Resistance Mechanisms of Saccharomyces cerevisiae to Commercial Formulations of Glyphosate Involve DNA Damage Repair, the Cell Cycle, and the Cell Wall Structure

• Main Authors: Apoorva Ravishankar, Amaury Pupo, Jennifer E. G. Gallagher
• Format: Article
• Language: English
• Published: Oxford University Press 2020-06-01
• Series: G3: Genes, Genomes, Genetics
• Subjects: commercial formulations of glyphosate; herbicide resistance; saccharomyces cerevisiae; cell wall; sed1; dip5; transcriptomics; whole-genome resequencing; in-lab evolutions
• Online Access: http://g3journal.org/lookup/doi/10.1534/g3.120.401183

The use of glyphosate-based herbicides is widespread and despite their extensive use, their effects are yet to be deciphered completely. The additives in commercial formulations of glyphosate, though labeled inert when used individually, have adverse effects when used in combination with other additives along with the active ingredient. As a species, Saccharomyces cerevisiae has a wide range of resistance to glyphosate-based herbicides. To investigate the underlying genetic differences between sensitive and resistant strains, global changes in gene expression were measured, when yeast were exposed to a glyphosate-based herbicide (GBH). Expression of genes involved in numerous pathways crucial to the cell’s functioning, such as DNA replication, MAPK signaling, meiosis, and cell wall synthesis changed. Because so many diverse pathways were affected, these strains were then subjected to in-lab-evolutions (ILE) to select mutations that confer increased resistance. Common fragile sites were found to play a role in adaptation to resistance to long-term exposure of GBHs. Copy number increased in approximately 100 genes associated with cell wall proteins, mitochondria, and sterol transport. Taking ILE and transcriptomic data into account it is evident that GBHs affect multiple biological processes in the cell. One such component is the cell wall structure which acts as a protective barrier in alleviating the stress caused by exposure to inert additives in GBHs. Sed1, a GPI-cell wall protein, plays an important role in tolerance of a GBH. Hence, a detailed study of the changes occurring at the genome and transcriptome levels is essential to better understand the effects of an environmental stressor such as a GBH, on the cell as a whole.