Maternal Transcript Degradation Research Articles

A maternal-to-zygotic-transition gene block on the zebrafish sex chromosome.

Wild zebrafish (Danio rerio) have a ZZ/ZW chromosomal sex-determination system with the major sex locus on the right arm of chromosome-4 (Chr4R) near the largest heterochromatic block in the genome, suggesting that Chr4R transcriptomics might differ from the rest of the genome. To test this hypothesis, we conducted an RNA-seq analysis of adult ZW ovaries and ZZ testes in the Nadia strain and identified 4 regions of Chr4 with different gene expression profiles. Unique in the genome, protein-coding genes in a 41.7 Mb section (Region-2) were expressed in testis but silent in ovary. The AB lab strain, which lacks sex chromosomes, verified this result, showing that testis-biased gene expression in Region-2 depends on gonad biology, not on sex-determining mechanism. RNA-seq analyses in female and male brains and livers validated reduced transcripts from Region-2 in somatic cells, but without sex specificity. Region-2 corresponds to the heterochromatic portion of Chr4R and its content of genes and repetitive elements distinguishes it from the rest of the genome. Region-2 lacks protein-coding genes with human orthologs; has zinc finger genes expressed early in zygotic genome activation; has maternal 5S rRNA genes, maternal spliceosome genes, a concentration of tRNA genes, and a distinct set of repetitive elements. The colocalization of (1) genes silenced in ovaries but not in testes that are (2) expressed in embryos briefly at the onset of zygotic genome activation; (3) maternal-specific genes for translation machinery; (4) maternal-specific spliceosome components; and (5) adjacent genes encoding miR-430, which mediates maternal transcript degradation, suggest that this is a maternal-to-zygotic-transition gene regulatory block.

Single-cell RNA-seq and single-cell bisulfite-sequencing reveal insights into yak preimplantation embryogenesis

Extensive epigenetic reprogramming occurs during preimplantation embryonic development. However, the impact of DNA methylation in plateau yak preimplantation embryos and how epigenetic reprogramming contributes to transcriptional regulatory networks are unclear. In this study, we quantified gene expression and DNA methylation in oocytes and a series of yak embryos at different developmental stages and at single-cell resolution using single-cell bisulfite-sequencing and RNA-seq. We characterized embryonic genome activation and maternal transcript degradation and mapped epigenetic reprogramming events critical for embryonic development. Through cross-species transcriptome analysis, we identified 31 conserved maternal hub genes and 39 conserved zygotic hub genes, including SIN3A, PRC1, HDAC1/2, and HSPD1. Notably, by combining single-cell DNA methylation and transcriptome analysis, we identified 43 candidate methylation driver genes, such as AURKA, NUSAP1, CENPF, and PLK1, that may be associated with embryonic development. Finally, using functional approaches, we further determined that the epigenetic modifications associated with the histone deacetylases HDAC1/2 are essential for embryonic development and that the deubiquitinating enzyme USP7 may affect embryonic development by regulating DNA methylation. Our data represent an extensive resource on the transcriptional dynamics of yak embryonic development and DNA methylation remodeling, and provide new insights into strategies for the conservation of germplasm resources, as well as a better understanding of mammalian early embryonic development that can be applied to investigate the causes of early developmental disorders.

SLAMseq resolves the kinetics of maternal and zygotic gene expression during early zebrafish embryogenesis.

The maternal-to-zygotic transition (MZT) is a key developmental process in metazoan embryos that involves the activation of zygotic transcription (ZGA) and degradation of maternal transcripts. We employed metabolic mRNA sequencing (SLAMseq) to deconvolute the compound embryonic transcriptome in zebrafish. While mitochondrial zygotic transcripts prevail prior to MZT, we uncover the spurious transcription of hundreds of short and intron-poor genes as early as the 2-cell stage. Upon ZGA, most zygotic transcripts originate from thousands of maternal-zygotic (MZ) genes that are transcribed at rates comparable to those of hundreds of purely zygotic genes and replenish maternal mRNAs at distinct timescales. Rapid replacement of MZ transcripts involves transcript decay features unrelated to major maternal degradation pathways and promotes de novo synthesis of the core gene expression machinery by increasing poly(A)-tail length and translation efficiency. SLAMseq hence provides insights into the timescales, molecular features, and regulation of MZT during zebrafish embryogenesis.

