MALE-STERILITY CAUSED BY SPERM CELL-SPECIFIC STRUCTURAL ABNORMALITIESIN EBOURIFFE, A NEW MUTATION OF THE HOUSE MOUSE

Citation
A. Lalouette et al., MALE-STERILITY CAUSED BY SPERM CELL-SPECIFIC STRUCTURAL ABNORMALITIESIN EBOURIFFE, A NEW MUTATION OF THE HOUSE MOUSE, Biology of reproduction, 55(2), 1996, pp. 355-363
Citations number
47
Categorie Soggetti
Reproductive Biology
Journal title
ISSN journal
00063363
Volume
55
Issue
2
Year of publication
1996
Pages
355 - 363
Database
ISI
SICI code
0006-3363(1996)55:2<355:MCBSCS>2.0.ZU;2-Z
Abstract
We have investigated the male sterility associated with a new recessiv e mutation of the house mouse: ebouriffe (ebo). All spermatozoa presen t in the epididymis showed severe malformations, mostly of the tail. L ight and electron microscopy showed a drastic decrease of the spermati d population, whereas spermatogonia and spermatocytes seemed moderatel y affected. This suggests that the mutation affects mostly spermiogene sis. Defects appeared during formation of the acrosome: the acrosomal granule was frequently vacuolated at stages II-III, giving rise first to abnormal acrosomes (stages VI-VII) with dilations and perforations, and then to an abnormal head and acrosome shape (stages IX-XI). Howev er, the most common malformations affected the flagella in elongated s permatids. Sometimes the centriole doublet did not move into the impla ntation fossa, causing an unattached and isolated flagellum. The major defect occurred in the midpiece region of differentiating spermatozoa : flagellar components were present but highly disorganized, and mitoc hondria were aggregated in a compact mass. Even though we have no evid ence that the ebo gene is a testis structural gene or a regulatory gen e that disrupts the complex spermatogenesis process, this mutation may provide an interesting tool for studying the late stages of spermatog enesis. Using an interspecific backcross, we localized the ebo mutatio n on chromosome 2, with no recombination out of 44 meioses with locus D2Mit32.