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The fecundity of female mammals is resolved by the limited size of the primordial follicle (PF) pool formed perinatally. The establishment of PF pool is accompanied by a significant programmed oocyte death. Long non-coding RNAs (lncRNA) are central modulators in regulating cell apoptosis or autophagy in multiple diseases, however, the significance of lncRNAs governing perinatal oocyte loss remains unknown. Here we find that Yin-Yang 1 (YY1) directly binds to the lncRNA X-inactive-specific transcript ( Xist ) promoter and facilitates  Xist  expression in the perinatal mouse ovaries.  Xist  is highly expressed in fetal ovaries and sharply downregulated along with the establishment of PF pool after birth. Gain or loss of function analysis reveals that  Xist  accelerates oocyte autophagy, mainly through binding to  pre-miR-23b  or  pre - miR-29a  in the nucleus and preventing the export of  pre-miR-23b / pre - miR-29a  to the cytoplasm, thus resulting in decreased mature of  miR-23b-3p / miR-29a-3p  expression and upregulation  miR-23b-3p / miR-29a-3p  co-target, STX17, which is essential for timely control of the degree of oocyte death in prenatal mouse ovaries. Overall, these findings identify  Xist  as a key non-protein factor that can control the biogenesis of  miR-23b-3p / miR-29a-3p , and this YY1- Xist - miR-23b-3p / miR-29a-3p -STX17 regulatory axis is responsible for perinatal oocyte loss through autophagy.

Long non-coding RNA Xist regulates oocyte loss via suppressing miR-23b-3p/miR-29a-3p maturation and upregulating STX17 in perinatal mouse ovaries