Meiotic resumption‐coupled degradation of maternal transcripts occurs during oocyte maturation in the absence of mRNA transcription. The CCR4–NOT complex has been identified as the main eukaryotic mRNA deadenylase. In vivo functional and mechanistic information regarding its multiple subunits remains insufficient. Cnot6l, one of four genes encoding CCR4–NOT catalytic subunits, is preferentially expressed in mouse oocytes. Genetic deletion of Cnot6l impaired deadenylation and degradation of a subset of maternal mRNAs during oocyte maturation. Overtranslation of these undegraded mRNAs caused microtubule–chromosome organization defects, which led to activation of spindle assembly checkpoint and meiotic cell cycle arrest at prometaphase. Consequently, Cnot6l−/− female mice were severely subfertile. The function of CNOT6L in maturing oocytes is mediated by RNA‐binding protein ZFP36L2, not maternal‐to‐zygotic transition licensing factor BTG4, which interacts with catalytic subunits CNOT7 and CNOT8 of CCR4–NOT. Thus, recruitment of different adaptors by different catalytic subunits ensures stage‐specific degradation of maternal mRNAs by CCR4–NOT. This study provides the first direct genetic evidence that CCR4–NOT‐dependent and particularly CNOT6L‐dependent decay of selective maternal mRNAs is a prerequisite for meiotic maturation of oocytes.

An important event of the maternal-to-zygotic transition (MZT) in animal embryos is the elimination of a subset of the maternal transcripts that accumulated during oogenesis. In both invertebrates and vertebrates, a maternally encoded mRNA decay pathway (M-decay) acts before zygotic genome activation (ZGA) while a second pathway, which requires zygotic transcription, subsequently clears additional mRNAs (Z-decay). To date the mechanisms that activate the Z-decay pathway in mammalian early embryos have not been investigated. Here, we identify murine maternal transcripts that are degraded after ZGA and show that inhibition of de novo transcription stabilizes these mRNAs in mouse embryos. We show that YAP1-TEAD4 transcription factor-mediated transcription is essential for Z-decay in mouse embryos and that TEAD4-triggered zygotic expression of terminal uridylyltransferases TUT4 and TUT7 and mRNA 3′-oligouridylation direct Z-decay. Components of the M-decay pathway, including BTG4 and the CCR4-NOT deadenylase, continue to function in Z-decay but require reinforcement from the zygotic factors for timely removal of maternal mRNAs. A long 3′-UTR and active translation confer resistance of Z-decay transcripts to M-decay during oocyte meiotic maturation. The Z-decay pathway is required for mouse embryo development beyond the four-cell stage and contributes to the developmental competence of preimplantation embryos.

To determine whether light quality affects the incidence of disease, we exposed cucumber (Cucumis sativus L. cv. Jinyan No. 4) plants at the 4-leaf stage to white and other monochromatic lights and tested the effects on plant response to Sphaerotheca fuliginea, defence-related gene expression and metabolic changes. Exposure to red light resulted in higher levels of H 2 O 2 and salicylic acid (SA), and stronger expression of defence genes such as PR-1 than exposure to white or other monochromatic lights. In comparison, plants grown under purple and blue light had higher activities of phenylalanine ammonialyase (PAL) and polyphenoloxidase (PPO) and higher level of flavonoids than plants grown under other lights. Furthermore, plants grown under red light were more resistant whilst plants grown under other monochromatic lights were less resistant to Sphaerotheca fuliginea than plants grown under white light. These results suggest a role of red light in lightenhanced resistance, which correlates with enhanced SA-dependent signaling pathway.

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