The mitochondrial sheath is composed of mitochondria that coil tightly around the midpiece of the sperm flagellum. Mitochondria are recruited from the cytoplasm to the flagellum late in spermatogenesis. Recruited mitochondria are initially spherical, but then elongate laterally to become crescent-like in shape. Subsequently, these crescent-like mitochondria elongate continuously to coil tightly around the flagellum. Mitochondrial sheath development in glycerol kinase 2 (Gk2)-disrupted mice, which show abnormal mitochondrial sheath formation, was observed using freeze-fracturing coupled with scanning electron microscopy (Shimada et al., Glycerol kinase 2 is essential for proper arrangement of crescent-like mitochondria to form the mitochondrial sheath during mouse spermatogenesis, pp. 155–162). Gk2-disrupted spermatids show abnormal localization of crescent-like mitochondria, despite initially exhibiting proper alignment of spherical mitochondria around the flagellum. These results indicate that GK2 is essential for proper arrangement of crescent-like mitochondria during mitochondrial sheath formation in mouse spermatogenesis.
Mammalian oocyte quality degrades over time after in vitro ovulation. As various oocyte manipulations employed in assisted reproductive technology are time consuming, post-ovulatory aging is a serious problem in reproductive medicine and ova research. Shimoi et al. investigated the effects of post-ovulatory aging on the incidence of chromosomal aneuploidy during meiosis II (MII), with a focus on the expression of functional proteins from the spindle assembly checkpoint (SAC) (Shimoi G et al.: Destabilization of spindle assembly checkpoint causes aneuploidy during meiosis II in murine post-ovulatory aged oocytes. pp. 57–66). This study showed that post-ovulatory oocyte aging inhibits MAD2 localization to the sister kinetochore. Furthermore, oocyte aging prevented cohesin subunits from being appropriately maintained or degraded. These results suggest that destabilization of SAC signaling causes sister chromatid segregation errors in MII oocytes and consequently increases the incidence of aneuploidy in early embryos.
The review article by Uenoyama et al. describes the roles of hypothalamic kisspeptin in the central mechanism regulating puberty and subsequent reproductive functions in mammals. The schematic illustration shows a possible mechanism regulating the pubertal augmentation of Kiss1 expression in the arcuate nucleus (ARC) to trigger pulsatile GnRH/gonadotropin secretion in rodents. The authors suspect that estrogen strongly suppresses ARC Kiss1 expression during the prepubertal period via direct and indirect pathways and that the sensitivity to estrogen negative feedback action on ARC Kiss1 expression decreases during the pubertal transition. The resultant increase in secretion of kisspeptin would trigger GnRH/gonadotropin secretion at pubertal onset (Uenoyama et al. The role of kisspeptin in the mechanism underlying reproductive function in mammals. pp. 469–476).
Monitoring Metabolic Health of Dairy Cattle in the Transition Period
Released: August 10, 2010 | Volume 56 Issue S Pages S29-S35
Follicular Growth and Atresia in Mammalian Ovaries: Regulation by Survival and Death of Granulosa Cells
Released: March 22, 2012 | Volume 58 Issue 1 Pages 44-50
Fuko MATSUDA, Naoko INOUE, Noboru MANABE, Satoshi OHKURA
Adaptations for Brood Parasitism in Cuculus Cuckoos
Released: October 20, 2010 | Volume 41 Issue 6 Pages j127-j133
Mammary Growth and Regression -Regulation of Milk Synthesis-
Released: October 20, 2010 | Volume 42 Issue 6 Pages j143-j150