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MSL3 coordinates a transcriptional and translational meiotic program in female Drosophila

ABSTRACT: MSL3 coordinates a transcriptional and translational meiotic program in female Drosophila

PROVIDER: PRJNA601455 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10899254.fastq.gz	Fastqsanger.gz
	SRR10899255.fastq.gz	Fastqsanger.gz
	SRR10899256.fastq.gz	Fastqsanger.gz
	SRR10899257.fastq.gz	Fastqsanger.gz
	SRR10899258.fastq.gz	Fastqsanger.gz

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MSL3 coordinates a transcriptional and translational meiotic program in female Drosophila

Project description:Gamete formation from germline stem cells (GSCs) is essential for sexual reproduction. However, the regulation of GSC differentiation and meiotic entry are incompletely understood. Set2, which deposits H3K36me3 modifications, is required for differentiation of GSCs during Drosophila oogenesis. We discovered that the H3K36me3 reader Male-specific lethal 3 (MSL3) and the histone acetyltransferase complex Ada2a-containing (ATAC) cooperate with Set2 to regulate entry into meiosis in female Drosophila. MSL3 expression is restricted to the mitotic and early meiotic stages of the female germline, where it promotes transcription of genes encoding synaptonemal complex components and a germline enriched ribosomal protein S19 paralog, RpS19b. RpS19b upregulation is required for translation of Rbfox1, a known meiotic cell cycle entry factor. Thus, MSL3 is a master regulator of meiosis, coordinating the expression of factors required for recombination and GSC differentiation. We find that MSL3 is expressed during mouse spermatogenesis, suggesting a conserved function during meiosis.

2021-12-09 | GSE143728 | GEO

Genome-wide analysis reveals a switch in the translational program upon oocyte meiotic resumption

Project description:Genome-wide analysis reveals a switch in the translational program upon oocyte meiotic resumption

| PRJNA559169 | ENA

High-resolution view of the yeast meiotic program revealed by ribosome profiling

Project description:Meiosis is a complex developmental process that generates haploid cells from diploid progenitors. We measured mRNA abundance and protein production through yeast sporulation and found strong temporal control for most genes, achieved through both mRNA levels and translational regulation. Monitoring the timing of protein production revealed novel factors involved in recombination and helped to illuminate the molecular basis of the broad restructuring of meiotic cells. We also found a strong increase in noncanonical translation at short open reading frames (sORFs) on unannnotated transcripts and upstream regions of known transcripts (uORFs). Ribosome occupancy at near-cognate uORFs was associated with more efficient ORF translation; while some AUG uORFs, often on regulated leader extensions, acted comptetitively. This work reveals a pervasive role for meiotic translational control and great complexity in genomic coding. Fine mapping of gene expression through meiosis reveals extensive regulation of protein synthesis and widespread non-canonical translation.

2012-01-06 | E-GEOD-34082 | biostudies-arrayexpress

Loss Of Function of Male-Specific Lethal 3 (Msl3) Does Not Affect Spermatogenesis in Rodents

Project description:Msl3 is a member of the chromatin-associated male-specific lethal MSL complex which is responsible for the transcriptional upregulation of genes on the X chromosome in males Drosophila. Although the dosage complex operates differently in mammals, the Msl3 gene is conserved from flies to humans. Msl3 is required for meiotic entry during Drosophila oogenesis. Recent reports indicate that also in primates, Msl3 is expressed in undifferentiated germline cells before meiotic entry. However, if Msl3 plays a role in the meiotic entry of mammals has yet to be explored. To study this, we used mouse spermatogenesis as a study model. Analyses of single cells RNA-seq data revealed that in mouse, differently from what was reported in primates, Msl3 is expressed in meiotic cells. To test the role of Msl3 in meiosis, we used a male germline-specific Stra8-iCre driver and a newly generated Msl3flox conditional knock-out mouse line. Msl3 conditional loss-of-function in spermatogonia did not cause spermatogenesis defects or changes in the expression of genes related to meiosis. Our data suggest that, in mice, Msl3 exhibits delayed expression compared to Drosophila and primates, and loss-of-function mutations disrupting the chromodomain or the MRG domain of Msl3 alone do not impede meiotic entry in rodents.

