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Outcomes of maternal nutrition. Factors affecting oocyte quality have long been a target of experimental inquiry and the effects of aging, metabolic disease, and environmental hazards have received particular attention. Murine systems are often most amenable to these experimental studies, but, although they are valuable, their relevance to the human might not be as clear as studies using domestic species or non-human primates. Kevin Sinclair's group at Nottingham has for the last several years been developing systems to assess the influence of diet and systemic physiology on oocyte quality in domestic species. In an article on page 918 they now have assessed the effects diet and body condition on oocyte developmental competence. They found that high levels of feeding improved the competence of oocytes to develop to the blastocyst stage when heifers are scored as low body condition (particularly lean). In contrast, this same feeding regimen resulted in reduced oocyte developmental competence when the body condition was good. This level of feeding also promoted hyperinsulinaemia in the normal body condition heifers, however, it is not yet clear whether the condition of hyperinsulinaemia is directly related to the reduced oocyte quality. These studies leave us excited about the prospects of using this system to assess the post-implantation effects of body condition and feeding and the potential for late onset health problems.
Defects in Secretory Pathway Trafficking During Sperm Development in Adam2 Knockout Mice. Kathryn K. Stein, Jowell C. Go, Paul Primakoff, and Diana G. Myles. Biol Reprod 2005; 73:1032–1038. Published online 13 July 2005; 10.1095/biolreprod.105.040972
Protein trafficking revealed. Mutant phenotypes often provide unexpected bonuses. A case in point is the phenotype of mice with targeted deletions of the genes encoding sperm ADAM (A Disintegrin And Metalloprotease) proteins. Male mice with a null mutation of the Adam2 gene (encoding ADAM2, also known as fertilin beta) are infertile and their sperm do not enter the oviduct. Surprisingly, other ADAM proteins, ADAM1B (fertilin alpha b) and ADAM3 (also known as cyritestin) are not present in the sperm from Adam2 KO mice. In a report on page 1032 of this issue, Stein et al elucidate the basic cell biology behind this surprising observation. Profiles of ADAM protein processing through the Golgi apparatus are similar in wild-type and mutant germ cells, but much of the "untargeted" ADAM protein fails to reach the cell surface in testicular sperm. Interestingly, this defect occurs at the same developmental stage when these proteins normally appear in a Triton X-100 insoluble compartment, which may reflect a specific protein "sorting" or "retention" pathway required for normal cell-surface expression. This suggests a previously unsuspected chaperone-like role for some ADAM proteins. This study reveals the cooperative nature of protein passage through the secretory pathway and thus addresses a fundamental question of sperm development, namely, how different surface components are targeted to specific domains.
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