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Birth weight is considered as an important indicator of environmental conditions during prenatal development. Molecular mechanisms, including epigenetic modifications, play central roles in the body's adaptation to ever-changing environmental conditions. Twin study designs offer a powerful approach for distinguishing environmental from genetic effects. Specifically, within-pair comparisons of monozygotic twins can be used to differentiate unique individual environmental factors from shared environmental and genetic contributions. Notably, numerous studies in monozygotic twins have shown associations between prenatal environment and birth weight discordance (BWD), and suggested a potential involvement of gene expression and epigenetic factors mediating the association. To conduct a scoping review of the literature on definitions of BWD and on epigenetic modifications and gene expression changes associated with BWD in twins. Following PRISMA guidelines, we searched PubMed and Ovid MEDLINE(R) databases and included 34 twin studies focusing on birth weight and epigenetic or gene expression outcomes. There is a lack of consensus on BWD values when comparing groups of twins for their risks of perinatal mortality and morbidity, which vary between 15-30% depending on the type of placentation and gestational age. The gene expression twin studies measured mostly metabolism-related candidate genes in placental tissues. Only small-scale twin studies measured BWD associated with gene expression patterns on genome-wide level using neonatal cells. Most DNA methylation twin studies conducted epigenome-level analyses, and studies differ substantially in terms of tissue type and age of the children. Differences in DNA methylation patterns measured in blood or saliva samples of the twins later in life were mostly in genes related to signal transduction, cell differentiation and proliferation processes. Transcriptional changes of placental glucose transporters and hypoxia-induced proteins possibly reflect compensatory processes in twin pregnancies. Gene ontology analysis of the differentially methylated genes associated with BWD pointed to transcription regulation and tissue development.

The glucocorticoid receptor (GR), which is encoded by the NR3C1 (Nuclear Receptor Subfamily 3 Group C Member 1) gene plays an important role in the modulation of the hypothalamic-pituitary-adrenal (HPA) axis activity by providing feedback regulation which allows termination of the stress response. Little is known about epigenetic programming at the level of NGFI-A (nerve growth factor-inducible protein A) putative binding site (CpG) of the NR3C1 exon 1F in dyads mother-child exposed to intimate partner violence (IPV) more specifically in an unstudied region such as the sub-Saharan Africa where levels of violence are very high. Examine NR3C1 exon 1F methylation in response to IPV and possible association with cortisol concentration and mental health. We recruited 20 mother-child dyads exposed to IPV and a control group of 20 mother-child dyads not exposed to IPV. We administered self-reported questionnaires to measure mother's mental health and collected saliva samples for cortisol dosage and bisulfite sequencing of DNA methylation. Regarding the mothers, our results showed a significant difference in methylation level at CpG 16-21 sites of the NR3C1 exon 1F promoter region between the groups. In the exposed group as compared to the control group, there was a significant positive association between the level of methylation at CpG 16-21 sites and mother's mental health in particular anxiety symptoms. However, we did not find any significant correlation between methylation level and cortisol concentration. In children, we did not find any significant results. This study highlights a NGFI-A putative binding site (CpG 16-21) that is more methylated in mothers exposed to IPV and which may have the potential to confer vulnerability for psychopathologies.

Background The glucocorticoid receptor (GR), which is encoded by the NR3C1 (Nuclear Receptor Subfamily 3 Group C Member 1) gene plays an important role in the modulation of the hypothalamic-pituitary-adrenal (HPA) axis activity by providing feedback regulation which allows termination of the stress response. Little is known about epigenetic programming at the level of NGFI-A (nerve growth factor-inducible protein A) putative binding site (CpG) of the NR3C1 exon 1F in dyads mother-child exposed to intimate partner violence (IPV) more specifically in an unstudied region such as the sub-Saharan Africa where levels of violence are very high. Objective Examine NR3C1 exon 1F methylation in response to IPV and possible association with cortisol concentration and mental health. Method We recruited 20 mother–child dyads exposed to IPV and a control group of 20 mother–child dyads not exposed to IPV. We administered self-reported questionnaires to measure mother’s mental health and collected saliva samples for cortisol dosage and bisulfite sequencing of DNA methylation. Results Regarding the mothers, our results showed a significant difference in methylation level at CpG 16–21 sites of the NR3C1 exon 1F promoter region between the groups. In the exposed group as compared to the control group, there was a significant positive association between the level of methylation at CpG 16–21 sites and mother’s mental health in particular anxiety symptoms. However, we did not find any significant correlation between methylation level and cortisol concentration. In children, we did not find any significant results. Conclusion This study highlights a NGFI-A putative binding site (CpG 16–21) that is more methylated in mothers exposed to IPV and which may have the potential to confer vulnerability for psychopathologies.

