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PubMed2004

Flutamide induces ultrastructural changes in spermatids and the ectoplasmic specialization between the Sertoli cell and spermatids in mouse testes.

Flutamide (Flu) is an anti-androgenic compound that disrupts development of male androgen-dependent tissues. The purpose of the present study was to investigate the effects of Flu on ICR mouse testes by electron microscopic observation. Newborn mice were subcutaneously injected with 0.00012, 0.0012, 0.012, 0.12, 1.2, 12 or 120 microg Flu/g body weight/shot on Days 2, 4, 6, 8, 10 and 12 (Day 1: day of birth). In addition, adult mice were injected with 0.0012, 0.012, 0.12 or 1.2 microg Flu/g body weight/day for 5 sequential days. Testes were processed for electron microscopy. In neonatal treatments, acrosomes and/or nuclei of the spermatids were deformed. In addition, the ectoplasmic specialization between the Sertoli cell and spermatids was partially or completely deleted. Stages of the seminiferous cycle were also disarranged in the neonatal treatments. There were no ultrastructural differences between the effects of neonatal and adult treatments, however, stage disarrangement was not observed in adult treatments. The percentages of abnormal spermatids were higher in neonatally treated mice than in mice treated as adults. Since similar observations were reported after treatment with beta-estradiol-3-benzoate (E2B), the presence of Flu may induce a "xenoestrogenic environment" in mouse testes.

Acrosome↗
PubMed1979

The induction of sex-chromosomal nondisjunction and diploid spermatids following x-irradiation of pre-spermatid stages in the northern vole Microtus oeconomus.

Chromosome nondisjunction seems to be one of the most important mutagenic effects occurring in man and makes an enormous contribution to human foetal wastage. As yet, little or no information is available on which environmental factors are important in inducing nondisjunction and accordingly we have investigated the effect of X-irradiation on inducing nondisjunction in male germ cells of an experimental mammal, the Northern vole-Microtus oeconomus. Using a staining technique based upon the presence of heterochromatin we have scored the number of sex chromosomes in early spermatids in both irradiated and unirradiated animals. A significant increase in nondisjunction, following treatment, was found with all doses between 25 and 200 R. However, variations in nondisjunction induction at various time intervals following irradiation suggest variations in cell stage sensitivity. More surprising was the large induction of diploid gametes which also demonstrated a significant induction with all irradiation doses. From the distribution of sex chromosomes we conclude that both nondisjunction and diploid gamete induction occur at both meiotic divisions. At present it is not possible to conclude whether the radiation response is linear and to define the cell-stage sensitivity with precision. The reasons for this appear to be variations in sensitivity between animals and also that there is a clear overlap between the duration of the early spermatid stage analyzed (4 days) and the interval between sampling times.

Animals↗
PubMed2002

Intracytoplasmic injection using spermatids and subsequent pregnancies: round versus elongated spermatids.

The purpose of this clinical trial study was to report the outcome of intracytoplasmic injection of round (RS) and elongated (ES) spermatids retrieved from the testis of nonobstructive men. Seven and three cycles using RS and ES injections were performed, respectively. Only one cycle utilizing the late stage of ES (Sd2) resulted in an on-going pregnancy. The remarkable low success rate following RS microinjection was established in this study.

Adult↗
PubMed1998

Multiple pregnancies obtained by testicular spermatid injection in combination with intracytoplasmic sperm injection.

