METTL7A improves bovine embryo competence by attenuating oxidative stress
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1136946 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29866241_1.fastq.gz | Fastqsanger.gz | |||
| SRR29866241_2.fastq.gz | Fastqsanger.gz | |||
| SRR29866242_1.fastq.gz | Fastqsanger.gz | |||
| SRR29866242_2.fastq.gz | Fastqsanger.gz | |||
| SRR29866243_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:In vitro fertilization (IVF) is currently one of the most used assisted reproductive technologies to achieve a successful pregnancy. However, the acquisition of oxidative stress in embryo in vitro culture impairs its competence. Here, we demonstrated that the S-adenosyl-L-methionine (SAMe)-dependent thiol methyltransferase, methyltransferase-like protein 7A (METTL7A) improves the developmental potential of bovine embryos. We found exogenous METTL7A modulates expression of genes involved in embryonic cell mitochondrial pathways and promotes trophectoderm development. Surprisingly, we discovered that METTL7A alleviates mitochondrial stress and DNA damage and promotes cell cycle progression during embryo cleavage. In summary, we have identified a novel mitochondria stress eliminate mechanism regulated by METTL7A that occurs during the acquisition of oxidative stress in embryo in vitro culture. This discovery lays the groundwork for the development of METTL7A as a promising therapeutic target for IVF embryo competence.
2025-02-12 | GSE272473 | GEO
Project description:In vitro fertilization (IVF) is a widely used assisted reproductive technology to achieve a successful pregnancy. However, the acquisition of oxidative stress in embryo in vitro culture impairs its competence. Here, we demonstrated that a nuclear coding gene, methyltransferase-like protein 7A (METTL7A), improves the developmental potential of bovine embryos. We found that exogenous METTL7A modulates expression of genes involved in embryonic cell mitochondrial pathways and promotes trophectoderm development. Surprisingly, we discovered that METTL7A alleviates mitochondrial stress and DNA damage and promotes cell cycle progression during embryo cleavage. In summary, we have identified a novel mitochondria stress eliminating mechanism regulated by METTL7A that occurs during the acquisition of oxidative stress in embryo in vitro culture. This discovery lays the groundwork for the development of METTL7A as a promising therapeutic target for IVF embryo competence.
| S-EPMC11702634 | biostudies-literature
Project description:Melatonin mediates stress defense and improves development competence of bovine oocytes
| PRJNA506215 | ENA
Project description:Histone deacetylase inhibitors (HDI) are among the growing class of epigenetic therapies used for the treatment of cancer. Although histone deacetylase inhibitors (HDIs) are effective in the treatment of T-cell lymphomas, solid tumors are largely resistant, and few mechanisms of resistance have been described. Overexpression of the multi-drug resistance gene ABCB1 that encodes P-glycoprotein (P-gp) is known to confer resistance to the HDI romidepsin, yet it is not associated with resistance in patients, suggesting other mechanisms of resistance arise in patients. To identify alternative romidepsin resistance mechanisms, we selected MCF-7 breast cancer cells with romidepsin in the presence of verapamil to reduce the chance of P-gp over-expression developing as a resistance mechanism. The resulting subline, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidpesin but not other HDIs such as belinostat, panobinostat, or vorinostat. RNA sequencing analysis demonstrated upregulation of the putative methyltransferase, METTL7A, a paralog of which, METTL7B, was found to methylate thiol groups on hydrogen sulfide and captopril. We hypothesized that METTL7A could methylate and inactivate romidepsin as well as other HDIs with a thiol as the zinc binding group. Here we show that expression of METTL7A is necessary for thiol-based HDI resistance in the MCF-7 DpVp300 cell line, and that expression of METTL7A or METTL7B in sensitive cells confers resistance to thiol based HDIs. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDIs by methylating and inactivating the zinc-binding thiol.
2025-05-13 | GSE217128 | GEO
Project description:Histone deacetylase inhibitors (HDI) are among the growing class of epigenetic therapies used for the treatment of cancer. Although histone deacetylase inhibitors (HDIs) are effective in the treatment of T-cell lymphomas, solid tumors are largely resistant, and few mechanisms of resistance have been described. Overexpression of the multi-drug resistance gene ABCB1 that encodes P-glycoprotein (P-gp) is known to confer resistance to the HDI romidepsin, yet it is not associated with resistance in patients, suggesting other mechanisms of resistance arise in patients. To identify alternative romidepsin resistance mechanisms, we selected MCF-7 breast cancer cells with romidepsin in the presence of verapamil to reduce the chance of P-gp over-expression developing as a resistance mechanism. The resulting subline, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidpesin but not other HDIs such as belinostat, panobinostat, or vorinostat. RNA sequencing analysis demonstrated upregulation of the putative methyltransferase, METTL7A, a paralog of which, METTL7B, was found to methylate thiol groups on hydrogen sulfide and captopril. We hypothesized that METTL7A could methylate and inactivate romidepsin as well as other HDIs with a thiol as the zinc binding group. Here we show that expression of METTL7A is necessary for thiol-based HDI resistance in the MCF-7 DpVp300 cell line, and that expression of METTL7A or METTL7B in sensitive cells confers resistance to thiol based HDIs. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDIs by methylating and inactivating the zinc-binding thiol.
