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Testis structure in the sys (symplastic spermatids) mouse.

L D Russell¹, A P Hikim, P A Overbeek

¹Department of Physiology, Southern Illinois University School of Medicine, Carbondale 62901.

The American Journal of Anatomy

|October 1, 1991

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The symplastic spermatids (sys) mutation in mice causes male infertility by disrupting spermatogenesis, leading to abnormal cell development and degeneration, with potential Sertoli cell involvement.

Area of Science:

Reproductive biology
Developmental biology
Genetics

Background:

The symplastic spermatids (sys) mutation is a recessive insertional mutation affecting male fertility in mice.
Homozygous (sys/sys) males exhibit infertility characterized by azoospermia due to spermatogenesis defects.

Purpose of the Study:

To investigate the structural and developmental abnormalities in the testes of mice with the symplastic spermatids (sys) mutation.
To elucidate the stage of spermatogenesis affected and identify potential cellular origins of the observed defects.

Main Methods:

Histological assessment of testicular tissues from mice with the symplastic spermatids (sys) mutation.
Microscopic examination to identify structural abnormalities in germ cells and Sertoli cells.

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Main Results:

Premature opening of intercellular bridges in round spermatids leads to the formation of large multinucleated symplasts (up to 285 nuclei).
Spermatid development arrests within symplasts, followed by degeneration and phagocytosis by Sertoli cells and macrophages.
Sertoli cells display prominent abnormalities including vacuolation, loss of apical processes, and degeneration, suggesting a potential primary role in germ cell demise.

Conclusions:

The symplastic spermatids (sys) mutation severely impairs spermatogenesis, resulting in male infertility.
Abnormalities in Sertoli cells are strongly implicated as a potential cause of germ cell degeneration in this model.
Further research is needed to pinpoint the primary cell type affected by the insertional inactivation.