Studies were conducted to determine how a serine to threonine mutation at position 264 on the Qb binding niche of the D1 protein [urea-resistant/triazine resistant (UR/TR biotype)] in common purslane (Portulaca oleracea) impacted carotenoid and chlorophyll pigment pools and measurements of photochemical and non-photochemical quenching (NPQ) following applications of various inhibitors of carotenoid biosynthesis (CBI) and the Photosystem II (PSII) inhibitor diuron when applied alone, or in mixtures, as compared to wildtype (WT) purslane. Non-photochemical quenching decreased 138 to 531% in comparison to the untreated checks following any herbicide application. Most CBI herbicides and diuron did not change chl a and chl b in the UR/TR biotype, while these same herbicide treatments tended to sharply decrease chlorophyll pigments in the WT population. Zeaxanthin levels were sharply elevated when CBI herbicides were applied alone to both purslane biotypes. β-carotene reduced in both biotypes following herbicide applications in comparison to the untreated check. Neoxanthin, antheraxanthin, and lutein were generally increased or remained similar to the un-treated controls in the herbicide treated UR/TR biotype, while levels of these carotenoids tended to decrease in the herbicide treated WT population. Diuron alone increased neoxanthin, antheraxanthin, lutein, and zeaxanthin by 4 to 200% in the UR/TR biotype, but decreased these same carotenoids 25 to 62% in the WT population. The applications of CBI and PSII herbicides demonstrate that redox signaling in response to this mutation in the D1 protein may impact the retention of plant pigment concentrations in the light harvesting complexes of PSII, which would be vital for stress tolerance in this biotype.