Glyphosate is a broad-spectrum, non-selective herbicide used widely in agriculture, forestry, and home gardening to control unwanted vegetation. Applied after plants emerge, it targets actively growing weeds. Its success stems from its ability to disrupt a fundamental life process within the plant.
Plant Uptake and Systemic Action
The primary method of application is foliar, where the liquid is sprayed directly onto the leaves and stems. Glyphosate is highly soluble, allowing it to pass through the waxy cuticle layer and enter the plant’s interior tissues. Once absorbed, the chemical is transported systemically throughout the plant’s vascular system.
The herbicide moves through the phloem, the tissue responsible for distributing sugars produced during photosynthesis. This movement directs glyphosate to metabolic “sinks,” or areas of rapid growth, such as meristems in the developing buds and root tips. The concentration of the herbicide in these actively growing areas initiates the mechanism of plant destruction. This efficient translocation is fundamental to its effectiveness against perennial weeds with extensive root systems.
Inhibiting the Shikimate Pathway
The chemical acts by interfering with the shikimate pathway, a specific chain of biochemical reactions. This unique metabolic process is found only in plants, fungi, algae, and certain bacteria, which explains the herbicide’s low toxicity profile in animals. The shikimate pathway synthesizes numerous aromatic compounds essential for plant life.
Glyphosate targets the enzyme 5-enolpyruvylshikimate-3-phosphate synthase, abbreviated as EPSP synthase. This enzyme catalyzes the sixth step in the shikimate pathway. The herbicide’s structure is similar to the enzyme’s natural substrate, phosphoenolpyruvate (PEP), allowing glyphosate to bind competitively to EPSP synthase.
Glyphosate acts as a transition state analog, binding tightly to the enzyme after the first substrate, shikimate-3-phosphate (S3P), has attached. This creates a stable, non-functional complex. By occupying the site where PEP normally binds, glyphosate effectively blocks the enzyme’s active site. This blockage completely shuts down the metabolic pathway at this step, preventing the production of the necessary intermediate compound, 5-enolpyruvylshikimate-3-phosphate (EPSP).
The Fatal Consequences of Enzyme Blockage
Blocking EPSP synthase immediately prevents the plant from completing the shikimate pathway. This metabolic failure halts the biosynthesis of the three aromatic amino acids: phenylalanine, tyrosine, and tryptophan. These amino acids are precursors for hundreds of compounds necessary for plant survival. Their absence prevents the synthesis of vital proteins, leading to a systemic shutdown of growth and development.
Tryptophan is the precursor for auxin, a major growth hormone, so its absence immediately impairs fundamental growth regulation. Phenylalanine and tyrosine are used to create secondary metabolites, including lignin for cell walls and defense compounds. Within days of application, the metabolic collapse becomes physically evident, starting with growth cessation. Plants then show chlorosis (yellowing of new leaves) followed by necrosis (tissue death), as the plant cannot sustain its most actively growing parts. The combination of protein depletion and the accumulation of pathway intermediates leads to the complete death of the plant, typically within one to three weeks.
Mechanisms of Plant Resistance
Widespread use of glyphosate has led to the development of methods by which plants survive exposure. One method is engineered resistance, incorporated into genetically modified crops like ‘Roundup Ready’ varieties. This is achieved by inserting a bacterial gene that produces a modified EPSP synthase enzyme. This bacterial enzyme, designated CP4 EPSPS, performs its normal function but is less susceptible to glyphosate inhibition, allowing the crop to thrive after application.
In natural weed populations, resistance has evolved through different physiological and genetic mechanisms. One mechanism is natural target-site resistance, often involving a single mutation in the native EPSP synthase gene that prevents glyphosate from binding effectively. Other weeds employ non-target-site mechanisms, which include:
Non-Target-Site Mechanisms
- Gene amplification, where the plant produces an excess of the EPSP synthase enzyme to overwhelm the inhibitor.
- Sequestration, where resistant weeds sequester the herbicide into vacuoles or rapidly degrade the chemical, preventing it from reaching the EPSP synthase enzyme.