The recurrent detection of the same specialized metabolite in a plant and one of its endophytes is frequently interpreted as evidence that both partners possess the capacity to synthesize that compound. This inference is stronger than the observation itself. Shared chemistry can arise through autonomous biosynthesis, host metabolic induction, microbial pathway activation, metabolite or precursor exchange, biotransformation, cultivation-dependent expression, or analytical misassignment. This article develops a proposed host–endophyte biosynthetic-attribution model that separates chemical identity from biosynthetic origin and integrates four principal evidence domains: isotope logic, genomic capacity, compartment evidence, and cultivation stability. The model treats these domains as complementary rather than interchangeable. Stable-isotope incorporation can constrain precursor routing but may remain ambiguous under cross-feeding; compatible biosynthetic genes indicate capacity but not expression; spatial localization constrains where metabolites occur but not necessarily where they are synthesized; and persistent axenic production strengthens microbial attribution without independently establishing pathway sufficiency. Higher confidence therefore arises from convergence among orthogonal observations and, where feasible, functional perturbation or pathway reconstruction. The proposed framework also accommodates competing explanations and evidence that decreases confidence, including metabolite disappearance during serial cultivation, absence of required enzymatic capacity, inconsistent spatial distributions, or failure of predictions under controlled testing. Its purpose is not to assign universal numerical scores or claim validated predictive performance, but to make biosynthetic claims more explicit, falsifiable, and experimentally prioritized. The framework is intended to improve interpretation of host–endophyte chemistry and reduce premature producer attribution in natural-product discovery.