Single-cell multi-omic analysis profiles defective genome activation and epigenetic reprogramming associated with human pre-implantation embryo arrest.

During pre-implantation stages of mammalian development, maternally stored material promotes both theerasure of the sperm and oocyte epigenetic profiles and is responsible for concomitant genome activation. Here, we have utilized single-cell methylome and transcriptome sequencing (scM&T-seq) to quantify both mRNA expression and DNA methylation in oocytes and a developmental series of human embryos at single-cell resolution. We fully characterize embryonic genome activation and maternal transcript degradation and map key epigenetic reprogramming events in developmentally high-quality embryos. Bycomparing these signatures with early embryos that have undergone spontaneous cleavage-stage arrest, as determined by time-lapse imaging, we identify embryos that fail to appropriately activate their genomes or undergo epigenetic reprogramming. Our results indicate that a failure to successfully accomplish these essential milestones impedes the developmental potential of pre-implantation embryos and is likely to have important implications, similar to aneuploidy, for the success of assisted reproductive cycles.

The Role of Vts1/Smaug in Adaptive Heritable Gene Expression

The ancient RNA Binding Protein (RBP) Vts1 has been identified to self‐assemble along with the Smaug regulator to produce enhancing non‐amyloid prions in mRNA decay. Seen in Drosophila, the sterile‐alpha‐motif (SAM) domain of Vts and the Smaug regulator acts as an embryonic regulator for maternal transcript degradation through cytoplasmic deadenylase in progeny development. Specifically, of Saccharomyces cerevisiae, the Vts/Smaug regulator forms condensates that self‐template to create prions functioning towards epigenetic heritable inheritance. The RBP Vts1 SAM domain recognizes in RNA hairpins Smaug recognition elements, SREs, initiating the process of degradation and self‐assembly. The structure of RBPs are composed of an ordered RNA binding domain, and an unventured intrinsically disordered region (IDR). At the quaternary level structure, the Vts1 protein matches as a hexamer of 489 kDa dominant peak with an oligomer of more than eight monomers, and the IDR is around 490 kDa as well while the RBD‐Vts1 is around 75 kDa. The condensed version of Vts1 fuse into structures of 10 micrometers due to the IDR driving self‐association to create oligomers. The RNA binding SAM domain and IDR have induced transcription degradation and post‐transcriptional regulation in a new mechanism, prompting adaptive gene expression for developmental decisions in organisms over evolutionary time periods. Though many RBP prion condensates are not heritable and inactivate protein function, the SMAUG+ prions of the condensed Vts1/Smaug protein in S. Cerevisiae instead respond to environmental stress and produce new emerging phenotypes that are actually heritable over a large biological time‐scale. Furthermore, SMAUG+ conversion is reversible and an enhancer of RBP Vts1 function, producing adaptive gene expression systems in fluctuating environments. In various yeast models, the SMAUG+ allows yeast to decide nutrient replenishment after starvation which creates a new adaptive advantage for organisms. The new cellular decision making regulated by the prion is in two forms of rapid mitosis or meiosis creating a non‐stress state; SMAUG+ has created an adaptive memory that can influence developmental and cellular decisions in addition to plant growth in limited nutrients. Such advancements in heritable prion inheritance can uncover the function of intrinsically disordered sequences. The Walton SMART team has designed a 3D model with MSOE Center for Biomolecular Modeling to investigate the SAM domain of Vts1 further and examine the role of SMAUG+ prions in adaptive heritable gene expression.

Role of miRNAs in preimplantation embryo development and their potential as embryo selection biomarkers.

MicroRNAs (miRNAs) play different roles in oocyte fertilisation, degradation of maternal transcripts, embryo development, and implantation. During in vitro fertilisation (IVF), different miRNAs are released from embryos into the spent culture media (SCM) that can potentially reflect the status of the embryo. This study is the assessment of miRNAs, which secreted in SCM during the IVF cycles can be used as noninvasive biomarkers to predict an embryo's ability to form a blastocyst, implant, and give live birth. Systematic literature search was conducted to review all recent studies about miRNAs as potential non-invasive biomarkers for selecting the best embryos in the assisted reproductive technology (ART) cycle. Studies have shown that levels of some miRNAs in the SCM have an association with the implantation potential and pregnancy outcome of the embryo. Embryo-secreted miRNAs can be used as potential non-invasive biomarkers for selecting the best embryos in the ART cycle. Unfortunately, few human studies evaluated the association between ART outcomes and miRNAs in SCM. This review can pave the way for further miRNAs transcriptomic studies on human embryo culture media and introducing a specific miRNA profile as a multivariable prediction model for embryo selection in IVF cycles.

