We have analyzed precursor pools in the chlorophyll (Chi) synthesis pathway for a set of eighteen well studied Chl b‐defident mutants in monocotyledonous (barley, maize and wheat) and dicotyledonous plants (Antirrhinum, Arabidopsis, soybean, tobacco and tomato) that form abnormal thylakoid membrane systems. All of these mutants have a partial block in Chl synthesis and nearly all of them accumulate protoporphyrin IX (Proto), the last porphyrin compound common to both heme and Chl synthesis. The large number of mutants at several genetic loci affecting this critical branchpoint in tetrapyrrole biosynthesis suggests that the Mg‐chelatase enzyme, catalyzing the first committed step of Chi biosynthesis, is a multimeric complex composed of the products of some of these genetic loci, and perhaps regulated by others. We hypothesize that these mutants are Chi b‐deficient and have reduced amounts of light‐harvesting antenna complexes (LHCs.) and develop abnormal thylakoid membranes as a direct result of limited Chl synthesis. The observed bottleneck in Chl synthesis can also explain the light‐intensity‐dependent and temperature‐dependent expression of the mutant phenotype. This hypothesis offers a simple explanation for the wide variety of pbenotypes that have been reported for the many Chl‐deficient mutants in the literature. Our findings are also consistent with the notion that Chl b is made from “left over” Chl a molecules and suggest that the Chi b‐deficient mutants should be considered more appropriately as leaky Chl‐deficient mutants.