Deletion of Mylk1 in Oocytes Causes Delayed Morula-to-Blastocyst Transition and Reduced Fertility Without Affecting Folliculogenesis and Oocyte Maturation in XXXX .

@entity1 @entity249 @entity19 @entity23452
UNASSIGNED: @entity1 oocyte undergos two asymmetric cell divisions during meiotic maturation and fertilization. Acentric spindle positioning and cortical polarity are major factors involved in asymmetric cell division, both of which are thought to depend on the dynamic interaction between myosin II and actin filaments. @entity23452 ( @entity23452 ) encoding by Mylk1 gene could directly phosphorylate and activate myosin II. To determine whether @entity23452 was required for oocyte asymmetric division, we specifically disrupted Mylk1 gene in oocytes by Cre-loxP conditional knockout system. We found that Mylk1 mutant female @entity19 showed severe @entity249 . Unexpectedly, contrary to previously reported in vitro findings, our data showed that oocyte meiotic maturation including spindle organization, polarity establishment, homologous chromosomes separation and polar body extrusion were not affected in Mylk1(fl/fl);GCre(+) females. Follicular development, ovulation and early embryonic develop to compact morula occurred normally in Mylk1(fl/fl);GCre(+) females, but deletion of @entity23452 caused delayed morula-to-blastocyst transition. More than a third of embryos were at morula stage at 3.5 days post coitum (dpc) in vivo. The delayed embryos could develop further to early blastocyst stage in vitro on Day 4 when most control embryos reached expanded blastocysts. Our findings provide evidence that @entity23452 is linked to timely blastocyst formation, though it is dispensable for oocyte meiotic maturation.
