Regulation of S-adenosyl methionine synthesis in the mouse embryo

Ménézo, Yves; Khatchadourian, Ch.; Gharib, Abdallah; Hamidi, Jamal; Greenland, Timothy; Sarda, Nicole

doi:10.1016/0024-3205(89)90455-4

Cited by 75 publications

(66 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SAM synthetase activity is required for DNA methylation activity through DMT (DNA methyl transferase), and has a high level of expression in both mouse and human oocytes and early preimplantation embryos [26]. The mechanism for direct reversal of damage, repairing alkylation damage in one step, is also expressed.…”

Section: Discussionmentioning

confidence: 99%

“…We also found a very high level of expression for H2AFX (H2A histone family member X) and CHAF1 (chromatin assembly factor 1), both involved in chromatin structure regulation during and after DNA repair. It must be pointed out that several types of regulation, in particular polyadenylation [17][18][19][20][21][22][23][24][25][26][27], will allow these mRNAs to be translated: portions of the mRNA can be lost both pre and post translation. Poly(A) binding proteins and the cytoplasmic polyadenylation elements are highly expressed in the oocyte (up to 500 times the background level).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

Ménézo

Russo

Tosti

et al. 2007

J Assist Reprod Genet

118

View full text Add to dashboard Cite

Purpose To determine the level of expression for mRNAs that regulate DNA repair activity in oocytes at the germinal vesicle (GV) stage. Reactive oxygen species (ROS) have been shown to play a major role in the appearance of deleterious DNA decays, and this study focuses on the repair of damage linked to decay caused by the action of ROS. The oocyte needs a mechanism for repairing DNA decays in the early preimplantation embryo before the onset of genomic activation, since in the absence of repair, residual DNA damage would lead to either apoptosis or tolerance. Tolerance of DNA damage is a source of potential mutations. Method GV oocytes were selected for this study, both for the ethical reason that they are unsuitable for patient treatment, and because no transcription takes place during the period from GV to MII and then prior to genomic activation. The GV oocyte is therefore a good model for looking at DNA during the first cleavages of early preimplantation development. Six cohorts of GV oocytes were pooled for extraction of mRNA; the DNA was analysed using Affimetrix HG-UG133 Plus 2, containing 54,675 probe sets; spike and housekeeping genes were also added as internal controls. Results In GV oocytes, DNA repair pathways for oxidized bases are redundant. One step repair procedure (OSR), BER (base excision repair), MMR (mismatch repair) and NER (Nucleotide excision repair) are present. All the recognition proteins are also present. The chromatin assembly factors necessary for the maintenance of genomic stability are highly expressed. Conclusion Gene expression analysis shows that the oocyte does not allow a high level of tolerance for DNA decays. This regulatory mechanism should avoid transmitting mutations into the next generation.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

Ménézo

Russo

Tosti

et al. 2007

J Assist Reprod Genet

118

View full text Add to dashboard Cite

show abstract

“…4 Methionine treatment was used as a concentration control. [26] reported that 1-2 cell murine embryos cultured in the presence of ethionine (100 μM) did not develop to the blastocyst stage. Although it remains unknown why the doses of ethionine that induce the developmental block are so different between murine and bovine embryos, the importance of methionine metabolism in preimplantation development is likely to be conserved between the species.…”

mentioning

confidence: 99%

Importance of Methionine Metabolism in Morula-to-blastocyst Transition in Bovine Preimplantation Embryos

