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in Triggering Ca2+ Oscillations During Fertilization. Jason G. Knott, Manabu Kurokawa, Rafael A. Fissore, Richard M. Schultz, and Carmen J. Williams. Biol Reprod 2005; 72:992996. Published 15 December 2004; 10.1095/biolreprod.104.036244
On page 992, Knott et al. provide new insight into processes of egg activation, which is a key event in reproductive and developmental biology. It initiates a cascade of processes necessary for the completion of meiosis, preventing polyspermy, pronuclear formation, and establishes the foundation for normal fetal development. Sperm initiate egg activation, and do so by releasing a factor, first known as oscillin, that causes a series of oscillations in free calcium within the egg cytoplasm. The number, frequency, and amplitude of these oscillations are crucial for driving the sequential processes of egg activation. Classic studies by Keith Jones, Karl Swann, and Shuichi Myazaki and colleagues pointed to a sperm-specific phospholipase C, PLC
, as the oscillin. Now, this paper by Knott et al., demonstrates the key physiological role of PLC
by using a transgenic RNAi approach to reduce the amount of PLC
in mouse sperm. The transgenic sperm trigger abnormal calcium oscillations in normal eggs, which terminate prematurely, and no transgenic offspring are born. These results strongly suggest that PLC
is a physiological trigger for the calcium oscillations that initiate development in mammals.
Increased Myogenic Responses in Uterine but not Mesenteric Arteries from Pregnant Offspring of Diet-Restricted Rat Dams. Denise G. Hemmings, Sukrutha Veerareddy, Philip N. Baker, and Sandra T. Davidge. Biol Reprod 2005; 72: 9971003. Published 15 December 2004; 10.1095/biolreprod.104.035675
On page 997, Hemmings et al. demonstrate enhanced myogenic responses in radial arteries of female offspring born to diet restricted mothers. This is another example of intergenerational effects of maternal environment on "early origins of health and disease." Myogenic responses were assessed in radial uterine arteries of pregnant female offspring to determine if diet restriction during pregnancy of their dams contributed to transgenerational effects. Female offspring from diet restricted and control dams had similar pregnancy weight gain, litter size, and fetal weights; however, placental size was significantly reduced in females from diet restricted dams. Interestingly, enhanced myogenic reactivity occurred in uterine, but not mesenteric arteries. Inhibition of nitric oxide synthase, but not prostaglandin H synthase, significantly increased myogenic responses in uterine arteries of females from control dams, but not diet restricted dams. The authors suggest that impaired uterine vascular function in diet restricted dams leads to similar impairment in their pregnant offspring and may provide a mechanism to explain transgenerational effects on unhealthy pregnancies.
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