Ythdf m6A Readers Function Redundantly during Zebrafish Development

During the maternal-to-zygotic transition (MZT), multiple mechanisms precisely control massive decay of maternal mRNAs. N6-methyladenosine (m6A) is known to regulate mRNA decay, yet how this modification promotes maternal transcript degradation remains unclear. Here, we find that m6A promotes maternal mRNA deadenylation. Yet, genetic loss of m6A readers Ythdf2 and Ythdf3 did not impact global maternal mRNA clearance, zygotic genome activation, or the onset of gastrulation, challenging the view that Ythdf2 alone is critical to developmental timing. We reveal that Ythdf proteins function redundantly during zebrafish oogenesis and development, as double Ythdf2 and Ythdf3 deletion prevented female gonad formation and triple Ythdf mutants were lethal. Finally, we show that the microRNA miR-430 functions additively with methylation to promote degradation of common transcript targets. Together these findings reveal that m6A facilitates maternal mRNA deadenylation and that multiple pathways and readers act in concert to mediate these effects of methylation on RNA stability.

Genome transfer for the prevention of female infertility caused by maternal gene mutation

Poor oocyte quality is associated with early embryo developmental arrest and infertility. Maternal gene plays crucial roles in the regulation of oocyte maturation, and its mutation is a common cause of female infertility. However, how to improve oocyte quality and develop effective therapy for maternal gene mutation remains elusive. Here, we use Zar1 as an example to assess the feasibility of genome transfer to cure maternal gene mutation–caused female infertility. We first discover that cytoplasmic deficiency primarily leads to Zar1-null embryo developmental arrest by disturbing maternal transcript degradation and minor zygotic genome activation (ZGA) during the maternal-zygotic transition. We next perform genome transfer at the oocyte (spindle transfer or polar body transfer) and zygote (early pronuclear transfer or late pronuclear transfer) stages to validate the feasibility of preventing Zar1 mutation–caused infertility. We finally demonstrate that genome transfer either at the oocyte or at the early pronuclear stage can support normal preimplantation embryo development and produce live offspring. Moreover, those pups grow to adulthood and show normal fertility. Therefore, our findings provide an effective basis of therapies for the treatment of female infertility caused by maternal gene mutation.

Two-Step Maternal-to-Zygotic Transition with Two-Phase Parental Genome Contributions

The maternal-to-zygotic transition (MZT) is an essential developmental turning point in both plants and animals. In plants, the timing of MZT and parental contributions to the zygotic transcriptome remain unclear. Here, by overcoming technical limitations, we characterize the Arabidopsis egg cell, zygote, and embryo transcriptomes across multiple stages. Using these datasets, we demonstrate that MZT occurs during zygote development and is a two-step interrelated process of rapid maternal transcript degradation followed by large-scale de novo transcription. Parental contributions to the zygotic transcriptome are stage-dependent: the spherical zygote is characterized by a maternally dominated transcriptome, whereas the elongated zygote transcriptome shows equal parental contributions. Our results show that plant MZT is similar to that in animals, showing a typical two-step process, and that zygotic genome activation is required for zygote elongation and division, indicating that de novo transcripts are essential for the establishment of zygote polarity and embryogenesis promotion.

Two-Step Maternal-to-Zygotic Transition with Two-Phases of Parental Genome Contributions

The maternal-to-zygotic transition (MZT) is an essential developmental turning point in both plants and animals. In animals, early embryogenesis is maternally controlled and zygotic genome activation (ZGA) starts much later. However, in plants, the timing of MZT and parental contributions to the zygotic transcriptome remain unclear. Here, we demonstrate that plant MZT occurs during the zygote development and is a two-step process, first involving rapid maternal transcript degradation and, second, large-scale de novo transcription. Parental contributions to the zygotic transcriptome are stage-dependent during zygote development; the spherical zygote is characterized by a maternally dominated transcriptome, whereas the elongated zygote genome shows equal parental contributions. Our results indicate that plant MZT is similar to that in animals, showing a typical two-step process; furthermore, we demonstrate that ZGA is required for zygote elongation and division, indicating that de novo transcripts are essential for the establishment of zygote polarity and promotion of embryogenesis.

