Expression of microRNAs and RNA-Binding Protein DND1 During Oocyte Maturation and Early Embryonic Development in the Pig.

Follicular development and oocyte maturation in mammals requires the temporal and spatial control of protein production. Consequently, it is hypothesised that the preovulatory follicle represses mRNA translation until specific proteins are required during oocyte maturation. Increasingly RNA-binding proteins are being recognised as important contributors to germ cell development, particularly during oocyte transcriptional quiescence. We have identified the presence of RNA-binding protein musashi-1 (Msi-1) mRNA within the mouse ovary and mature mouse oocyte, where the protein is believed to act as a translational repressor by binding to specific sequences within the 3' UTR of target mRNA molecules. Recent studies in various mammalian systems have identified p21 WAF1, cdkn2a, notch and m-numb as potential targets of Msi-1. We have also identified morf4l1 as a potential target through preliminary pulldown and microarray analysis using a GST tagged Msi-1 recombinant protein. To further study these potential targets, a transgenic Msi-1 mouse was produced to overexpress the RNA-binding protein in the developing oocyte. Real time PCR, performed on intact ovaries of WT and Tg mice, has so far demonstrated a 1.5-fold increase in Msi-1 expression in tgMsi-1/+ ovaries, above WT ovary expression. Real time PCR analysis of Msi-1 target mRNA expression has also shown an overall increase in expression in the tgMsi-1/+ ovaries of p21 WAF1 (~2.5-fold), cdkn2a (~2-fold), and notch (~3-fold). However m-numb and morf4l1 do not appear to be targets of Msi-1 in the oocyte, with no significant difference in expression between the WT and tgMsi-1/+ ovaries analysed. Functional quantification of oocyte development reveals a significantly less oocytes produced from superovulated juvenile mice compared with wild type litter mates. Therefore, preliminary analysis suggests that Msi-1 may play a role in binding the transcripts of genes necessary for cell cycle regulation and chromatin remodelling, characteristic of meiotic progression and oocyte development.

Download Full-text

Expression profile of the RNA-binding protein genehermes during chicken embryonic development

Developmental Dynamics ◽

10.1002/dvdy.20392 ◽

2005 ◽

Vol 233 (3) ◽

pp. 1045-1051 ◽

Cited By ~ 12

Author(s):

Helen P. Wilmore ◽

Peter J. McClive ◽

Craig A. Smith ◽

Andrew H. Sinclair

Keyword(s):

Embryonic Development ◽

Expression Profile ◽

Rna Binding ◽

Binding Protein ◽

Rna Binding Protein

Download Full-text

The RNA-Binding Protein, ZFP36L2, Influences Ovulation and Oocyte Maturation

PLoS ONE ◽

10.1371/journal.pone.0097324 ◽

2014 ◽

Vol 9 (5) ◽

pp. e97324 ◽

Cited By ~ 18

Author(s):

Christopher B. Ball ◽

Karina F. Rodriguez ◽

Deborah J. Stumpo ◽

Fernando Ribeiro-Neto ◽

Kenneth S. Korach ◽

...

Keyword(s):

Oocyte Maturation ◽

Rna Binding ◽

Binding Protein ◽

Rna Binding Protein

Download Full-text

The RNA binding protein DAZL functions as repressor and activator of maternal mRNA translation during oocyte maturation

10.1101/598805 ◽

2019 ◽

Author(s):

Cai-Rong Yang ◽

Gabriel Rajkovic ◽

Enrico Maria Daldello ◽

Xuan G. Luong ◽

Jing Chen ◽

...

Keyword(s):

Oocyte Maturation ◽

Rna Binding ◽

Binding Protein ◽

Rna Binding Protein ◽

Mrna Translation ◽

Critical Function ◽

Translational Repressor ◽

Maternal Mrna ◽

Maternal Transcripts ◽

Deleted In Azoospermia

AbstractDeleted in azoospermia like (DAZL) is an RNA-binding protein playing critical function during gamete development. In fully-grown oocytes, DAZL protein is detected in prophase and levels increase four to five fold during reentry into the meiotic cell cycle. Here, we have investigated the functional significance of this DAZL accumulation in maturing oocytes. Oocyte depletion of DAZL prevents progression to MII. This maturation block is associated with widespread disruption in the pattern of maternal transcripts loading on ribosomes and their translation measured using a RiboTag IP/RNASeq or qPCR strategy. In addition to decreased ribosome loading of a subset of transcripts, we found that DAZL depletion causes also translational activation of distinct subset of mRNAs. DAZL binds to mRNAs whose translation is both repressed and activated during oocyte maturation. Unexpectedly, DAZL depletion also causes increased ribosome loading of a subset of mRNAs in quiescent GV-arrested oocytes. This dual role of repression and activation is recapitulated by using YFP reporters including the 3’UTR of DAZL targets. Injection of recombinant DAZL protein in DAZL-depleted oocytes rescues the translation of these targets as well as maturation to MII. Mutagenesis of putative DAZL-binding sites in these candidate mRNAs mimics the effect of DAZL depletion. These findings demonstrate that DAZL regulates translation of maternal mRNAs in mature oocytes, functioning both as translational repressor and activator.

Download Full-text

The RNA-Binding Protein Elavl1/HuR Is Essential for Placental Branching Morphogenesis and Embryonic Development

Molecular and Cellular Biology ◽

10.1128/mcb.01393-08 ◽

2009 ◽

Vol 29 (10) ◽

pp. 2762-2776 ◽

Cited By ~ 113

Author(s):

Vicky Katsanou ◽

Stavros Milatos ◽

Anthie Yiakouvaki ◽

Nikos Sgantzis ◽

Anastasia Kotsoni ◽

...

Keyword(s):

Gene Expression ◽

Embryonic Development ◽

Rna Binding ◽

Developmental Stages ◽

Binding Protein ◽

Dominant Role ◽

Meta Analysis ◽

Rna Binding Protein ◽

Branching Morphogenesis ◽

Genetic Ablation

ABSTRACT HuR is an RNA-binding protein implicated in a diverse array of pathophysiological processes due to its effects on the posttranscriptional regulation of AU- and U-rich mRNAs. Here we reveal HuR's requirement in embryonic development through its genetic ablation. Obligatory HuR-null embryos exhibited a stage retardation phenotype and failed to survive beyond midgestation. By means of conditional transgenesis, we restricted HuR's mutation in either embryonic or endothelial compartments to demonstrate that embryonic lethality is consequent to defects in extraembryonic placenta. HuR's absence impaired the invagination of allantoic capillaries into the chorionic trophoblast layer and the differentiation of syncytiotrophoblast cells that control the morphogenesis and vascularization of the placental labyrinth and fetal support. HuR-null embryos rescued from these placental defects proceeded to subsequent developmental stages but displayed defects in skeletal ossification, fusions in limb elements, and asplenia. By coupling gene expression measurements, data meta-analysis, and HuR-RNA association assays, we identified transcription and growth factor mRNAs controlled by HuR, primarily at the posttranscriptional level, to guide morphogenesis, specification, and patterning. Collectively, our data demonstrate the dominant role of HuR in organizing gene expression programs guiding placental labyrinth morphogenesis, skeletal specification patterns, and splenic ontogeny.

Download Full-text