Summary1. PGM phenotypes have been determined by starch‐gel electrophoresis in more than 2000 unrelated ‘ English’ people and several smaller samples from other populations.2. Besides the three common phenotypes (PGM 1, 2–1 and 2), eleven rare phenotypes have been identified, and their genetical basis investigated.3. Nine of the new phenotypes, PGM 3–1, 3–2, 4–1, 4–2, 5–2, 6–1, 6–2, 7–1 and 7–2, appear to represent heterozygous combinations of one or another of a series of rare alleles, PGM31, PGM41, PGM51, PGM61 and PGM71, with either PGM11 or PGM21. Each of these alleles probably determines the formation of two new isoenzyme components which are homologous with components a and c determined by PGM11 and components b and d determined by PGM21.4. The ‘Atkinson’ and ‘Palmer’ phenotypes are thought to represent heterozygotes for alleles at a different locus, PGM2. The common allele at this locus is designated PGM12 and the postulated genotype for the ‘Atkinson’ phenotype is PGM12PGM22 and for the ‘Palmer’ pheno‐type is POM12PGM32. It is suggested that PGM12 determines isoenzyme components e, f and g and that PGM22 and PGM32 each determine three isoenzyme components which are electrophoretically different from but homologous with e, f and g.5. The ‘Atkinson’ phenotype appears to have an appreciable incidence in Negro populations and has so far not been observed in any non‐Negro group.

HOPKINSON, D. A., & HARRIS, H. (1966). Rare phosphoglucomutase phenotypes. Annals of Human Genetics, 30(2), 167–181. Portico.