Mitochondria and the death of oocytes

Gloria I. Perez, Alexander M. Trbovich, Roger G. Gosden and Jonathan L. Tilly ()
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Gloria I. Perez: Vincent Center for Reproductive Biology, Massachusetts General Hospital/Harvard Medical School, VBK137E-GYN
Alexander M. Trbovich: Vincent Center for Reproductive Biology, Massachusetts General Hospital/Harvard Medical School, VBK137E-GYN
Roger G. Gosden: Centre for Reproduction, Growth and Development, University of Leeds, Leeds General Infirmary
Jonathan L. Tilly: Vincent Center for Reproductive Biology, Massachusetts General Hospital/Harvard Medical School, VBK137E-GYN

Nature, 2000, vol. 403, issue 6769, 500-501

Abstract: Abstract In females of many species, over half of the germ-cell (oocyte) population dies by apoptosis before birth1. For example, germ-cell numbers peak at 5–7×106 at week 20 of gestation in humans, but drop to less than 1×106 in the early neonatal period2,3. Apparent germ-cell wastage occurs on a similar scale in female rodents, falling from 6.4×104 at day 17.5 of pregnancy to 1.9×104 shortly after birth4. Krakauer and Mira5 have interpreted this death of germ cells as a developmental solution to the accumulation of mutations in mitochondria, proposing that prenatal oocyte apoptosis effectively removes oocytes carrying mutant mitochondria. Here we test whether mitochondria can actually influence oocyte fate by microinjecting small numbers of mitochondria into mouse oocytes and find that this prevents these cells from undergoing apoptosis. We also show that a common mitochondrial DNA deletion occurs more frequently in unfertilized, as compared with fertilized, human oocytes.

Date: 2000
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DOI: 10.1038/35000651

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