The purpose of the present series of experiments was to test the hypothesis that treatment of bovine oocytes with MG132 at the end of maturation would improve developmental competence of the oocytes and resultant embryos while addition of MG132 at the beginning of maturation would reduce oocyte competence. An additional goal was to assess specific proteins whose relative abundance in the oocyte was altered by MG132 late in maturation with the goal of identifying candidate molecules responsible for actions of MG132 on oocyte competence. Oocyte competence for nuclear maturation, fertilization and ability to support embryonic development was affected by addition of the proteasomal inhibitor MG132 during the maturation process. Actions of MG132 depended on the time of addition. Oocyte competence was improved when MG132 was added during the last 6 h of maturation and reduced when added during the first 6 h of maturation. It is well established that proteasomal activity is required for completion of meiosis I. Proteasomal cleavage of ubiquitinated cyclin B1 leads to the inactivation of MPF required for completion of meiosis I. Inhibition of meiosis is likely a major cause for reduced oocyte competence caused by addition of MG132 from 0�C6 h of maturation because MG132 treatment at this time tended to reduce the proportion of oocytes that L-161,982 reached MII at the end of maturation. Inhibition of other proteasome-mediated events early in maturation may also be involved in reduced oocyte competence. For example, in the pig, MG132 can affect cumulus cells by reducing progesterone production and expression of genes involved in expansion of the extracellular matrix. The finding that treatment with MG132 late in maturation improves oocyte competence is consistent with other results showing beneficial effects of MG132 on aged mouse oocytes fertilized by intracytoplasmic sperm injection and parthenogenetically activated pig oocytes. Beneficial effects of MG132 on nuclear Lisuride maleate remodeling, transcript abundance and embryonic development have also been shown for embryos constructed by somatic cell nuclear cloning in mice, rats, goats and pigs. Unlike for addition from 0�C6 h, MG132 added from 16�C22 h did not improve oocyte competence by improving nuclear maturation because the percentage of oocytes that were MII at the end of maturation was not affected by MG132 later in maturation. Rather, some of the beneficial effect of MG132 from 16�C22 h on the percentage of oocytes that became blastocysts was due to 1) increased cleavage rate through actions not involving fertilization rate and 2) increased competence of the fertilized oocyte to develop to the blastocyst stage. Indeed, the potential of a newly formed embryo to become a blastocyst was improved by addition of MG132 from 16�C22 h in two of three experiments evaluated, as indicated by a significant improvement in the percentage of cleaved embryos that became blastocysts.