Recent studies have shown that the injection of spermatid cells into the human oocyte can result in normal fertilization, embryo development and even delivery of live, healthy offspring. In our study, 23 azoospermic cases with severe spermatogenetic defects in their testicular biopsy are presented. The serum follicle stimulating hormone (FSH) concentrations and histopathological results of these males have been documented and compared in terms of fertilization and embryo development. The mean FSH value of the azoospermic males was 15.8 +/- 2.3 mIU/l, ranging from 1.6 to 39 mIU/l. Elongated spermatids were used in three cases only, as these more mature forms were mostly present in the testicular sample. In the remaining 20 cases, only round spermatids were found for use in intracytoplasmic sperm injection (ICSI). The fertilization rate with two pronuclei was 31.3%. The fertilization rate was found to be as high as 71% in three patients in the elongating and elongated spermatids group and as low as 25.6% in the round spermatid group. A few immature, non-motile spermatozoa were seen in only two cases from the elongated spermatid group. However, in the remaining cases, no spermatozoa were observed. The number of pronuclear (PN) arrest was quite high when only round spermatids were used (36.1%). Total fertilization failure was observed in two cases from the round spermatid group with Sertoli cell only and germ cell aplasia. A total of three pregnancies was achieved in 23 cases (13.0%), two from the elongated spermatid group and one from the round spermatid group. One biochemical pregnancy with a round spermatid resulted in an early spontaneous abortion and surprisingly, the remaining pregnancies were achieved with elongated spermatids resulting in multiple pregnancies. One twin and one triplet pregnancy were established following four embryo transfers in each patient. The twin pregnancy resulted in a live birth with two healthy babies; unfortunately, the triplet pregnancy ended in an abortion at 11 weeks. The use of testicular spermatids in the treatment of non-obstructive azoospermia may give hope by offering a novel treatment model. In cases with very severe spermatogenetic defect, even multiple pregnancies can be achieved with elongated spermatid cells by yielding a high implantation rate. However, the efficiency of round spermatids in achieving fertilization and pregnancy was disappointing.

Adult↗
PubMed1996

Hormonal dependency of neural cadherin in the binding of round spermatids to Sertoli cells in vitro.

The procession of round spermatids through stages VII and VIII of the rat spermatogenic cycle is critically dependent on testosterone (T). When intratesticular T levels are reduced, round spermatids appear to slough from the seminiferous epithelium, resulting in the disappearance of elongated spermatids. We hypothesized that T-dependent cell adhesion molecules are involved in Sertoli cell-round spermatid interactions. This study examined the hormonal regulation of one candidate cell adhesion molecule, N-cadherin, in vitro and its participation in Sertoli cell-round spermatid adhesion in coculture. Sertoli cells were isolated from 20-day-old Sprague-Dawley rats; treated with FSH and T, alone or in combination; and incubated for 48 h before determination of N-cadherin concentrations in Sertoli cell extracts by RIA. Both FSH and T significantly increased the cellular content of N-cadherin (3.7-fold), whereas FSH or T alone had no effect. Round spermatids were isolated from adult rats, and their adhesion to Sertoli cells was assessed in a 48-h coculture in the presence of FSH, T, or FSH plus T. Adherent round spermatids were quantitated by histological evaluation after staining with the periodic acid-Schiff reaction. A dose-dependent increase in round spermatid density (number of round spermatids bound per 10,000-microns2 Sertoli cell culture surface area) was observed with increasing T doses (7-28 ng/ml) in the presence of FSH (1 microgram/ml), whereas FSH and T alone at these doses produced no effect. T also increased the N-cadherin content of the cocultures in a dose-dependent manner in the presence of FSH. Addition of an N-cadherin antiserum to the Sertoli cell-round spermatid coculture in the presence of FSH and T significantly (P < 0.0001) reduced round spermatid density by 65%. It is concluded that both the production of N-cadherin by Sertoli cells and the binding of round spermatids to Sertoli cells are stimulated in a synergistic manner by T and FSH. Furthermore, the immunoneutralization data suggest the active involvement of N-cadherin in round spermatid-Sertoli cell adhesion in vitro. N-Cadherin may be one of the factors that subserve the androgen-dependent process of round to elongated spermatid maturation.

Amino Acid Sequence↗
PubMed1996

Testosterone withdrawal promotes stage-specific detachment of round spermatids from the rat seminiferous epithelium.

Testosterone (T) has been shown to be essential for the completion of spermiogenesis. Our previous studies showed that when intratesticular T was suppressed for 11 wk, the conversion of round spermatids between stages VII and VIII of the spermatogenic cycle was markedly suppressed and that elongated spermatids were undetectable. The fate of the round spermatids that did not proceed through this conversion was unclear. The current study aimed to investigate this T-dependent loss of round spermatids during stages VII and VIII. Adult male Sprague-Dawley rats received 24-cm T implants for 1 wk to suppress LH while maintaining spermatogenesis. The T24 implants were removed and replaced with 3-cm T plus 0.4-cm estradiol (TE treatment) to suppress intratesticular T and spermatogenesis, and animals were killed at 0 and 4 days and 1, 2, 3, 4, and 6 wk later. The number of homogenization-resistant elongated spermatids in the testis was counted, and round spermatid populations in stages VII and VIII were quantified using stereological techniques. The hourly production rates (HPR) were calculated, and a ratio was made between the HPR of round spermatids in stages VII and VIII to assess the efficiency of their conversion through these stages. Testicular T levels were suppressed to 2-4% of control values by TE treatment. After 2 wk of TE treatment, the number of homogenization-resistant elongated spermatids was significantly suppressed, falling to < 0.5% of the control value by 6 wk. The HPR of round spermatids in stages VII and VIII was not affected by up to 2 wk of TE treatment, nor was the conversion between these stages interrupted. After 3 wk of TE treatment, the HPR of round spermatids in stages VII and VIII was significantly suppressed, as was the conversion between these stages, the ratio falling to 27% of the control value by 6 wk. In rats treated with TE, histological examination of the cauda epididymidis showed occasional round spermatids after 3 wk of treatment, and large numbers after 6 wk. We conclude that the failure of round spermatids to complete spermiogenesis following T withdrawal is due to stage-specific detachment of round spermatids between stages VII and VIII.

