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Genetic control of voltinism characteristics in European corn borer races assessed with a marker gene
Author(s) -
Glover Thomas J.,
Robbins Paul S.,
Eckenrode Charles J.,
Roelofs Wendell L.
Publication year - 1992
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/arch.940200203
Subject(s) - voltinism , biology , diapause , genetics , zoology , larva , ecology
The post‐diapause development (PDD) time for univoltine European corn borers (ECB) under diapause breaking conditions averages approximately 44 days, whereas the PDD time for bivoltine ECB under the same conditions is approximately 15 days. This difference is the principal component of the life cycle that determines the number of generations possible in a summer. Previous workers have demonstrated some genetic control of differences in voltinism among populations, including apparent control by sex‐linked (Z‐linked) genes. In the present study allozymes of the enzyme, triose phosphate isomerase (TPI), were used as markers of the Z chromosomes in crosses of a bivoltine colony (Tpi‐1) and a univoltine colony (Tpi‐2). The F 1 resulting from a cross of univoltine females (Z 2 W) and bivoltine males (Z 1 Z 1 ) consisted of hemizygous Tpi‐1 females (Z 1 W) with a mean PDD time of 19 days and heterozygous Tpi‐1/Tpi‐2 males (Z 1 Z 2 ) with a mean PDD time of 34 days. The F 2 progeny consisted of Tpi‐1 females (Z 1 W) (mean PDD time = 15 days), Tpi‐2 females (Z 2 W) (mean PDD time = 40 days), homozygous Tpi‐1 males (Z 1 Z 1 ) (mean PDD time = 16 days), and heterozygous Tpi‐1/Tpi‐2 males (Z 1 Z 2 ) (mean PDD time = 25 days). The close correlation of TPI phenotypes and PDD times in these crosses, along with similar results for the maternal and paternal backcrosses of the F 1 individuals, indicates that the PDD time is principally controlled by genes on the Z chromosome and that heterozygous males exhibit incomplete or partial dominance of these genes. © 1992 Wiley‐Liss, Inc.