Chloroplasts generate important cellular signals and synthesize diverse products. The chloroplast-localized protein, Nitric Oxide Associated-1 (NOA1), is implicated in nitric oxide (NO) accumulation and linked to the methylerythritol phosphate (MEP) pathway, but its role is undefined. I report that NOA1 is not essential for NO accumulation because the noa1 mutant accumulates NO when provided sucrose-supplemented media. Therefore, chloroplast function and fixed carbon, but not NOA1 are likely critical for plant NO accumulation. noa1 is also resistant to fosmidomycin, an inhibitor of the MEP pathway. This phenotype led to uncovering a potential link between the MEP and tetrapyrrole pathways. I report that fosmidomycin toxicity is light dependent and reduced by phytol supplementation. Downregulation of the tetrapyrrole pathway enhances fosmidomycin resistance, suggesting that reduced tetrapyrrole biosynthesis alleviates fosmidomycin toxicity. These findings reveal new insight into how impairment of the MEP pathway affects plants and the importance of metabolic balance for chloroplast function.