Does cDC2/SPDY transiently associate with endoplasmic reticulum exit sites during oocyte maturation?
Our data demonstrate the presence of a novel structure in the cortex of porcine oocytes that comprises ERES and transiently accumulates CDC2 prior to germinal vesicle breakdown. In addition, we show that SPDY, but not cyclin B, localizes to this ERES cluster together with CDC2.
The novel nonsense mutation we detected-EMX2, p.E142X- resulted in a dominant negative effect. The functional data were exemplified in HEK293FT cells. This reinforced the likelihood that EMX2 contributed to the pathophysiology of IMF. Although it is uncommon (0.19%), EMX2 is the first gene identified that if perturbed may cause isolated IMF.