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Maternal MicroRNAs are Essential for Mouse Zygotic Development

ABSTRACT: MicroRNAs (miRNAs) have been shown to have important functions in a variety of cellular processes. Here we report on miRNA expression and their dynamic regulation during mouse oogenesis and early embryos. We show that following specific deletion of Dicer from growing oocytes, the mutant oocytes cease development and were unable to progress through the first cell division. While the mutant mature oocytes seemed morphologically normal, they had disorganized spindle. Using detailed single cell cDNA microarray analysis of normal versus mutant oocytes, we found that a large proportion of maternal genes, including C-mos, are under the control of miRNAs. This study provides strong evidence that maternal miRNAs are essential for the earliest stages of mouse embryonic development. mRNA expression was compared with miRNA expression in dicer knockout and wild-type mouse mature oocyte.

ORGANISM(S): Mus musculus

SUBMITTER: Kaneda Masahiro

PROVIDER: E-GEOD-6806 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Maternal microRNAs are essential for mouse zygotic development.

Tang Fuchou F Kaneda Masahiro M O'Carroll Dónal D Hajkova Petra P Barton Sheila C SC Sun Y Andrew YA Lee Caroline C Tarakhovsky Alexander A Lao Kaiqin K Surani M Azim MA

Genes & development 20070301 6

MicroRNAs (miRNAs) have important roles in diverse cellular processes, but little is known about their identity and functions during early mammalian development. Here, we show the effects of the loss of maternal inheritance of miRNAs following specific deletion of Dicer from growing oocytes. The mutant mature oocytes were almost entirely depleted of all miRNAs, and they failed to progress through the first cell division, probably because of disorganized spindle formation. By comparing single-cel ...[more]

PMID: 17369397

Similar Datasets

Maternal MicroRNAs are Essential for Mouse Zygotic Development

Project description:MicroRNAs (miRNAs) have been shown to have important functions in a variety of cellular processes. Here we report on miRNA expression and their dynamic regulation during mouse oogenesis and early embryos. We show that following specific deletion of Dicer from growing oocytes, the mutant oocytes cease development and were unable to progress through the first cell division. While the mutant mature oocytes seemed morphologically normal, they had disorganized spindle. Using detailed single cell cDNA microarray analysis of normal versus mutant oocytes, we found that a large proportion of maternal genes, including C-mos, are under the control of miRNAs. This study provides strong evidence that maternal miRNAs are essential for the earliest stages of mouse embryonic development. Keywords: mRNA and miRNA expression comparison

2007-03-16 | GSE6806 | GEO

MicroRNA function is globally suppressed in mouse oocytes and early embryos

Project description:Dicer, which is required for the processing of both microRNAs (miRNAs) and small interfering RNAs (siRNAs), is essential for oocyte maturation. Oocytes express both miRNAs and endogenous siRNAs (endo-siRNAs). To determine whether the abnormalities in Dicer knockout oocytes during meiotic maturation are secondary to the loss of endo-siRNAs and/or miRNAs, we deleted Dgcr8, which encodes a RNA binding protein specifically required for miRNA processing. In striking contrast to Dicer, Dgcr8 deficient oocytes matured normally and, when fertilized with wild-type sperm, produced healthy appearing offspring, even though miRNA levels were reduced to similar levels as Dicer deficient oocytes. Furthermore, the deletion of both maternal and zygotic Dgcr8 alleles did not impair preimplantation development including the determination of the inner cell mass (ICM) and trophectoderm. Most surprisingly, the mRNA profiles of wild-type and Dgcr8 null oocytes were essentially identical while Dicer null oocytes showed hundreds of misregulated transcripts. These findings show that miRNA function is globally suppressed during oocyte maturation and preimplantation development and that endo-siRNAs, rather than miRNAs, underlie the Dicer knockout phenotype in oocytes. We used microarrays to understand at the global level how loss of miRNAs and/or siRNAs is impacting mRNA levels in mouse oocytes.