Animals↗
PubMedDate not supplied

Diagnostic value of differential quantification of spermatids in obstructive azoospermia.

Testicular biopsies from 80 azoospermic young men were revised and the average numbers per cross-sectioned tubule of each germ cell type were calculated and compared with those of control normal testes. In 53 patients, azoospermia had an obstructive cause, and in 22 of those 53 patients more adult spermatids were found by testicular biopsy than young spermatids (over 100% in some testes), in one or both testes. However, in normal testes fewer mature spermatids than young spermatids (23.3%) were found. In the 22 patients, the causes of azoospermia were: vasectomy (7 patients), bilateral agenesis of the vas deferens (3 patients), Young syndrome (3 patients), bilateral cysts in the caput epididymidis (1 patient), bilateral inguinal herniorrhaphy (1 patient), left varicocele (1 patient), and unknown causes (6 patients). Biopsies were bilateral except for 3 cases (a vasectomized patient, a patient with Young syndrome, and a patient with obstruction due to an unknown cause). Hormonal levels were normal in the 22 patients. In addition, testicular biopsies of 3 twisted testes from 3 young adult men showing a number of adult spermatids higher than that of young spermatids were also included in the study. All testicular biopsies-including those of the twisted testes-showed an obstructive histologic pattern, consisting of a mosaic distribution of testicular lesions: mainly tubular ectasis and germ cell sloughing into the adluminal compartment of seminiferous tubules. The increase in the number of adult spermatids was bilateral in 1 of the 6 vasectomized men who underwent bilateral biopsy, and in 7 of the 11 bilaterally biopsied patients with obstructive azoospermia due to other causes. The most probable explanation for the increased number of adult spermatids is stagnation of testicular fluid, caused by sperm excretory duct obstruction. The unilateral increase in the number of adult spermatids in vasectomized men might be related to the occurrence of a spermatic granuloma (a frequent finding in vasectomy) in the proximal end of the sectioned ductus deferens ipsilateral to the testis with nonincreased adult spermatid numbers, and the absence of spermatic granuloma in the ductus deferens ipsilateral to the testis with increased adult spermatid numbers. This granuloma would produce, in addition to spermatozoon destruction, reabsorption of the testicular and epididymal fluids. The higher rate of bilateral increase, in the number of young spermatids observed in the patients with congenital lesions of the ductus deferens or the ductus epididymidis, might be related to the absence of spermatic granulomas in congenital obstructions.

Adult↗
PubMed1997

Human fertilization with round and elongated spermatids.

Human spermatids from ejaculate and testicular tissue have been utilized for evaluating human fertilization by intracytoplasmic sperm injection (ICSI) and, where possible, compared with spermatozoa utilizing sibling oocytes. Round and elongated spermatids obtained from ejaculates were either prepared through Percoll gradients or isolated and washed individually using subzonal insemination needles (SUZI; 10-14 microm internal diameter). Seminiferous tubules obtained after biopsy were placed into HEPES-buffered Earle's medium and dissected using 21-gauge needles. Spermatogenic cells and spermatozoa were isolated and washed individually using SUZI needles. Spermatozoa were subsequently injected into the ooplasm using 5 microm (internal diameter) ICSI needles, whereas 8-9 microm (internal diameter) needles were used for spermatid injection. Only metaphase II oocytes (n = 207) were injected: 64 with round spermatids, 92 with elongated spermatids and 51 with spermatozoa; the fertilization rate was 30, 24 and 67% respectively. There was a significant (P < 0.001) increase in the fertilization rate using spermatozoa compared with spermatids. The fertilization rate was not different between round and elongated spermatids, although the fertilization rates for round and elongated spermatids in the ejaculate were 33 and 18% respectively, compared with 22 and 38% respectively when testicular spermatids were utilized. In three patients sibling oocytes were used to compare round and elongated spermatids found in the ejaculate with spermatozoa extracted from seminiferous tubules. The fertilization rate was 24% for spermatids and 79% for testicular spermatozoa. This result suggests that, should only spermatids be available in the ejaculate, a testicular biopsy in the hope of obtaining testicular spermatozoa would be worth while.

