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Several recent in vitro and germ cell transplantation studies have shown that multipotent or pluripotent cells can be derived from the postnatal testis. However, the source of the cells has been a matter of disagreement. One hypothesis is that testis-derived pluripotent cells arise from primordial germ cells (PGCs) that are remnants from fetal development that failed to differentiate into spermatogonia. An alternative hypothesis is that the pluripotent cells arise from spermatogonial stem cells that dedifferentiate to a pluripotent state in culture. In a paper on p. 681 of this issue, Kanatsu-Shinohara and co-workers provide evidence in favor of the latter hypothesis. They demonstrate that a single clone of germline stem (GS) cells can give rise both to cells with restricted potential to produce spermatogenesis and to multipotent GS (mGS) cells, but that the GS cells lose their spermatogenic potential when they become mGS cells. Although the fate and potential of PGCs is unresolved, these interesting results firmly demonstrate that multipotentiality is an inherent feature of spermatogonial stem cells.
Pluripotency of a Single Spermatogonial Stem Cell in Mice. Mito Kanatsu-Shinohara, Jiyoung Lee, Kimiko Inoue, Narumi Ogonuki, Hiromi Miki, Shinya Toyokuni, Masahito Ikawa, Tomoyuki Nakamura, Atsuo Ogura, and Takashi Shinohara. Biol Reprod 2008; 78:681-687. Published online in BOR-Papers In Press 16 January 2008; DOI 10.1095/biolreprod.107.066068
Recent evidence has suggested a role for prenatal programming in reproductive success. Using a sheep model of prenatal androgen exposure, the Padmanabhan group has provided further insights into how prenatal conditions can alter postnatal fertility. In a paper on p. 648 of this issue, Manikkam et al. show that anterior pituitary responsiveness is increased not only to the primary neuroendocrine drive, GnRH, but also to paracrine modulators through altered gene expression ultimately amplifying LH release and leading to acyclicity. And in another paper in this issue, on p. 636, by Veiga-Lopez et al., the same model was used to illustrate how reproductive defects induced by prenatal androgen exposure develop over time to produce a spectrum of reproductive impairment. These data add to a growing body of evidence in multiple species that prenatal exposure to androgens produces reproductive and metabolic consequences that resemble polycystic ovary syndrome, a leading cause of human infertility.
Developmental Programming: Impact of Prenatal Testosterone Excess on Pre- and Postnatal Gonadotropin Regulation in Sheep. Mohan Manikkam, Robert C. Thompson, Carol Herkimer, Kathleen B. Welch, Jonathan Flak, Fred J. Karsch, and Vasantha Padmanabhan. Biol Reprod 2008; 78:648-660. Published online in BOR-Papers In Press 19 December 2007; DOI 10.1095/biolreprod.107.063347
Developmental Programming: Deficits in Reproductive Hormone Dynamics and Ovulatory Outcomes in Prenatal, Testosterone-Treated Sheep. A. Veiga-Lopez, W. Ye, D. J. Phillips, C. Herkimer, P. G. Knight, and V. Padmanabhan. Biol Reprod 2008; 78:636-647. Published online in BOR-Papers In Press 19 December 2007; DOI 10.1095/biolreprod.107.065904
It has been notoriously difficult to predict fertility from semen or sperm parameters, both in the livestock industry and in the human infertility clinic. For bulls, the most valuable field fertility measurement has been the "non-return rate" (NRR), which is a measure of conception within a defined interval. Now, in a paper on p. 618 of this issue, Lalancette et al. profile "high fertile" and "low fertile" sperm RNAs. Interestingly, a high NRR RNA library has higher representation of transcripts associated with known functions than does a low NRR library, which is enriched for sequences of unknown function. Such transcriptome profiles might be useful for fertility assessment, but more importantly could provide insight into infertility of unknown etiology.
Transcriptome Analysis of Bull Semen with Extreme Nonreturn Rate: Use of Suppression-Subtractive Hybridization to Identify Functional Markers for Fertility. C. Lalancette, C. Thibault, I. Bachand, N. Caron, and N. Bissonnette. Biol Reprod 2008; 78:618-635. Published online in BOR-Papers In Press 14 November 2007; DOI 10.1095/biolreprod.106.059030
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