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Publication : Prevention of maternal aging-associated oocyte aneuploidy and meiotic spindle defects in mice by dietary and genetic strategies.

First Author  Selesniemi K Year  2011
Journal  Proc Natl Acad Sci U S A Volume  108
Issue  30 Pages  12319-24
PubMed ID  21730149 Mgi Jnum  J:174362
Mgi Id  MGI:5085932 Doi  10.1073/pnas.1018793108
Citation  Selesniemi K, et al. (2011) From the Cover: Prevention of maternal aging-associated oocyte aneuploidy and meiotic spindle defects in mice by dietary and genetic strategies. Proc Natl Acad Sci U S A 108(30):12319-24
abstractText  Increased meiotic spindle abnormalities and aneuploidy in oocytes of women of advanced maternal ages lead to elevated rates of infertility, miscarriage, and trisomic conceptions. Despite the significance of the problem, strategies to sustain oocyte quality with age have remained elusive. Here we report that adult female mice maintained under 40% caloric restriction (CR) did not exhibit aging-related increases in oocyte aneuploidy, chromosomal misalignment on the metaphase plate, meiotic spindle abnormalities, or mitochondrial dysfunction (aggregation, impaired ATP production), all of which occurred in oocytes of age-matched ad libitum-fed controls. The effects of CR on oocyte quality in aging females were reproduced by deletion of the metabolic regulator, peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha). Thus, CR during adulthood or loss of PGC-1alpha function maintains female germline chromosomal stability and its proper segregation during meiosis, such that ovulated oocytes of aged female mice previously maintained on CR or lacking PGC-1alpha are comparable to those of young females during prime reproductive life.
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