Cell Size↗
PubMed1991

Hormonal regulation of spermatid binding.

A Sertoli-spermatid coculture model is described in which a large percentage (greater than 76%) of round spermatids remain viable for 48 h and bind to Sertoli cells. The effects of follicle-stimulating hormone (FSH) and testosterone on spermatid binding (expressed as the spermatid density; SD = the number of spermatids per unit area of Sertoli cell cytoplasm), ultrastructure of the Sertoli-spermatid junctional complex, and distribution in the Sertoli cell of junction-related F-actin and vinculin are described. Following 48 h of incubation, neither FSH alone nor testosterone alone affected spermatid binding to Sertoli cells beyond that observed in control cocultures. However, the combination of FSH and testosterone (FSH + testosterone) resulted in a significant increase in the density of spermatids bound to Sertoli cells. Junction-related structure of the Sertoli cell cytoskeleton between the Sertoli cell and the pre-step 8 spermatid was different than that observed between the Sertoli cell and the post-step 8 spermatid. The junction-related cytoskeletal modification of the Sertoli cell (JCMS) in the latter was similar in appearance to the well-described 'Sertoli ectoplasmic specialization' observed adjacent to post-step 8 spermatids in vivo. FSH + testosterone and FSH alone, but not testosterone alone, resulted in the peripheral distribution of actin and vinculin, which otherwise remained in stress fiber-like structures throughout the Sertoli cell. Results show that maximal spermatid binding to Sertoli cells in vitro requires FSH + testosterone and is associated with the peripheral distribution of actin and vinculin.

Actins↗
PubMed2001

Development of blastocyst-stage embryos after round spermatid injection in patients with complete spermiogenesis failure.

PURPOSE: Our purpose was to evaluate the progression of embryos derived from round spermatid injection to the blastocyst stage and compare the results with those obtained by the use of testicular or epididymal spermatozoa. METHODS: Thirty-eight patients with azoospermia enrolled in this study. In 29 patients with obstructive or nonobstructive azoospermia, spermatozoa were recovered from epididymis or testis. In the remaining nine cases with nonobstructive azoospermia, only round spermatids were found in seven, whereas in two of the patients, there were no elongated or round spermatids. Six of these cases underwent round spermatid injection. RESULTS: Twenty-one of 29 patients with injection of spermatozoa underwent embryo transfer on day 3, and 10 pregnancies (47.6%) were obtained. In eight cycles, embryos were further cultured for delayed transfer. In six cases undergoing round spermatid injection, no transfer was performed on day 3 and extended culture with delayed embryo transfer was applied. The mean number of fertilized oocytes and mean number of embryos on day 3 and also the fertilization rate and mean number of good-quality embryos on day 3, mainly grade 1 or 2, were statistically significantly higher in the spermatozoa group than the round spermatid injection group. Compared to the spermatozoa group, the number of arrested embryos was significantly higher and the number of blastocyst-stage embryos and number of good-quality blastocysts were significantly lower in the spermatid injection group. No blastocysts developed in two spermatid cycles and embryo transfer was not possible, and in the remaining four cycles, after at least one blastocyst transfer, no pregnancies were achieved. However, in eight cycles with extended culture in the spermatozoa group, embryo transfers were achieved in all and three pregnancies, for a pregnancy rate of 37.5%, were obtained after blastocyst transfer. CONCLUSIONS: Our preliminary results showed that round spermatid injection was associated with a significantly lower fertilization and embryo development rate and a significantly higher developmental arrest rate compared with the injection of spermatozoa. Extended culture and delayed embryo transfer did not improve the clinical outcome after round spermatid injection, and these results suggested a developmental failure in embryos preventing successful implantation after round spermatid injection.