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

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 ofmaternal 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.

The following five articles for this Special Issue were previously published and can be found in their respective issues or online

Metabolic stress induces modifications in the epigenetic program of preimplantation bovine embryos (85:2)https://onlinelibrary.wiley.com/doi/10.1002/mrd.22941Impact of preimplantational oral low‐dose estradiol‐17β exposure on the endometrium: The role of miRNA (85:5)https://onlinelibrary.wiley.com/doi/10.1002/mrd.22975Long term effects of ART: What do animals tell us? (85:4)https://onlinelibrary.wiley.com/doi/10.1002/mrd.22970Testicular development in male lambs prenatally exposed to a high‐starch diet (85:5)https://onlinelibrary.wiley.com/doi/10.1002/mrd.22974Delay in maternal transcript degradation in ovine embryos derived from low competence oocytes (85:5)https://onlinelibrary.wiley.com/doi/10.1002/mrd.22977

Delay in maternal transcript degradation in ovine embryos derived from low competence oocytes.

Oocytes from prepubertal animals have a reduced ability to undergo embryo development and produce viable offspring. The present work used an ovine model consisting of oocytes derived from adult and prepubertal donors to assess the molecular status of oocytes and preimplantation embryos with different developmental competence. The lower potential of oocytes of young donors was confirmed in terms of in vitro developmental capabilities and kinetics. A panel of genes including maternal effect (DPPA3, GDF9, NMP2, ZAR1) and housekeeping genes (ACTB, RPL19, SDHA, YWHAZ, ATP1A1), genes involved in DNA methylation (DNMT1, DNMT3A, DNMT3B), genomic imprinting (IGF2R), pluripotency (NANOG, POU5F1) and cell cycle regulation (CCNB1, CDK1, MELK) was relatively quantified. Temporal analysis during oocyte maturation and preimplantation embryo development evidenced patterns associated with donor age. With a few gene-specific exceptions, the differential model showed a reduced transcript abundance in immature prepubertal oocytes that completely reversed trend after fertilization, when higher mRNA levels were consistently observed in early embryos, indicating a delay in maternal transcript degradation. We propose that the molecular shortage in the prepubertal oocyte may affect its developmental potential and impair the early pathways of maternal mRNA clearance in the embryo. While confirming the different potential of oocytes derived from adult and prepubertal donors, our work showed for the first time a consistent delay in maternal transcript degradation in embryos derived from low competence oocytes that interestingly recalls the delayed developmental kinetics. Such abnormal transcript persistence may hinder further development and represents a novel perspective on the complexity of developmental competence.

The maternal-zygotic transition and zygotic activation of the Mnemiopsis leidyi genome occurs within the first three cleavage cycles.

The maternal-zygotic transition (MZT) describes the developmental reprogramming of gene expression marked by the degradation of maternally supplied gene products and activation of the zygotic genome. While the timing and duration of the MZT vary among taxa, little is known about early-stage transcriptional dynamics in the non-bilaterian phylum Ctenophora. We sought to better understand the extent of maternal mRNA loading and subsequent differential transcript abundance during the earliest stages of development by performing comprehensive RNA-sequencing-based analyses of mRNA abundance in single- and eight-cell stage embryos in the lobate ctenophore Mnemiopsis leidyi. We found 1,908 contigs with significant differential abundance between single- and eight-cell stages, of which 1,208 contigs were more abundant at the single-cell stage and 700 contigs were more abundant at the eight-cell stage. Of the differentially abundant contigs, 267 were exclusively present in the eight-cell samples, providing strong evidence that both the MZT and zygotic genome activation (ZGA) have commenced by the eight-cell stage. Many highly abundant transcripts encode genes involved in molecular mechanisms critical to the MZT, such as maternal transcript degradation, serine/threonine kinase activity, and chromatin remodeling. Our results suggest that chromosomal restructuring, which is critical to ZGA and the initiation of transcriptional regulation necessary for normal development, begins by the third cleavage within 1.5 hr post-fertilization in M. leidyi.

Cohesin facilitates zygotic genome activation in zebrafish.

