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Gonosome-autosome translocations in fowl: the development of chromosomally unbalanced embryos sired by singly and doubly heterozygous cockerels

Published online by Cambridge University Press:  14 April 2009

W. F. Blazak  and
N. S. Fechheimer
W. F. Blazak
Affiliation:
Department of Dairy Science, The Ohio State University, Columbus, Ohio 43210, U.S.A.
N. S. Fechheimer
Affiliation:
Department of Dairy Science, The Ohio State University, Columbus, Ohio 43210, U.S.A.
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Cockerels singly or doubly heterozygous (t1/ +, t2/ + and tl/t2, respectively; collectively heterokaryotypic, HTK) for two different Z-autosome translocations (t1, t2) produce an array of chromosomally balanced and unbalanced spermatozoa owing to adjacent segregation and nondisjunction at the first meiotic division. This study addresses the developmental capacity of embryos derived from matings of control ( + / + ) and HTK (tl/ +, t2/ +, tl/t2) cockerels with hens bearing normal chromosome complements (+ /W).

Estimates of the hatchability of fertile eggs sired by + / +, tl/ +, t2/ + and tl/t2 cockerels were 82·8%, 43·0%, 41·3% and 10·9%, respectively. Approximately 75% of the mortality observed in embryos sired by HTK cockerels occurred by four days of incubation. Developmental arrest generally occurred earlier in embryos sired by t2/+ and tl/t2 cockerels than in those by tl/ + cockerels. These differences reflect variation in the degree of embryonic chromosome unbalance expected among embryos of the different sire groups. The pattern of mortality after three days was similar in embryos sired by HTK cockerels. In control embryos, mortality was highest on days 20–21 of incubation.

Chromosome analysis of 16/18 h embryos, day 1/5 embryos and hatched chicks sired by HTK cockerels revealed that most, if not all, chromosomally unbalanced embryos died during development; the majority before three days of incubation. Partial monosomy for chromosome one was found to be more deleterious to embryonic development than partial trisomy.

Type
Research Article
Information
Genetics Research , Volume 37 , Issue 2 , April 1981 , pp. 161 - 171
Copyright
Copyright © Cambridge University Press 1981

References

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