Methionine (Met) is an essential amino acid that limits the nutritional value of many crop plants, yet its steady-state level in plant tissues is remarkably low. At the same time, Met is a central metabolic hub supporting protein synthesis and, through S-adenosylmethionine (SAM), drives the production of hormones, vitamins, polyamines, and epigenetic marks. The primary objective of this review is to understand why and how plants maintain low steady-state Met levels, and what occurs when Met content is elevated, a question of growing importance for Met biofortification. We first summarize evidence that flux through the Met/SAM pathway is high while Met pools remain small, because Met is rapidly diverted to SAM, S-methylmethionine (SMM), and other metabolites. We then describe how increasing Met at the genetic level alters development, primary metabolism, and stress responses, enhancing amino acids and sugars in leaves and proteins and starch in seeds, but often causing growth defects and stress hypersensitivity. However, moderate exogenous Met can improve growth and stress tolerance. Finally, we highlight how changes in Met/SAM levels affect DNA and histone methylation, as well as transposable-element silencing. Together, these findings suggest that plants limit Met to control metabolic, redox, and epigenetic modification, constraining Met biofortification strategies and seed nutritional improvement efforts.
Amir et al. (2026) studied this question.