The First Successful Pregnancy Following Injection of Testicular Round Spermatid in Iran

Saremi, A.T.; Esfandiari, Navid; Salehi, N Mohammad; Saremi, M. R.

doi:10.1080/01485010290031637

Cited by 13 publications

(6 citation statements)

References 22 publications

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“…In infertility clinics, ICSI has been widely used as the method of choice to overcome infertility of patients with oligozoospermia, azoospermia, teratozoopermia, and asthenozoospermia. Although testicular spermatozoa or elongated spermatids are almost as effective as ejaculated spermatozoa in producing live offspring by human ICSI (30,31), the success and failure of human ROSI have been controversial (32)(33)(34)(35). Although it is possible that nuclei and centrosomes of human round spermatids are not quite ready for syngamy and embryonic development, the problem could be simply technical.…”

Section: Discussionmentioning

confidence: 99%

Production of fertile offspring from genetically infertile male mice

Yanagimachi

Wakayama

Kishikawa

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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A number of recessive autosomal genes cause male infertility. Male mice homozygous for the blind-sterile (bs͞bs) and quaking-sterile (qk͞qk) gene mutations are sterile, because they either do not produce any spermatozoa or produce only a few abnormal spermatozoa. Mice lacking the cyclic AMP responsive-element modulator gene are sterile due to failure of spermiogenesis. All these mice, however, are able to produce fertile offspring when their spermatozoa or round spermatids are injected into oocytes of normal females. This implies that genetic and epigenetic elements necessary for syngamy and embryonic development are established in round spermatids and spermatozoa of these animals, even though their spermatogenic cells are destined to die (bs͞bs and qk͞qk) or are programmed to undergo apoptosis (cyclic AMP responsive-element modulator-null) without becoming functional spermatozoa. In all vertebrates, with few possible exceptions, female germ cells become fertilization-competent at the metaphase of the second meiotic division (1, 2). In contrast, male germ cells become fertilization-competent only after the completion of meiosis and their transformation into motile spermatozoa. In mammals, spermatozoa in the testis are virtually immotile. They must undergo maturation in the epididymis and capacitation in the female genital tract before gaining the ability to interact with mature oocytes (2, 3). Spermatozoa become able to fuse with oocytes only after the acrosome reaction, which normally takes place immediately before passing through noncellular coats surrounding individual oocytes (4). An important question is whether all postmeiotic modifications of male germ cells are necessary for syngamy and embryonic development. Are all genes involved in postmeiotic modifications necessary for the development of new individuals?We found that mouse oocytes fused or injected with round spermatids were able to develop into normal offspring (5, 6). Because secondary, and even late primary, spermatocytes were able to produce normal offspring after injection into oocytes (7-9), we inferred that all genomic and epigenetic elements necessary for embryonic development are established before spermatogenic cells become motile spermatozoa. In other words, all postmeiotic modifications of male germ cells are considered processes solely dedicated for the delivery of male genomes into the oocytes. However, it should be pointed out that all these experiments were performed by using male germ cells from normal fertile male mice. Thereby, a question arises: Would male germ cells that are unable to differentiate into spermatozoa because of genetic causes be able to produce normal offspring? Here, we have used three different mutant mice that display spermiogenic defects at different levels. Mice homozygous for blind-sterile (bs͞bs) and quaking-sterile (qk͞qk) gene mutations produce a few spermatozoa, but none are fertile (10-12). Male mice homozygous for a mutation in the cyclic AMP responsive-element modulator (CREM) gene are unable to start...

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Section: Discussionmentioning

confidence: 99%

Production of fertile offspring from genetically infertile male mice

Yanagimachi

Wakayama

Kishikawa

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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“…It is currently unclear whether human embryogenesis follows a similar pattern, however there is evidence for preferential inactivation of the paternal X in extra-embryonic tissue, suggesting that the same situation applies (Uehara et al, 2000). If so, if the epigenetic marks set during spermatogenesis have effects following fertilisation, this would have an impact on current methods of treatment for infertility-in particular ICSI has been performed with immature sperm and even round spermatids (Silber et al, 1996;Saremi, Esfandiari, Salehi, & Saremi, 2002;Mansour et al, 2003), in which the various imprints may not yet have been correctly established. Interestingly, a recent study (Dumoulin et al, 2005) showed that human preimplantation XX embryos grow slower than XY embryos if produced via ICSI, but not if produced via IVF, and that the differential growth is due to reduced proliferation of extraembryonic cells.…”

Section: Potential Wider Implications Of Sex Chromosome Dynamicsmentioning

confidence: 96%

Spermatogenesis and sex chromosome gene content: An evolutionary perspective

Ellis¹,

Affara²

2006

Human Fertility

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Mammalian sex chromosomes are highly diverged and heteromorphic: a comparatively large and gene-rich X chromosome contrasting with a small, largely heterochromatic and degenerate Y chromosome. Both gonosomes are however uniquely important in male-specific functions such as spermatogenesis. In this review, we examine the evolutionary pressures that have driven the divergence of the sex chromosomes from their ancestral state, and show how these have shaped the gene content of both chromosomes. Their shared history of gene acquisition and loss, differentiation, degeneration and intragenomic warfare has far-reaching consequences for their functionality in spermatogenesis, and may also have potential clinical implications.

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“…ROSNI is proposed as a treatment for men in whom other more mature sperm forms (elongating spermatids or sperm) cannot be identified for ICSI [72]. It is not widely performed, not as successful as ICSI and is still an experimental procedure.…”

Section: Injection With Immature Spermmentioning

confidence: 99%