Adult↗
PubMed1997

Fertilization with human testicular spermatids: four successful pregnancies.

Between July 1995 and May 1996, 36 patients with non-obstructive azoospermia of secretory origin underwent intracytoplasmic injection of spermatids. A previous histological biopsy was performed on all patients: 15 had spermatogenic arrest, a further 13 had Sertoli cell-only syndrome, and the remaining eight had post-cryptorchidism tubal atrophy. The ejaculate was duly examined and a complete absence of spermatozoa and spermatids was confirmed, with only bacteria and debris being found. Testicular sperm extraction (TESE) was then performed. In 19 out of 36 cases round spermatids only were found, while elongated spermatids were found in the remaining 17. Both round and elongated spermatids were isolated and used for injection. A total of 135 oocytes at metaphase II were recovered from 19 partners and injected with round spermatids, while 123 mature oocytes from 17 partners were injected with elongated spermatids. The number of oocytes fertilized, as judged by the presence of two pronuclei, was 75 (55.5%) and 71 (57.7%) respectively. By 34 h after injection, the number of embryos which had cleaved to the 2-cell stage was 56 (74.6%) with round spermatids and 55 (77.4%) with elongated spermatids. All cleaved embryos were transferred into the uterus of the partners. Clinical pregnancies were established in two cases of round spermatid cycles (10.5%) (both are still ongoing), and three cases of elongated spermatid cycles (17.6%) (two are still ongoing; one was lost after 8 weeks of gestation). Chromosomal analysis showed that all fetuses had a normal karyotype (three male and one female) with no chromosomal abnormalities.

Female↗
PubMed1999

On-stage selection of single round spermatids using a vital, mitochondrion-specific fluorescent probe MitoTracker(TM) and high resolution differential interference contrast microscopy.

The selection of individual round spermatids for round spermatid injection (ROSI), a prerequisite for the successful application of this infertility treatment, has been hampered by the ambiguous definition of a round spermatid and the lack of specific vital and non-vital markers. Using cells from rhesus monkey and bull, we describe a non-invasive method for the on-stage selection of individual round spermatids for ROSI, based on the polarized patterns of mitochondria, visualized in live round spermatid cells by epifluorescence microscopy after incubation with MitoTracker(TM), a vital, mitochondrion-specific fluorescent probe. The correct identification of live round spermatid was confirmed by the presence of the acrosomal granule or acrosomal cap in parallel observations by Nomarski differential interference contrast microscopy. The existence of mitochondrial polarization was first established by the labelling of MitoTracker-tagged round spermatids with spermatid-specific antibodies against proteins of nascent sperm accessory structures combined with antibodies against a nuclear pore complex component, known to disappear at the round spermatid stage. Using an inverted microscope equipped with epifluorescence, the round spermatids can be individually selected from a heterogeneous population of testicular cells labelled with MitoTracker dyes. A major advantage of this approach is that the dyes are incorporated into the paternal mitochondria, destined for rapid elimination after fertilization. In addition, the relatively high excitation and emission wavelengths of MitoTracker dyes are less harmful to DNA after their photon excitation. Before the appropriate clinical testing is conducted, the MitoTracker-based round spermatid selection may be instrumental in the training of clinical staff.

Animals↗
PubMed2001

Differential gene expression in pre-implantation embryos from mouse oocytes injected with round spermatids or spermatozoa.

BACKGROUND: The use of immature male germ cells to fertilize human oocytes raises several questions. Spermatozoa are normally quiescent, but many genes are transcribed post-meiotically in round spermatids. This creates a novel situation for the oocyte. We have therefore explored the effects on early embryonic development of introducing a fully transcriptionally active round spermatid into the oocyte. METHODS AND RESULTS: Following the micro-injection of spermatozoa or spermatids into mouse oocytes we have analysed the expression, at various times, of six genes in the resulting embryo. Spermatozoa and spermatids produced similar fertilization rates. Hprt was expressed in all embryos at all stages tested. Hsp70.1 was found normally during the 2-cell stage and repressed by the 4-cell stage in embryos from both spermatozoa and round spermatids. However, the amplitude of the signal was greatly reduced in 2-cell embryos from round spermatids. Smcy also showed a disturbed pattern of expression in embryos from round spermatids. Protamine 2, which is normally restricted to the spermatid stage, was expressed following fertilization with round spermatids, but was already repressed at the two pronuclei stage. Ube1Y, which is normally expressed post-meiotically and not during the post-implantatory development, was expressed up to the 2-cell stage in embryos from round spermatids only, and then repressed. Ube1X was also expressed up to the 2-cell stage, but in both embryo types. CONCLUSIONS: We therefore suspect that in embryos fertilized with round spermatids, regulatory mechanisms for inhibiting the inappropriate transcription of male post-meiotically expressed genes are activated following fertilization, permitting the zygotic genome activation to occur, though with some disturbances.

