Inheritance of sperm head abnormality types in mice – the role of the Y chromosome

Author:

Krzanowska Halina

Abstract

SUMMARYFour inbred strains of mice were used, differing in the total percentages of spermatozoa with abnormal heads (KE, 22·1%; C57, 26·4%; KP, 7·7%; CBA, 5·5%) and in the frequency distribution of abnormality types, as divided into four arbitrary classes. The most variable class 2 (narrow heads with canals inside the nuclear material) accounted for 47% of all abnormalities in KE strain, was common in CBA (29%) and almost missing in KP and C57 strains. F1 hybrids from the diallel crosses of these strains exhibited highly significant heterosis effects and significant reciprocal differences in the total percentage of abnormalities. The relative frequency of class 2 ranked in F1 hybrids in a similar order as calculated from the mid-parental values. After seven generations of backcrosses performed to introduce the Y chromosome from CBA to the genetical background of the KE strain, the total percentage of abnormalities was significantly reduced, although the relative proportion of class 2 was similar to that in KE strain. Also the Y chromosome from C57 strain, introduced into the genetical background of KE strain, caused a significant reduction of total abnormalities, but again the relative frequency of class 2 was not affected. It is concluded that the Y chromosome plays an important role in determining the total percentage of sperm head abnormalities, but does not seem to be involved in influencing specific abnormality types.

Publisher

Hindawi Limited

Subject

Genetics,General Medicine

Reference18 articles.

1. Chemical induction of sperm abnormalities in mice.

2. Krzanowska H. (1976). Types of sperm-head abnormalities in four inbred strains of mice. Acta Biologica Cracoviensia (Series Zoologia) 19 (in press).

3. Inheritance of reduced male fertility, connected with abnormal spermatozoa, in mice;Krzanowska;Acta Biologica Oracoviensia,1966

4. CHANGES IN DEOXYRIBONUCLEOPROTEIN DURING SPERMIOGENESIS IN THE BULL: INCREASED [3H]ACTINOMYCIN D BINDING TO NUCLEAR CHROMATIN OF MORPHOLOGICALLY ABNORMAL SPERMATOZOA

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