Testis structure in the sys (symplastic spermatids) mouse

Abstract

Testes of mice with the recessive insertional mutation termed symplastic spermatids (sys) were assessed for structural and developmental abnormalities. Homozygous (sys/sys) males are infertile due to an abnormality in spermatogenesis leading to azoospermia. The major interruption to spermatogenesis occurs when the intercellular bridges that connect round spermatids open prematurely resulting in the formation of symplasts. Symplasts contain as many as 285 nuclei. Development of spermatids within symplasts is arrested just before, or just after, elongation of the spermatid nuclei begins. Symplasts degenerate and appear to be phagocytized by Sertoli cells and by intratubular macrophages. In addition, degeneration of young round spermatids and also spermatocytes occasionally is observed. Spermatocyte degeneration is substantial in some tubules and leaves them depleted of cells other than basal compartment cells. Sertoli cell abnormalities are prominent and include intracellular vacuolation, absence of apical processes surrounding round spermatids, degeneration, and occasional sloughing. Although reduplication and infolding of the basal lamina is also seen, this does not appear as a common phenomenon. The sys phenotype is first manifest in animals between 19 days and 22 days of age. Considerable variability is seen in testis histology of prepubertal animals; some display degenerating pachytene spermatocytes and virtually no Sertoli cell vacuoles, while others display vacuoles without apparent elevated numbers of degenerating spermatocytes. Although this study has not revealed the primary cell type(s) affected by the insertional inactivation event, it is possible that the abnormalities in the Sertoli cells are responsible for germ cell degeneration as it is generally recognized that deficits in the Sertoli cell can result in major germ cell abnormalities but not vice versa.

Germinative Testicular Cells and Bone Marrow Mononuclear Cells Transplanted to a Rat Model of Testicular Degeneration

“…The present results are in agreement to (Russel et al 1991) who described that it takes around 13 days to a single A spermatogonia from starting division until becoming an elongated spermatid. In this study, the germ cell transplant showed to be an effective method to recover spermatogenesis in degenerated rat testis caused by Busulfan treatment.…”

“…A single A spermatogonia (As) is the stem cell of spermatogenesis. After a number of spermatogonial divisions, this cell gives rise to spermatocytes, which after meiotic divisions, produce spermatids that develop into spermatozoa (Russel et al, 1991). The process of regeneration through stem cells in the testis was described in mice exposed to neutron radiation (Meistrich et al, 1978).…”

PLAG1 deficiency impairs spermatogenesis and sperm motility in mice

“…Symplasts originate when the intercellular bridges between round spermatids collapse and form a multinucleated cell that displays arrested development. These symplasts eventually undergo degeneration and are phagocytised by Sertoli cells and intratubular macrophages 28 .…”

Proliferative and Nonproliferative Lesions of the Rat and Mouse Male Reproductive System

“…Multinucleated giant cells may be more prevalent among immature animals; only frequency levels occurring noticeably beyond those among concurrent control animals should be recorded. In the sys mouse, the major interruption to spermatogenesis occurs when the intercellular bridges that connect round spermatids open prematurely resulting in the formation of symplasts (MacGregor et al 1990;Russell et al 1991 If it is unilateral, the probable cause is efferent duct blockage. The efferent ducts are the major site of reabsorption of seminiferous tubule fluid, which is secreted by the Sertoli cells (Hess 2002).…”