Animals↗
PubMed1994

Testosterone promotes the conversion of round spermatids between stages VII and VIII of the rat spermatogenic cycle.

Several spermatogenic cell types have been reported to be responsive to testosterone (T) in vivo. We have proposed that the principal action of T is to facilitate the maturation of round to elongated spermatids during spermiogenesis. To identify T-dependent cell types during spermiogenesis, round spermatid populations were counted using stereological techniques in adult rats after T withdrawal and replacement. The number of round spermatids per testis in stages I-III, IV-VI, VII, and VIII of the spermatogenic cycle were determined and, based on the known duration of each stage, the hourly production rates of round spermatid populations calculated. Sprague-Dawley rats received 3 cm T and 0.4 cm estradiol implants (TE treatment) for 11 weeks to suppress LH, testicular T levels, and spermatogenesis. To restore sperm production, high-dose T (24 cm) implants were then given, and animals were perfused 0, 2, 4, and 7 days later. Total testicular T levels were suppressed to 2.9% of control levels by TE treatment and significantly increased (P < 0.05) after 2 days of high-dose T, to remain between 7-12% of control. The hourly production rates of round spermatids between stages I and VII were suppressed to 29-35% of control by TE treatment and remained unchanged by high-dose T administration. Stage VIII round spermatid hourly production rates however, were markedly reduced to 5% of control by TE treatment and increased significantly (P < 0.05) to 27% of control after 4 days of high-dose T. The efficiency of conversion of spermatids through spermiogenesis was estimated from the ratios of the hourly production rates of successive spermatid groups. The conversion of spermatids between stages I-VII of the cycle did not differ from control regardless of the treatment. However, the conversion of round spermatids between stages VII and VIII was markedly suppressed to 16% of control by TE treatment and was then normalized after 4 days of high-dose T administration. We conclude that the conversion of round spermatids between stages VII and VIII is a highly T-dependent step during spermiogenesis.

Animals↗
PubMed2004

The acrosome-acroplaxome-manchette complex and the shaping of the spermatid head.

A combination of exogenous contractile forces generated by a stack of F-actin-containing hoops embracing the apical region of the elongating spermatid nucleus and an endogenous modulating mechanism dependent on the spermatid-containing acrosome-acroplaxome-manchette complex may play a cooperative role in the shaping of the spermatid head. In addition, the manchette is a key element in the transport of vesicles and macromolecules to the centrosome and developing spermatid tails as well as in nucleocytoplasmic transport. The proposed model of spermatid head shaping is based on: 1) currently known structural and molecular components of the F-actin hoops, the main cytoskeletal element of the Sertoli cell ectoplasmic specializations; 2) the molecular features of acrosome biogenesis; 3) the assembly of a subacrosomal cytoskeletal plate called the acroplaxome; and 4) the spatial relationship of the acrosome-acroplaxome complex with the manchette, a transient microtubular/actin-containing structure. During acrosome biogenesis, the acroplaxome becomes the nucleation site to which Golgi-derived proacrosomal vescicles tether and fuse. The acroplaxome has at least two functions: it anchors the developing acrosome to the elongating spermatid head. It may also provide a mechanical scaffolding plate during the shaping of the spermatid nucleus. The plate is stabilized by a marginal ring with junctional complex characteristics, adjusting to exogenous clutching forces generated by the stack of Sertoli cell F-actin-containing hoops applied to the elongating spermatid head. A tubulobulbar complex, formed by cytoplasmic processes protruding from the elongating spermatid head extending into the adjacent Sertoli cell, is located at the concave side of the spermatid head. The tubulobulbar complex might provide stabilizing conditions, together with the actin-afadin-nectin-2/nectin-3 adhesion unit, to enable sustained and balanced clutching exogenous forces applied during the elongation of the spermatid head.

Acrosome↗