At zygotic genome activation (ZGA), changes in chromatin structure are associated with new transcription immediately following the maternal-to-zygotic transition (MZT). The nuclear architectural proteins cohesin and CCCTC-binding factor (CTCF) contribute to chromatin structure and gene regulation. We show here that normal cohesin function is important for ZGA in zebrafish. Depletion of the cohesin subunit Rad21 delays ZGA without affecting cell cycle progression. In contrast, CTCF depletion has little effect on ZGA, whereas complete abrogation is lethal. Genome-wide analysis of Rad21 binding reveals a change in distribution from pericentromeric satellite DNA and other locations, including the miR-430 locus (the products of which are responsible for maternal transcript degradation), to genes, as embryos progress through the MZT. After MZT, a subset of Rad21 binding overlaps the pioneer factor Pou5f3, which activates early expressed genes. Rad21 depletion disrupts the formation of nucleoli and RNA polymerase II foci, suggestive of global defects in chromosome architecture. We propose that Rad21/cohesin redistribution to active areas of the genome is key to the establishment of chromosome organization and the embryonic developmental program.

Irregular transcriptome reprogramming probably causes thec developmental failure of embryos produced by interspecies somatic cell nuclear transfer between the Przewalski's gazelle and the bovine.

BackgroundInterspecies somatic cell nuclear transfer (iSCNT) has been regarded as a potential alternative for rescuing highly endangered species and can be used as a model for studying nuclear–cytoplasmic interactions. However, iSCNT embryos often fail to produce viable offspring. The alterations in normal molecular mechanisms contributing to extremely poor development are for the most part unknown.ResultsPrzewalski’s gazelle–bovine iSCNT embryos (PBNT) were produced by transferring Przewalski’s gazelle fibroblast nuclei into enucleated bovine oocytes. The percentages of PBNT embryos that developed to morula/blastocyst stages were extremely low even with the use of various treatments that included different SCNT protocols and treatment of embryos with small molecules. Transcriptional microarray analyses of the cloned embryos showed that the upregulation of reprogramming-associated genes in bovine–bovine SCNT (BBNT) embryos was significantly higher than those observed in PBNT embryos (1527:643). In all, 139 transcripts related to various transcription regulation factors (TFs) were unsuccessfully activated in the iSCNT embryos. Maternal degradation profiles showed that 1515 genes were uniquely downregulated in the BBNT embryos, while 343 genes were downregulated in the PBNT embryos. Incompatibilities between mitochondrial DNA (mtDNA) and nuclear DNA revealed that the TOMM (translocase of outer mitochondrial membrane)/TIMM (translocase of inner mitochondrial membrane) complex-associated genes in BBNT embryos had the highest expression levels, while the PBNT embryos exhibited much lower expression rates.ConclusionsImproper degradation of maternal transcripts, incomplete activation of TFs and abnormal expression of genes associated with mitochondrial function in PBNT embryos likely contributed to incomplete reprogramming of the donor cell nuclei and therefore led to the developmental failure of these cloned embryos.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-1113) contains supplementary material, which is available to authorized users.

Losing Mom’s Message: Requirement for DCP1A and DCP2 in the Degradation of Maternal Transcripts During Oocyte Maturation1

Losing Mom’s Message: Requirement for DCP1A and DCP2 in the Degradation of Maternal Transcripts During Oocyte Maturation1

Knockdown of Maternal Homeobox Transcription Factor SEBOX Gene Impaired Early Embryonic Development in Porcine Parthenotes

A number of germ cell-specific transcription factors essential for ovarian formation and folliculogenesis have been identified and studied. However, the role of these factors during early embryonic development has been poorly explored. In the present study, we investigated the role of SEBOX, a maternal homeobox transcription factor, during early embryonic development in porcine parthenotes. mRNA for SEBOX is preferentially expressed in oocytes, and expression persists until embryonic genome activation (EGA). Knockdown of SEBOX by siRNA disrupted early embryonic development, but not oocyte maturation. Many maternal genes essential for early embryonic development were upregulated in SEBOX-depleted embryos. Moreover, some pluripotency-associated genes, including SOX2 and NANOG, were upregulated when SEBOX was knocked down. Therefore, our data demonstrate that SEBOX is required for early embryonic development in pigs and appears to regulate the degradation of maternal transcripts and the expression of pluripotency genes.

