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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

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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.

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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

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Gene expression profile of Dicer-deficient oocytes

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

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