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Highlights

Intra-uterine migration and spacing of embryos occurs in most species with multiple ovulations but is critical in litter-bearing species to optimally distribute blastocysts within each uterine horn for adequate endometrial surface area for implantation and placentation. In a paper on p. 954, Hama et al. provide evidence that lysophosphatidic acid (LPA), acting through its receptor LPA3, plays critical roles in establishment of pregnancy by affecting embryo spacing and subsequent implantation. Targeted deletion of the Lpa3 gene in mice results in delayed implantation and embryo crowding that are associated with decreases in uterine production of prostaglandins and myometrial contractions. Exogenous prostaglandins rescued delayed implantation, but not defects in embryo spacing in Lpa3-null mice. Using embryo transfer, the authors determined that mechanisms for embryo spacing and implantation are segregated events with LPA3 signaling regulating uterine contractions to control embryo spacing and LPA3-mediated uterine production of prostaglandin signaling to mediate implantation of blastocysts. These findings may be relevant to development of strategies to ameliorate poor rates of implantation following assisted reproductive technologies in women.

Kotaro Hama, Junken Aoki, Asuka Inoue, Tomoko Endo, Tomokazu Amano, Rie Motoki, Motomu Kanai, Xiaoqin Ye, Jerold Chun, Norio Matsuki, Hiroshi Suzuki, Masakatsu Shibasaki, and Hiroyuki Arai. Embryo Spacing and Implantation Timing Are Differentially Regulated by LPA3-Mediated Lysophosphatidic Acid Signaling in Mice. Biol Reprod 2007; 77:954–959. Published online in BOR-Papers In Press 5 September 2007; DOI 10.1095/biolreprod.107.060293

Yo-yo-ing in the seminiferous epithelium.

Spermatids differentiate in intimate contact with their surrounding Sertoli cells, which form ectoplasmic specializations at sites of their adhesion to the germ cells. During their differentiation, spermatids move "down," or basally, in the seminiferous epithelium, and subsequently "up" to the apical, luminal region. Previous work from the Vogl laboratory (Guttman et al. 2000, J Cell Sci 113:2167) demonstrated that isolated ectoplasmic specializations support microtubule transport in both directions, leading to the hypotheses that dynein might be responsible for upward movement and a kinesin for downward movement. Now, in a paper on p. 1037, Vaid et al. provide important information bolstering this interesting hypothesis: with combined approaches of mass spectrometry, gene chip analyses, and immunolocalization, they demonstrate that a kinesin, KIF20A, is expressed in the right place and time to be responsible for downward movement of spermatids mediated by ectoplasmic specializations. This is a nice example of how an in vitro model can direct protein discovery. Confirmation of KIF20A function, e.g., by gene knockout, will lead to greater understanding of active dynamics of germ cells in the seminiferous epithelium and possibly even to contraceptive targets.

Kuljeet S Vaid, Julian A Guttman, Roshni R Singaraja, and A. Wayne Vogl. A Kinesin is Present at Unique Sertoli/Spermatid Adherens Junctions in Rat and Mouse Testes. Biol Reprod 2007; 77:1037–1048. Published online in BOR-Papers In Press 12 September 2007; DOI 10.1095/biolreprod.107.063735

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