![]() These observations raise intriguing questions regarding how mRNA decay is regulated during meiotic maturation. Indeed, oocytes that undergo delayed RNA decay exhibit a reduced polar body extrusion (PBE) rate, distorted spindles and embryo development arrest 3, 4. Therefore, the maintenance and timely decay of maternal transcripts is a prerequisite for the acquisition of full developmental competence in oocytes. Consequently, by the 2-cell stage, approximately 90% of cellular RNAs in mouse embryos are degraded 2. ![]() Transcription does not resume until zygotic genome activation (ZGA) after fertilization. Once oocytes develop to the full-grown germinal vesicle (GV) stage, extensive but target-selective maternal RNA decay is triggered by gonadotropin, and de novo transcription ceases. In growing oocytes, maternal RNAs are robustly transcribed and stored to support further oocyte maturation and embryo development. The intricately orchestrated transition from oocyte to embryo is accompanied by dynamic changes in maternal transcripts 1. Overall, this work identifies ALKBH5 as a key determinant of oocyte quality and unveil the facilitating role of ALKBH5-mediated m 6A removal in maternal RNA decay. Additionally, reducing IGF2BP2 in Alkbh5-depleted oocytes partially rescued these defects. A distinct subset of transcripts with persistent m 6A peaks are recognized by the m 6A reader IGF2BP2 and thus remain stabilized, resulting in impaired RNA clearance. ![]() Analysis of m 6A dynamics demonstrated that ALKBH5-mediated m 6A demethylation ensures the timely degradation of maternal RNAs, which is severely disrupted following Alkbh5 −/− depletion. Temporal profiling of the maternal transcriptomes revealed striking RNA accumulation in Alkbh5 −/− oocytes during meiotic maturation. Here, we show that Alkbh5 depletion causes a wide range of defects in oocyte meiosis and results in female infertility. However, the specific role of ALKBH5 in oocyte maturation remains elusive. ![]() One regulator of m 6A, ALKBH5, reverses m 6A deposition and is essential in RNA metabolism. N 6-methyladenosine (m 6A) maintains maternal RNA stability in oocytes. ![]()
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