Open AccessGenetic polymorphism of amylase isoenzymes in feral populations of the house mouse
Author(s) -
NIELSEN JØRN TØNNES,
SICK KNUD
Publication year - 1975
Publication title -
hereditas
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.819
H-Index - 50
eISSN - 1601-5223
pISSN - 0018-0661
DOI - 10.1111/j.1601-5223.1975.tb01484.x
Subject(s) - biology , linkage disequilibrium , locus (genetics) , genetics , chromosomal polymorphism , allele , amylase , population , house mice , evolutionary biology , zoology , haplotype , chromosome , gene , karyotype , enzyme , biochemistry , demography , sociology
By means of agar gel electrophoresis the polymorphisms in salivary and pancreatic amylases of the house mouse ( Mus musculus ) have been explored in 26 wild populations and 10 colony‐bred stocks of different geographic origin. New evidence is presented showing that these salivary and pancreatic polymorphisms are controlled by two separate but very closely linked loci: Amy‐1 and Amy‐2 . A third monomorphic locus Amy‐3 takes part in the formation of the pancreatic amylase. Two alleles, A and B, occur in both the Amy‐1 and the Amy‐2 locus. Chromosomes of type Amy ‐1 A Amy‐2 B and type Amy ‐1 B Amy‐2 B totally dominate in the material, whereas chromosomes of type Amy‐1 A Amy‐2 B and Amy‐1 B Amy‐2 A occur very rarely. Even polymorphic populations in which both chromosomes, Amy ‐1 A Amy ‐2 A and Amy ‐1 B Amy‐2 B , attain appreciable frequencies are lacking in the recombinant types and are thus in extreme linkage disequilibrium. The geographic distribution of monomorphic and polymorphic populations is rather patchy both globally and locally. The strong linkage disequilibrium seen in the latter is attributed to population mixture, rather than to selection.