Evaluating Causal Claims in Plant Developmental Metabolism: A When–Where–How Framework

Metabolic changes are often described as drivers of plant development even when the evidence establishes only association or a permissive requirement. This review separates biological role from causal status and evaluates claims across seven dimensions: association, necessity, localization, transport, rescue and mediation, sufficiency, and quantitative-threshold testing. We apply a when–where–how framework to four cases. Perturbations of T6P, SnRK1, and TOR support T6P-dependent kinase regulation as a mediator of lateral-root development and are consistent with a context-dependent candidate gate, but its window and threshold remain unresolved. Circadian regulation of AHA3 and SUC2 by CCA1 provides the most complete chain, combining cell-specific perturbation, transport, and rescue. The OsARF18–OsARF2–OsSUT1 pathway supports sucrose transport as a mediator of rice fertility, although receiving-cell necessity and quantitative restoration remain unresolved. H+-ATPase perturbations identify apoplastic pH as a proximal mediator of Arabidopsis hypocotyl and cotton-fiber elongation, with context-dependent optima rather than a shared threshold. Nutrient and redox regulation, specialized metabolism, stress, and senescence provide boundary comparisons. Causal confidence depends on claim-matched evidence for responding cells and developmental windows and, where relevant, transport routes, mechanisms, and whole-plant trade-offs. The framework can guide AI-assisted breeding by prioritizing genotype-, stage-, and tissue-specific interventions for prospective perturbation and rescue.