Ikeda

Sugimoto

Kume

2012

Journal of Reproduction and Development

View full text Add to dashboard Cite

Abstract. The roles of methionine metabolism in bovine preimplantation embryo development were investigated by using ethionine, an antimetabolite of methionine. In vitro produced bovine embryos that had developed to the 5-cell stage or more at 72 h after the commencement of in vitro fertilization (IVF) were then cultured until day 8 (IVF = day 0) in medium supplemented with 0 (control), 1, 5 and 10 mM ethionine. Compared with the blastocyst development in the control (40.0%), ethionine at 10 mM almost completely blocked blastocyst development (1.1%, P<0.001), and this concentration was used in the following experiments. Methionine added at the same concentration (10 mM, a concentration control of ethionine) did not cause such an intense developmental inhibition. Development to the compacted morula stage on day 6 was not affected by 10 mM ethionine treatment. S-adenosylmethionine (SAM) added to the ethionine treatment partly restored the blastocyst development. Semiquantitative reverse transcription-polymerase chain reaction analysis of cell lineage-related transcription factors in day 6 compacted morulae showed that the expressions of NANOG and TEAD4 were increased by ethionine treatment relative to the control (P<0.01). Furthermore, immunofluorescence analysis of 5-methylcytosine revealed that DNA was hypomethylated in the ethionine-treated day 6 morulae compared with the control (P<0.001). These results demonstrate that the disruption of methionine metabolism causes impairment of the morula-toblastocyst transition during bovine preimplantation development in part via SAM deficiency, indicating the indispensable roles of methionine during this period. The disruption of methionine metabolism may cause hypomethylation of DNA and consequently lead to the altered expression of developmentally important genes, which then results in the impairment of blastocyst development. Key words: Bovine, Methionine, One-carbon metabolism, Preimplantation embryo, S-adenosylmethionine (J. Reprod. Dev. 58: [91][92][93][94][95][96][97] 2012) M ethionine is a dietary essential amino acid that plays multiple biological roles, including those as the initiating amino acid in eukaryotic protein synthesis, a precursor of the essential methyl donor for methylation reactions (S-adenosylmethionine, SAM) and a source of redox regulators (cysteine and glutathione) [1,2]. Methionine metabolism can be seen as the trans-and remethylation cycle of methionine (methionine cycle) that intertwines with the cycle of folate metabolism (folate cycle) and the transsulfuration pathway from homocysteine, an intermediate in the methionine cycle [3], and these combined metabolic networks are called one-carbon metabolism [4,5]. Recently, mammalian oocytes and preimplantation embryos have been reported to express the key regulatory enzymes in one-carbon metabolism [6][7][8], suggesting that mammalian oocytes and preimplantation embryos can independently utilize and metabolize nutrients in one-carbon metabolism, such as methionine, choline, betaine, folates a...

show abstract

“…2). Homocysteine also competes with methionine for uptake into the embryo (11), and this hinders the formation of S-Adenosyl methionine, the universal methylation agent. The most important pathway for Hcy recycling is the folate pathway, which requires vitamins B3, B9 (folic acid) and B12.…”

mentioning

confidence: 99%

Autism, imprinting and epigenetic disorders: a metabolic syndrome linked to anomalies in homocysteine recycling starting in early life??

Ménézo¹,

Marès

Cohen³

et al. 2011

J Assist Reprod Genet

View full text Add to dashboard Cite

An association between imprinting syndromes and ART is now common knowledge. Imprinting problems are roughly linked to DNA methylation disorders, and clinical reports of ART-linked imprinting syndromes have implicated hypomethylation of the maternal alleles (1). Kattari et al. (2), examining DNA methylation in 700 genes, observed different levels of methylation between children conceived in vitro and in vivo. They also found that the differences observed in DNA methylation in the children conceived in vitro involved differences in gene expression for both imprinted and non-imprinted genes. This effect is observed even when maternal age is taken into account. We recently pointed out some aspects of in vitro and in vivo parameters that could be responsible for impairment of methylation processes in ART patients (3), in particular an increased concentration of homocysteine (Hcy) in the oocyte environment.Further to these observations, two articles recently presented at the International meeting for autism research in Philadelphia pointed out a correlation between Assisted Reproductive Technology and Autism. 111 women who had a child with an autism spectrum disorder (ASD) took part in the Nurses' Health Study II, which revealed that about 4% of mothers who took fertility drugs had a child with an ASD, compared to about 2% who did not take fertility drugs. In a second study, an Israeli group also observed an increased frequency in babies with ASD after ART: 10.5% of 461 children diagnosed with a disorder on the autism spectrum were conceived using IVF, significantly higher than the 3.5% autism rate in the general Israeli population. Two major metabolic problems are commonly involved in Autism disorders: altered thiol metabolism and increased homocysteine levels, and oxidative stress including mitochondrial dysfunction (4-8) In many cases a correlation is found with alterations in the mothers of autistic children (9, 10).One mechanism that oxidative stress/thiol metabolism and methylation (imprinting) have in common is the recycling of homocysteine (see Fig. 1). Recycling of homocysteine is a Capsule Monitoring and early supplementation with parameters linked to homocysteine metabolism immediately before and during pregnancy, as well as during early infancy of the child, could limit the risks of developing autism spectrum and imprinting related disorders.

show abstract

Regulation of S-adenosyl methionine synthesis in the mouse embryo

Cited by 75 publications

References 15 publications

Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

Expression profile of genes coding for DNA repair in human oocytes using pangenomic microarrays, with a special focus on ROS linked decays

Importance of Methionine Metabolism in Morula-to-blastocyst Transition in Bovine Preimplantation Embryos

Autism, imprinting and epigenetic disorders: a metabolic syndrome linked to anomalies in homocysteine recycling starting in early life??

Contact Info

Product

Resources

About