Fertility is compromised after oocyte-specific deletion of Katanin A-subunit,Katna1, but notKatnal1

Abstract

AbstractKatanins are microtubule severing enzymes that play roles in shaping diverse microtubule-based structures during all cell cycle stages. To address the role of katanin A-subunits in mammalian oocytes, we have used theZp3-CreLoxapproach to specifically delete katanin A1 (Katna1) and katanin A-like 1 (Katnal1) from the start of oocyte growth in mice. Here, we show thatKatnal1is not required for normal female fertility, but that deletion ofKatna1causes a 50% decrease in fertility. Further investigation inKatna1-/-oocytes revealed no effect on MI spindle morphology but a significant effect on the morphology of MII spindles. This was accompanied by a decreased rate of fertilisation. ResultantKatna1+/-heterozygous embryos that reached the 2-cell stage developed at normal rates to the blastocyst stage. Diploid homozygous parthenotes derived fromKatna1-/-oocytes revealed a reduced rate of blastocyst formation, decreased cell number and increased nuclear size. The ability of the paternal allele to rescue preimplantation development suggests the origin of the decrease in the fertility of conditionalKatna1-/-mice lies in abnormalities arising in the egg to embryo transition prior to embryonic genome activation.