Chromatin remodeling provides essential transcriptional regulation for all biological processes. In Caenorhabditis elegans , the chromatin remodeler LET-418, a homolog of the human Mi-2β protein, plays a critical role in regulating development, organogenesis, tissue maintenance, stress resistance and lifespan. LET-418 is part of several chromatin remodeling complexes and contributes significantly to the balance between growth and defense mechanisms, yet its target genes remain unclear. Using DNA methylation profiling, we identified genomic binding sites and associated target genes of LET-418 and its MEC-complex-specific interactor MEP-1 in the intestine. Consistent with their presence in the same complex, the two proteins shared more than half of their target genes. Functional analysis revealed that LET-418 and MEP-1 target genes are highly active in the intestine and are involved in repressing innate immune responses, including the intracellular pathogen response (IPR). Consistently, in let-418 mutants, IPR-induced genes, such as pals-5 or pals-2 are strongly upregulated, in a manner dependent on ZIP-1, a major transcription factor for IPR. Additionally, we found pathogen levels of the natural intracellular intestinal pathogen Nematocida parisii significantly reduced in let-418 mutants, supporting the observation of increased IPR in this mutant. Altogether, these findings reveal a crucial role for LET-418 as a modulator of the IPR, aligning with its role in maintaining the balance between development and defense.

Today, agriculture around the world is challenged by parasitic nematode infections. Plant-parasitic nematodes (PPNs) can cause significant damage and crop loss and are a threat to food security. For a long time, the management of PPN infection has relied on nematicides that impact not only parasitic nematodes but also other organisms. More recently, new nematicides have been developed that appear to specifically target PPN. Cyclobutrifluram belongs to this new category of nematicides. Using the nematode Caenorhabditis elegans as a model organism, we show here that cyclobutrifluram strongly impacts the survival and fertility rates of the worm by decreasing the number of germ cells. Furthermore, using a genetic approach, we demonstrate that cyclobutrifluram functions by inhibiting the mitochondrial succinate dehydrogenase (SDH) complex. Transcriptomic analysis revealed a strong response to cyclobutrifluram exposure. Among the deregulated genes, we found genes coding for detoxifying proteins, such as cytochrome P450s and UDP-glucuronosyl transferases (UGTs). Overall, our study contributes to the understanding of the molecular mode of action of cyclobutrifluram, to the finding of new approaches against nematicide resistance, and to the discovery of novel nematicides. Furthermore, this study confirms that C. elegans is a suitable model organism to study the mode of action of nematicides.

The Green Fluorescent Protein (GFP) has been tremendously useful in investigating cell architecture, protein localization, and protein function. Recent developments in transgenesis and genome editing methods now enable working with fewer transgene copies and, consequently, with physiological expression levels. However, lower signal intensity might become a limiting factor. The recently developed mNeonGreen protein is a brighter alternative to GFP in vitro. The goal of the present study was to determine how mNeonGreen performs in vivo in Caenorhabditis elegans—a model used extensively for fluorescence imaging in intact animals. We started with a side-by-side comparison between cytoplasmic forms of mNeonGreen and GFP expressed in the intestine, and in different neurons, of adult animals. While both proteins had similar photostability, mNeonGreen was systematically 3–5 times brighter than GFP. mNeonGreen was also used successfully to trace endogenous proteins, and label specific subcellular compartments such as the nucleus or the plasma membrane. To further demonstrate the utility of mNeonGreen, we tested transcriptional reporters for nine genes with unknown expression patterns. While mNeonGreen and GFP reporters gave overall similar expression patterns, low expression tissues were detected only with mNeonGreen. As a whole, our work establishes mNeonGreen as a brighter alternative to GFP for in vivo imaging in a multicellular organism. Furthermore, the present research illustrates the utility of mNeonGreen to tag proteins, mark subcellular regions, and describe new expression patterns, particularly in tissues with low expression.

Chromatin condition is crucial for the cells to respond to their environment. In C. elegans, post-embryonic development is accompanied by the exit of progenitor cells from quiescence in response to food. The chromatin protein LET-418/Mi2 is required for this transition in development indicating that proper chromatin structure in cells of the freshly hatched larvae is important to respond to food. However, the identity of the tissue or cells where LET-418/Mi2 is required, as well as the developmental signals that it is modulating have not been elucidated. By restoring the activity of LET-418/Mi2 in specific tissues, we demonstrate that its activity in the intestine and the hypodermis is able to promote in a cell non-autonomous manner the exit of blast cells from quiescence and further development. Furthermore, we identify the IIS (insulin/insulin-like growth factor signaling) pathway to be one of the signaling pathways that is conveying LET-418/Mi2 cell non-autonomous effect on development.

