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CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE118564 | GEO | 2018/11/23

REPOSITORIES: GEO

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CNOT6L couples the selective degradation of maternal transcripts to meiotic cell cycle progression in mouse oocyte.

Project description: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.

| S-EPMC6293276 | biostudies-literature

CNOT6L Couples Selective Maternal Transcript Degradation to Meiotic Cell Cycle Progression in Oocyte

Project description: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-zygotic transition licensing factor BTG4, which interacts with catalytic subunits CNOT7 and -8 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.

| S-SCDT-EMBOJ-2018-99333 | biostudies-other

CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [polysome RNA-seq]

Project description:Purpose: The goals of this study are to study the function of Cnot6l during oocyte maturation . Methods: Comparing the polysome-bounded transcripts at GV, MI and MII stage in WT and Cnot6l-/- oocytes by RNA sequencing. Results: Using an optimized data analysis workflow, we mapped about 15 million sequence reads per sample to the mouse genome (build mm9) and identified 23236 transcripts with TopHat workflow. Conclusions: CNOT6L stimulated degradation of maternal transcriptsto oocyte meiotic maturation.

2018-11-23 | GSE118563 | GEO

CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [total RNA-seq]

Project description:Purpose: The goals of this study are to study the function of Cnot6l during oocyte maturation and the differences between loss of Cnot6l and Btg4 during oocyte maturation. Methods:Comparing the degration of transcripts at different stage in WT, Btg4-/- and Cnot6l-/- oocytes by RNA sequencing. Results: Using an optimized data analysis workflow, we mapped about 15 million sequence reads per sample to the mouse genome (build mm9) and identified 23236 transcripts with TopHat workflow. Conclusions: CNOT6L stimulated degradation of maternal transcriptsto oocyte meiotic maturation.

2018-11-23 | GSE118562 | GEO

CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte

Project description:CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte

| PRJNA486092 | ENA

CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [total RNA-seq]

Project description:CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [total RNA-seq]

| PRJNA486094 | ENA

CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [polysome RNA-seq]

Project description:CNOT6L Couples the Selective Degradation of Maternal Transcriptsto Meiotic Cell Cycle Progression in Mouse Oocyte [polysome RNA-seq]

| PRJNA486095 | ENA

MAPK signaling couples SCF-mediated degradation of translational regulators to oocyte meiotic progression.

Project description:RNA-binding proteins (RBPs) are important regulators of gene expression programs, especially during gametogenesis. How the abundance of particular RBPs is restricted to defined stages of meiosis remains largely elusive. Here, we report a molecular pathway that subjects two nonrelated but broadly evolutionarily conserved translational regulators (CPB-3/CPEB and GLD-1/STAR) to proteosomal degradation in Caenorhabditis elegans germ cells at the transition from pachytene to diplotene of meiotic prophase. Both RBPs are recognized by the same ubiquitin ligase complex, containing the molecular scaffold Cullin-1 and the tumor suppressor SEL-10/FBXW7 as its substrate recognition subunit. Destabilization of either RBP through this Skp, Cullin, F-box-containing complex (SCF) ubiquitin ligase appears to loosen its negative control over established target mRNAs, and presumably depends on a prior phosphorylation of CPB-3 and GLD-1 by MAPK (MPK-1), whose activity increases in mid- to late pachytene to promote meiotic progression and oocyte differentiation. Thus, we propose that the orchestrated degradation of RBPs via MAPK-signaling cascades during germ cell development may act to synchronize meiotic with sexual differentiation gene expression changes.

| S-EPMC5866554 | biostudies-literature

Cep55 regulates spindle organization and cell cycle progression in meiotic oocyte.

Project description:Cep55 is a relatively novel member of the centrosomal protein family. Here, we show that Cep55 is expressed in mouse oocytes from the germinal vesicle (GV) to metaphase II (MII) stages. Immuostaining and confocal microscopy as well as time lapse live imaging after injection of mRNA encoding fusion protein of Cep55 and GFP identified that Cep55 was localized to the meiotic spindle, especially to the spindle poles at metaphase, while it was concentrated at the midbody in telophase in meiotic oocytes. Knockdown of Cep55 by specific siRNA injection caused the dissociation of ?-tubulin from the spindle poles, resulting in severely defective spindles and misaligned chromosomes, leading to metaphase I arrest and failure of first polar body (PB1) extrusion. Correspondingly, cyclin B accumulation and spindle assembly checkpoint (SAC) activation were observed in Cep55 knockdown oocytes. Our results suggest that Cep55 may act as an MTOC-associated protein regulating spindle organization, and thus cell cycle progression during mouse oocyte meiotic maturation.

| S-EPMC4652202 | biostudies-literature

The chromatin remodeler Snf2h is essential for oocyte meiotic cell cycle progression.

Project description:Oocytes are indispensable for mammalian life. Thus, it is important to understand how mature oocytes are generated. As a critical stage of oocytes development, meiosis has been extensively studied, yet how chromatin remodeling contributes to this process is largely unknown. Here, we demonstrate that the ATP-dependent chromatin remodeling factor Snf2h (also known as Smarca5) plays a critical role in regulating meiotic cell cycle progression. Females with oocyte-specific depletion of Snf2h are infertile and oocytes lacking Snf2h fail to undergo meiotic resumption. Mechanistically, depletion of Snf2h results in dysregulation of meiosis-related genes, which causes failure of maturation-promoting factor (MPF) activation. ATAC-seq analysis in oocytes revealed that Snf2h regulates transcription of key meiotic genes, such as Prkar2b, by increasing its promoter chromatin accessibility. Thus, our studies not only demonstrate the importance of Snf2h in oocyte meiotic resumption, but also reveal the mechanism underlying how a chromatin remodeling factor can regulate oocyte meiosis.

| S-EPMC7000916 | biostudies-literature

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