2023-10-05 | GSE235777 | GEO

High-resolution view of the yeast meiotic program revealed by ribosome profiling

2012-01-06 | GSE34082 | GEO

SWI/SNF chromatin remodeling complex coordinates the meiotic gene activation via promoter remodeling and Meiosin activation in female germline

Project description:In mammals, primordial germ cells (PGCs) enter meiosis and differentiate to primary oocytes in embryonic ovaries. Previously, we demonstrated that SWI/SNF chromatin remodeling complex is required for induction of the meiotic prophase genes and meiotic initiation in female germline, using conditional knockout (CKO) mice lacking the Smarcb1 (also known as Snf5) gene, which encodes a core subunit of the SWI/SNF complex. Here, we show that the meiotic prophase genes expressed at lower levels in the Snf5 CKO females can be classified into two groups, based on the promoter accessibility. The promoters of 74% of these genes showed lower accessibility in the mutant mice whereas those of remaining genes were opened equivalently in control and the mutant mice. The former genes include the Meiosin that encodes the transcription regulator essential for activation of the meiotic prophase genes. Furthermore, the promoters of the former and the latter genes were largely modified with H3K27me3/bivalent histone marks and H3K4me3, respectively. Collectively, we provide the mechanistic model by which SWI/SNF complex remodels the meiotic prophase genes repressed by polycomb repressive complex (PRC), including the Meiosin, and then MEIOSIN together with STRA8 activates the meiotic prophase genes in female germline.

2022-11-17 | GSE203588 | GEO

ZAR1 and ZAR2 are Required for Oocyte Meiotic Maturation by Regulating the Maternal Transcriptome and mRNA Translational Activation

Project description:Zar1 was the first mammalian maternal-effect gene to be identified. Embryos derived from Zar1-null female mice are blocked before zygotic genome activation; however, the underlying mechanism remains unclear. By knocking out Zar1 and its homolog Zar2 in mice, we revealed a novel function of these genes in oocyte meiotic maturation. Zar1/2-deleted oocytes displayed delayed meiotic resumption and polar body-1 emission and a higher incidence of abnormal meiotic spindle formation and chromosome aneuploidy. The grown oocytes of Zar1/2-null mice contained fewer total mRNAs and displayed a reduced level of protein synthesis. Key maturation-associated changes failed to occur in the Zar1/2-null oocytes, including the translational activation of maternal mRNAs encoding the cell cycle proteins cyclin B1 and WEE2, as well as maternal-to-zygotic transition (MZT) licensing factor BTG4. Consequently, maternal mRNA decay was impaired and MZT was abolished. ZAR1/2 bound mRNAs to regulate the translational activity of their 3ʹ-UTRs and interacted with other oocyte proteins, including mRNA-stabilizing protein MSY2 and cytoplasmic lattice components. These results countered the traditional view that ZAR1 only functions after fertilization and highlight a previously unrecognized role of ZAR1/2 in regulating the maternal transcriptome and translational activation in maturing oocytes.

2019-09-25 | GSE135787 | GEO

A Rapid Translational Immune Response Program in CD8 Memory T Lymphocytes

Project description:A Rapid Translational Immune Response Program in CD8 Memory T Lymphocytes

| PRJNA707537 | ENA

LIN-41 and OMA ribonucleoprotein complexes mediate a translational repression-to-activation switch controlling oocyte meiotic maturation and the oocyte-to-embryo transition in Caenorhabditis elegans

Project description:An extended meiotic prophase is a hallmark of oogenesis. Hormonal signaling activates the CDK1/cyclin B kinase to promote oocyte meiotic maturation, which involves nuclear and cytoplasmic events. Nuclear maturation encompasses nuclear envelope breakdown, meiotic spindle assembly, and chromosome segregation. Cytoplasmic maturation involves major changes in oocyte protein translation and cytoplasmic organelles and is poorly understood. In the nematode Caenorhabditis elegans, sperm release the major sperm protein (MSP) hormone to promote oocyte growth and meiotic maturation. Large translational regulatory ribonucleoprotein (RNP) complexes containing the RNA-binding proteins OMA-1, OMA-2, and LIN-41 regulate meiotic maturation downstream of MSP signaling. To understand the control of translation during meiotic maturation, we purified LIN-41-containing RNPs and characterized their protein and RNA components. Protein constituents of LIN-41 RNPs include essential RNA-binding proteins, the GLD-2 cytoplasmic poly(A) polymerase, the CCR4-NOT deadenylase complex, and translation initiation factors. RNA sequencing defined mRNAs associated with both LIN-41 and OMA-1, as well as sets of mRNAs associated with either LIN-41 or OMA-1. Genetic and genomic evidence suggests that GLD-2, which is a component of LIN-41 RNPs, stimulates the efficient translation of many LIN-41-associated transcripts. We analyzed the translational regulation of two transcripts specifically associated with LIN-41 that encode the RNA regulators SPN-4 and MEG-1. We found that LIN-41 represses translation of spn-4 and meg-1, whereas OMA-1 and OMA-2 promote their expression. Upon their synthesis, SPN-4 and MEG-1 assemble into LIN-41 RNPs prior to their functions in the embryo. This study defines a translational repression-to-activation switch as a key element of cytoplasmic maturation.

2017-06-02 | GSE98130 | GEO

SWI/SNF chromatin remodeling complex coordinates the meiotic gene activation via promoter remodeling and Meiosin activation in female germline

Project description:SWI/SNF chromatin remodeling complex coordinates the meiotic gene activation via promoter remodeling and Meiosin activation in female germline

| PRJNA841501 | ENA

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