Background: The experience of intimate partner violence (IPV) is stressful. One objective way to monitor it is to assess victims' stress response by measuring the concentration of their salivary cortisol, the major stress hormone released by the hypothalamic-pituitary-adrenal axis. Objective: We investigated how the IPV experienced by women in Cameroon affects their stress levels and those of their children. Method: We recruited 50 mother-child dyads exposed to IPV and a control group of 25 mother-child dyads. All mothers completed questionnaires, including the Revised Conflict Tactics Scale to assess IPV, the Sense of Coherence Scale, and the Self-Esteem Scale, to assess their psychological resources. Mothers were asked to collect 3 saliva samples from themselves and 3 from their children on a single weekday: immediately after waking up, 30 minutes after waking up, and 45 minutes after waking up. The total cortisol secretion over the first hour after awakening was determined by calculating the area under the curve with respect to the ground (AUCg). Results: Mothers exposed to IPV exhibited higher total post-awakening cortisol concentrations compared with those in the control group. However, no significant difference was found between exposed and non-exposed children. In addition, higher IPV, specifically injuries, was significantly and positively associated with greater AUCg among mothers exhibiting lower self-esteem. When self-esteem was high, however, no significant effect of IPV on AUCg was observed. Conclusions: Of particular clinical significance is that self-esteem can modulate the stress levels of women exposed to IPV, a valuable insight into the development of effective psychosocial interventions to support IPV victims in sub-Saharan Africa. Victims of intimate partner violence (IPV) experience extreme stress through elevated cortisol levels. Our results showed that higher cortisol levels was associated with lower self-esteem and a lower sense of coherence, thus implying that self-esteem may serve as a moderator.

Background Epimorphic regeneration of a missing appendage in fish and urodele amphibians involves the creation of a blastema, a heterogeneous pool of progenitor cells underneath the wound epidermis. Current evidence indicates that the blastema arises by dedifferentiation of stump tissues in the vicinity of the amputation. In response to tissue loss, silenced developmental programs are reactivated to form a near-perfect copy of the missing body part. However, the importance of chromatin regulation during epimorphic regeneration remains poorly understood. Results We found that specific components of the Nucleosome Remodeling and Deacetylase complex (NuRD) are required for fin regeneration in zebrafish. Transcripts of the chromatin remodeler chd4a /Mi-2, the histone deacetylase hdac1 /HDAC1/2, the retinoblastoma-binding protein rbb4 /RBBP4/7, and the metastasis-associated antigen mta2 /MTA were specifically co-induced in the blastema during adult and embryonic fin regeneration, and these transcripts displayed a similar spatial and temporal expression patterns. In addition, chemical inhibition of Hdac1 and morpholino-mediated knockdown of chd4a , mta2 , and rbb4 impaired regenerative outgrowth, resulting in reduction in blastema cell proliferation and in differentiation defects. Conclusion Altogether, our data suggest that specialized NuRD components are induced in the blastema during fin regeneration and are involved in blastema cell proliferation and redifferentiation of osteoblast precursor cells. These results provide in vivo evidence for the involvement of key epigenetic factors in the cellular reprogramming processes occurring during epimorphic regeneration in zebrafish.

Mi2 proteins are evolutionarily conserved, ATP-dependent chromatin remodelers of the CHD family that play key roles in stem cell differentiation and reprogramming. In Caenorhabditis elegans, the let-418 gene encodes one of the two Mi2 homologs, which is part of at least two chromatin complexes, namely the Nucleosome Remodeling and histone Deacetylase (NuRD) complex and the MEC complex, and functions in larval development, vulval morphogenesis, lifespan regulation, and cell fate determination. To explore the mechanisms involved in the action of LET-418/Mi2, we performed a genome-wide RNA interference (RNAi) screen for suppressors of early larval arrest associated with let-418 mutations. We identified 29 suppressor genes, of which 24 encode chromatin regulators, mostly orthologs of proteins present in transcriptional activator complexes. The remaining five genes vary broadly in their predicted functions. All suppressor genes could suppress multiple aspects of the let-418 phenotype, including developmental arrest and ectopic expression of germline genes in the soma. Analysis of available transcriptomic data and quantitative PCR revealed that LET-418 and the suppressors of early larval arrest are regulating common target genes. These suppressors might represent direct competitors of LET-418 complexes for chromatin regulation of crucial genes involved in the transition to postembryonic development.