2025-05-13 | GSE217127 | GEO
Project description:Histone deacetylase inhibitors (HDI) are among the growing class of epigenetic therapies used for the treatment of cancer. Although histone deacetylase inhibitors (HDIs) are effective in the treatment of T-cell lymphomas, solid tumors are largely resistant, and few mechanisms of resistance have been described. Overexpression of the multi-drug resistance gene ABCB1 that encodes P-glycoprotein (P-gp) is known to confer resistance to the HDI romidepsin, yet it is not associated with resistance in patients, suggesting other mechanisms of resistance arise in patients. To identify alternative romidepsin resistance mechanisms, we selected MCF-7 breast cancer cells with romidepsin in the presence of verapamil to reduce the chance of P-gp over-expression developing as a resistance mechanism. The resulting subline, MCF-7 DpVp300, does not express P-gp and was found to be selectively resistant to romidpesin but not other HDIs such as belinostat, panobinostat, or vorinostat. RNA sequencing analysis demonstrated upregulation of the putative methyltransferase, METTL7A, a paralog of which, METTL7B, was found to methylate thiol groups on hydrogen sulfide and captopril. We hypothesized that METTL7A could methylate and inactivate romidepsin as well as other HDIs with a thiol as the zinc binding group. Here we show that expression of METTL7A is necessary for thiol-based HDI resistance in the MCF-7 DpVp300 cell line, and that expression of METTL7A or METTL7B in sensitive cells confers resistance to thiol based HDIs. We thus propose that METTL7A and METTL7B confer resistance to thiol-based HDIs by methylating and inactivating the zinc-binding thiol.
2025-05-13 | GSE217129 | GEO
Project description:Interleukin-6 supplementation improves bovine conceptus elongation and transcriptomic indicators of developmental competence
| PRJNA1088457 | ENA
Project description:Oxidative stress has been suggested to negatively affect oocyte and embryo quality and developmental competence, resulting in failure to reach full term. In this study, we investigated the effect of N-acetyl-L-cysteine (NAC), a cell-permeating antioxidant, on developmental competence and the quality of oocytes and embryos upon supplementation (0.1-10 mM) in maturation and culture medium in vitro using slaughterhouse-derived oocytes and embryos. The results show that treating oocytes with 1.0 mM NAC for 8 h during in vitro maturation attenuated the intracellular reactive oxygen species (ROS) (p < 0.05) and upregulated intracellular glutathione levels (p < 0.01) in oocytes. Interestingly, we found that NAC affects early embryonic development, not only in a dose-dependent, but also in a stage-specific, manner. Significantly (p < 0.05) decreased cleavage rates (90.25% vs. 81.46%) were observed during the early stage (days 0-2), while significantly (p < 0.05) increased developmental rates (38.20% vs. 44.46%) were observed during the later stage (from day 3) of embryonic development. In particular, NAC supplementation decreased the proportion of apoptotic blastomeres significantly (p < 0.05), resulting in enhanced hatching capability and developmental rates during the in vitro culture of embryos. Taken together, our results suggest that NAC supplementation has beneficial effects on bovine oocytes and embryos through the prevention of apoptosis and the elimination of oxygen free radicals during maturation and culture in vitro.
| S-EPMC8229896 | biostudies-literature
Project description:Oocyte quality, which is directly related to reprogramming competence, is a major important limiting factor in animal cloning efficiency. Compared with oocytes matured in vivo, in vitro matured (IVM) oocytes exhibit lower oocyte quality and reprogramming competence primarily because of their higher levels of reactive oxygen species (ROS). In this study, we investigate whether supplementing the oocyte maturation medium with melatonin, a free radical scavenger, could improve oocyte quality and reprogramming competence. We found that 10−9 M melatonin effectively alleviated oxidative stress, markedly decreased early apoptosis levels, recovered the integrity of mitochondria, ameliorated the spindle assembly and chromosome alignment in oocytes, and significantly promoted subsequent cloned embryo development in vitro. We also analyzed the effects of melatonin on epigenetic modifications in bovine oocytes. Melatonin increased the global H3K9 acetylation levels, reduced the H3K9 methylation levels, and minimally affected DNA methylation and hydroxymethylation. Genome-wide expression analysis of genes affected by melatonin during oocyte maturation was conducted by high-throughput scRNA sequencing. We found that several important genes altered by melatonin were involved in oocyte stress defense. These genes included GSTP1, mitochondrial DNA polymerase POLG, mitochondrial ATP synthase ATP5E, centriole-enriched gene CEP295, spindle assembly-related gene TCTP, cytoprotection, and anti-apoptosis-related gene HSP27. Our results indicated critical roles of melatonin during bovine oocyte maturation and development.
2018-11-21 | GSE122738 | GEO
Project description:The aberrant gene expression of early bovine embryos are a major cause for developemtal arrest. Therefore our aim was to detect transcriptomic fingerprints which correlate with the subsequent developmental competence of a two cell stage embryo.
2012-05-16 | GSE37986 | GEO