Correction: Genome-wide microarray analysis leads to identification of genes in response to herbicide, metribuzin in wheat leaves.

[This corrects the article DOI: 10.1371/journal.pone.0189639.].

Genome-wide microarray analysis leads to identification of genes in response to herbicide, metribuzin in wheat leaves.

Herbicides are an important component of weed management in wheat, particularly in the southeastern US where weeds actively compete with wheat throughout the winter for nutrients and reduce tillering and ultimately the yield of the crop. Some wheat varieties are sensitive to metribuzin, a low-cost non-selective herbicide, leading to leaf chlorosis, stand loss, and decreased yield. Knowledge of the genetics of herbicide tolerance in wheat is very limited and most new varieties have not been screened for metribuzin tolerance. The identification of genes associated with metribuzin tolerance will lead to the development of molecular markers for use in screening breeding lines for metribuzin tolerance. AGS 2035 and AGS 2060 were identified as resistant and sensitive to metribuzin in several previous field screening experiments as well as controlled condition screening of nine varieties in the present study. Genome-wide transcriptome profiling of the genes in AGS 2035 and AGS 2060 through microarray analysis identified 169 and 127 genes to be significantly (2-fold, P>0.01) up- and down-regulated, respectively in response to metribuzin. Functional annotation revealed that genes involved in cell wall biosynthesis, photosynthesis and sucrose metabolism were highly responsive to metribuzin application. (Semi)quantitative RT-PCR of seven selected differentially expressed genes (DEGs) indicated that a gene coding for alkaline alpha-galactosidase 2 (AAG2) was specifically expressed in resistant varieties only after one and two weeks of metribuzin application. Integration of the DEGs into our ongoing mapping effort and identification of the genes within the QTL region showing significant association with resistance in future will aid in development of functional markers for metribuzin resistance.

Genomic and genotoxic responses to controlled weathered-oil exposures confirm and extend field studies on impacts of the Deepwater Horizon oil spill on native killifish.

To understand the ecotoxicological impacts of the Deepwater Horizon oil spill, field studies provide a context for ecological realism but laboratory-based studies offer power for connecting biological effects with specific causes. As a complement to field studies, we characterized genome-wide gene expression responses of Gulf killifish (Fundulus grandis) to oil-contaminated waters in controlled laboratory exposures. Transcriptional responses to the highest concentrations of oiled water in the laboratory were predictive of field-observed responses that coincided with the timing and location of major oiling. The transcriptional response to the low concentration (∼ 10-fold lower than the high concentration) was distinct from the high concentration and was not predictive of major oiling in the field. The high concentration response was characterized by activation of the molecular signaling pathway that facilitates oil metabolism and oil toxicity. The high concentration also induced DNA damage. The low concentration invoked expression of genes that may support a compensatory response, including genes associated with regulation of transcription, cell cycle progression, RNA processing, DNA damage, and apoptosis. We conclude that the gene expression response detected in the field was a robust indicator of exposure to the toxic components of contaminating oil, that animals in the field were exposed to relatively high concentrations that are especially damaging to early life stages, and that such exposures can damage DNA.

Common mechanism underlies repeated evolution of extreme pollution tolerance.

Human alterations to the environment can exert strong evolutionary pressures, yet contemporary adaptation to human-mediated stressors is rarely documented in wildlife populations. A common-garden experimental design was coupled with comparative transcriptomics to discover evolved mechanisms enabling three populations of killifish resident in urban estuaries to survive normally lethal pollution exposure during development, and to test whether mechanisms are unique or common across populations. We show that killifish populations from these polluted sites have independently converged on a common adaptive mechanism, despite variation in contaminant profiles among sites. These populations are united by a similarly profound desensitization of aryl-hydrocarbon receptor-mediated transcriptional activation, which is associated with extreme tolerance to the lethal effects of toxic dioxin-like pollutants. The rapid, repeated, heritable and convergent nature of evolved tolerance suggests that ancestral killifish populations harboured genotypes that enabled adaptation to twentieth-century industrial pollutants.