Analysis of microRNAs and their precursors in bovine early embryonic development

In animals, the maternal-to-embryonic transition (MET) occurs in the first days of early development and involves the degradation of maternal transcripts that have been stored during oogenesis. Moreover, precise and specific control mechanisms govern the adequate synchronization of the MET events to promote the activation of the embryonic genome. These mechanisms are not well understood, but it is believed that microRNAs (miRNAs) could be one of the mechanisms involved. After a microarray screening study, we analysed the expression of specific miRNA during oocyte maturation and early embryo development until preimplantation stages. Two differentially expressed candidates were selected for further analysis. Mature and precursor forms of miR-21 and miR-130a were quantified by qRT-PCR in pools of 20 oocytes at GV (germinal vesicle), GV breakdown and metaphase II stages as well as in pools of embryos at the 2-cell, 4-cell, 8-cell and blastocyst stages. The results showed a linear increase during the 1-8 cell stage for the mature forms of miR-130a and miR-21 (P < 0.05 and P < 0.003, respectively) and for the precursor form of miR-130a (P < 0.002). To see if this increase was due to minor transcriptional activity, 2-cell embryos were exposed to α-amanitin for 30-34 h. Results showed a significant decrease in miR-21, pre-miR-21, miR-130a and SRFS3 in α-amanitin-treated embryos (P < 0.05). Considering the potential regulatory role of these miRNA, the bovine genome was screened to identify putative targets with a 3'UTR exact seed match. This study suggests that miRNAs could be important players in the MET, as expression profiles suggest a potential regulation role during early development steps.

6 CLONING AND EXPRESSION OF BOVINE FACTOR IN THE GERMLINE ALPHA (FIGLA) IN OOCYTES AND EARLY EMBRYOS: A POTENTIAL TARGET OF microRNA-212

Factor In the GermLine Alpha (FIGLA), a basic helix-loop-helix transcription factor, was first identified in regulating coordinate expression of zona pellucida genes in mice. It plays a crucial role in the formation of primordial follicles and lack of FIGLA in mice alters the expression of many oocyte specific genes that are required for fertilization and early embryonic survival. The objective of this study was to characterise the expression and regulation of bovine FIGLA during early embryogenesis. The cloned bovine FIGLA cDNA is 660 bp in length, which encodes a protein of 165 amino acids. Expression of bovine FIGLA mRNA is restricted to ovarian tissue and can be detected in fetal ovaries harvested as early as 90 days of gestation when primordial follicles start to form. Expression analysis demonstrated that FIGLA mRNA is abundant in germinal vesicle and metaphase II stage oocytes, as well as in embryos from pronuclear to 8-cell stage, but barely detectable in embryos collected at morula and blastocyst stages, suggesting that FIGLA might be a maternal effect gene. Recent studies in zebrafish have highlighted the importance of non-coding small RNAs (microRNAs) as key regulatory molecules targeting maternal mRNAs for degradation during embryonic development. We hypothesised that FIGLA, as a maternal transcript, is regulated by microRNAs during early embryogenesis. Using microInspector, an algorithm for detection of possible interactions between microRNAs and target mRNA sequences, a microRNA binding site (miR-212) was identified in the 3′-UTR of the bovine FIGLA mRNA. Alignment of the 3′-UTR of FIGLA mRNAs from bovine, human and mouse shows complete conservation of the ‘seed’ region indicating that miR-212 might be a post-transcriptional regulator of FIGLA and the microRNA: mRNA interaction is evolutionary conserved. Expression analysis indicates that bovine miR-212 is expressed in oocytes and tends to increase at the 4-cell and 8-cell stage embryos followed by a decline at morula and blastocyst stages, indicating that miR-212 is presumably of maternal origin and potentially involved in maternal transcript degradation during the maternal-to-embryonic transition. To validate the role of miR-212 in silencing FIGLA, a luciferase reporter assay was performed using HeLa cells. The luciferase activity in cells expressing a luciferase construct containing the entire 3′ UTR of bovine FIGLA was suppressed by ∼40% in the presence of miR-212. We also investigated the stability of FIGLA mRNA in cells transfected with bovine FIGLA expression plasmid in the presence or absence of miR-212. Expression of bovine FIGLA mRNA was significantly reduced in the presence of mir-212 compared to control cells transfected with FIGLA construct alone. In summary, our data establish miR-212 as a potential post-transcriptional regulator of FIGLA during the maternal-to-embryonic transition in bovine embryos. Future studies aim to determine if miR-212 mimic can inhibit endogenous FIGLA expression in bovine embryos and its effect on subsequent embryonic development.