a genome-wide association study (GWAS) to determine key molecular-genetic factors governing safener-mediated signaling mechanisms and/or herbicide detoxification. GWAS revealed a significant single nucleotide polymorphism (SNP) associated with safener-induced response on chromosome 9, located within a phi-class SbGST gene and about 15-kb from a different phi-class SbGST. Lastly, the expression of these two candidate SbGSTs was quantified in etiolated shoot tissues of sorghum inbred BTx623 in response to fluxofenim treatment. SbGSTF1 and SbGSTF2 transcripts increased within 12-hr after fluxofenim treatment but the level of safener-induced expression differed between the two genes. In addition to identifying specific GSTs potentially involved in the safener-mediated detoxification pathway, this research elucidates a new direction for studying both constitutive and inducible mechanisms for chemical defense in cereal crop seedlings.

Highlights

  • Plants have the unique capability of stimulating selective signaling pathways in response to diverse stimuli, including natural and synthetic compounds as well as abiotic and biotic stresses

  • Plant defense mechanisms elicited under biotic and abiotic stress are typically activated through plant hormone-mediated signaling (Bari and Jones, 2009), which may include the upregulation of detoxification enzymes that recognize and metabolize a diverse range of natural and synthetic compounds

  • This study provides novel insights pertaining to how safeners reprogram the plant transcriptome and elucidates mechanisms involved in detoxification reactions in grain sorghum seedlings

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Summary

Introduction

Plants have the unique capability of stimulating selective signaling pathways in response to diverse stimuli, including natural and synthetic compounds as well as abiotic and biotic stresses. Plant defense mechanisms elicited under biotic and abiotic stress are typically activated through plant hormone-mediated signaling (Bari and Jones, 2009), which may include the upregulation of detoxification enzymes that recognize and metabolize a diverse range of natural and synthetic compounds (xenobiotics; Edwards et al, 2000; Cummins et al, 2011). One of the most well-studied xenobiotic responses is the herbicide detoxification pathway, consisting of a complex, multistep process that metabolizes different herbicide substrates These detoxification processes occur in three sequential phases: Phase I involves hydrolysis or oxidation and Phase II involves conjugation with endogenous sugars or reduced glutathione (GSH). The predominant mechanisms for safener-induced plant detoxification include an enhanced rate of herbicide metabolic detoxification and/or sequestration (Davies and Caseley, 1999; Hatzios and Burgos, 2004; Riechers et al, 2010; Edwards et al, 2011)

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