2010-02-05 | GSE19894 | GEO

Adenylation of maternally inherited microRNAs by Wispy

Project description:Early development depends heavily on accurate control of maternally inherited mRNAs, and yet it remains unknown how maternal microRNAs (miRNAs) are regulated during maternal to zygotic transition (MZT). We here find that maternal miRNAs are highly adenylated at their 3' ends in mature oocytes and early embryos. Pervasive adenylation is observed in oocytes of fly, sea urchin and mouse, indicating that maternal miRNA adenylation may be widely conserved in animals. We identify Wispy as the enzyme responsible for miRNA adenylation in flies. Wispy is known to be expressed specifically in oocytes and early embryos and function as a noncanonical poly(A) polymerase. Knockout of wispy abrogates miRNA adenylation and induces miRNA accumulation in fly eggs whereas overexpression of Wispy increases adenylation and reduces miRNA levels in S2 cells. Adenylation occurs on both the 5p and 3p miRNAs, indicating that Wispy acts on miRNAs after Dicer processing. We further find that Wispy interacts with Ago1 through protein-protein interaction, which may allow the effective and selective adenylation of miRNAs. Thus, adenylation may contribute to the clearance of maternally deposited miRNAs during MZT. Our work provides the first mechanistic insights into the regulation of maternal miRNAs and illustrates the importance of RNA tailing in development. MiRNA expression and modification profile during early embryo development of fruit fly and zebra fish using high throughput sequencing

2014-10-01 | E-GEOD-61931 | biostudies-arrayexpress

Gene expression profile of Dicer-deficient oocytes

Project description:Small RNAs, such as miRNAs and siRNAs, are involved in gene regulation in a variety of systems, including mouse oocytes. Dicer is a ribonuclease III enzyme essential for miRNA and siRNA biosynthesis. In an effort to uncover the function of small RNAs during oocyte growth, we specifically deleted Dicer in growing oocytes and analyzed the global pattern of gene expression in these Dicer-deficient oocytes. Germinal vesicle-intact, fully grown oocytes were collected from eCG-primed wild-type or Dicer-deficient female mice and freed of attached cumulus cells by pipetting. Twenty oocytes per mouse were used for RNA extraction and hybridization on the MOE430 v2 Affymetrix microarray platform. Oocytes from four wild-type and four Dicer-knockout mice were analyzed.

2010-04-06 | E-GEOD-17985 | biostudies-arrayexpress

Adenylation of maternally inherited microRNAs by Wispy

2014-10-01 | GSE61931 | GEO

Gene expression profile of Dicer-deficient oocytes

2010-03-05 | GSE17985 | GEO

Transcriptome profile of oocytes expressing a catalytically inactive knock-in allele of Ago2

2015-01-20 | GSE57514 | GEO

A novel miRNA processing pathway independent of Dicer requires Argonaute2 catalytic activity

Project description:Here we identify a Dicer-independent miRNA biogenesis pathway that employs the slicer catalytic activity of Argonaute2 (Ago2). To uncover Dicer-independent miRNAs, we sequenced small RNAs in wild type, maternal-zygotic dicer (MZdicer) and MZago2 mutants, using zebrafish as a model system. We find that, in contrast to other miRNAs, miR-451 levels were increased in MZdicer but drastically reduced in the MZago2 mutants. We show that pre-miR-451 processing requires Ago2 catalytic activity in vivo. MZago2 mutant embryos display delayed erythrocyte maturation that can be rescued by wild type Ago2 or miR-451 duplex but not catalytically dead Ago2. We propose that Ago2-mediated cleavage of a subset of pre-miRNAs, followed by uridylation and trimming, generates functional miRNAs in a Dicer-independent manner.

2010-07-01 | GSE21503 | GEO

Transcriptome profile of oocytes expressing a catalytically inactive knock-in allele of Ago2

Project description:The RNase III enzyme DICER generates both microRNAs (miRNAs) and endogenous short interfering RNAs (endo-siRNAs). Dicer deletion in mouse oocytes leads to female infertility due to defects during meiosis I. Because miRNA function is suppressed in mouse oocytes, it has been proposed that endo-siRNAs may have a role during female meiosis. By utilizing a catalytically inactive knock-in allele of AGO2 specifically in oocytes, we disrupt the function of siRNAs and analyze the transcriptome of these oocytes in comparison with Ago2 null, and Dicer null oocytes. Germinal vesicle-intact, full-grown oocytes were collected from eCG-primed females expressing a catalytically inactive knock-in allele of Ago2 (Ago2 ADH) specifically in oocytes. Oocytes were also collected from Ago2 null and Ago2 fl/fl oocytes, as well as Dicer wild-type and null mice. Oocytes were freed of attached cumulus cells by pipetting. Twenty oocytes collected from 3 different mice were used for high-throughput RNA sequencing. Three replicates for all genotypes except Ago2 null (two). The mouse background strain is "mostly" C57BL6, i.e., it is a cross between 3 different transgenic mice of different strains.

2015-01-20 | E-GEOD-57514 | biostudies-arrayexpress

A novel miRNA processing pathway independent of Dicer requires Argonaute2 catalytic activity

2010-07-01 | E-GEOD-21503 | biostudies-arrayexpress

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