Excited States of Proton-bound DNA/RNA Base Homo-dimers: Pyrimidines

We are presenting the electronic photo fragment spectra of the protonated pyrimidine DNA bases homo-dimers. Only the thymine dimer exhibits a well structured vibrational progression, while protonated monomer shows broad vibrational bands. This shows that proton bonding can block some non radiative processes present in the monomer.Comment: We acknowledge the use of the computing facility cluster GMPCS of the LUMAT federation (FR LUMAT 2764

Power management and control strategies for off-grid hybrid power systems with renewable energies and storage

This document is the Accepted Manuscript of the following article: Belkacem Belabbas, Tayeb Allaoui, Mohamed Tadjine, and Mouloud Denai, 'Power management and control strategies for off-grid hybrid power systems with renewable energies and storage', Energy Systems, September 2017. Under embargo. Embargo end date: 19 September 2018. The final publication is available at Springer via https://doi.org/10.1007/s12667-017-0251-y.This paper presents a simulation study of standalone hybrid Distributed Generation Systems (DGS) with Battery Energy Storage System (BESS). The DGS consists of Photovoltaic (PV) panels as Renewable Power Source (RPS), a Diesel Generator (DG) for power buck-up and a BESS to accommodate the surplus of energy, which may be employed in times of poor PV generation. While off-grid DGS represent an efficient and cost-effective energy supply solution particularly to rural and remote areas, fluctuations in voltage and frequency due to load variations, weather conditions (temperature, irradiation) and transmission line short-circuits are major challenges. The paper suggests a hierarchical Power Management (PM) and controller structure to improve the reliability and efficiency of the hybrid DGS. The first layer of the overall control scheme includes a Fuzzy Logic Controller (FLC) to adjust the voltage and frequency at the Point of Common Coupling (PCC) and a Clamping Bridge Circuit (CBC) which regulates the DC bus voltage. A maximum power point tracking (MPPT) controller based on FLC is designed to extract the optimum power from the PV. The second control layer coordinates among PV, DG and BESS to ensure reliable and efficient power supply to the load. MATLAB Simulink is used to implement the overall model of the off-grid DGS and to test the performance of the proposed control scheme which is evaluated in a series of simulations scenarios. The results demonstrated the good performance of the proposed control scheme and effective coordination between the DGS for all the simulation scenarios considered.Peer reviewedFinal Accepted Versio

Paternal methotrexate exposure affects sperm small RNA content and causes craniofacial defects in the offspring

Folate is an essential vitamin for vertebrate embryo development. Methotrexate (MTX) is a folate antagonist that is widely prescribed for autoimmune diseases, blood and solid organ malignancies, and dermatologic diseases. Although it is highly contraindicated for pregnant women, because it is associated with an increased risk of multiple birth defects, the effect of paternal MTX exposure on their offspring has been largely unexplored. Here, we found MTX treatment of adult medaka male fish (Oryzias latipes) causes cranial cartilage defects in their offspring. Small non-coding RNA (sncRNAs) sequencing in the sperm of MTX treated males identify differential expression of a subset of tRNAs, with higher abundance for specific 5′ tRNA halves. Sperm RNA methylation analysis on MTX treated males shows that m5C is the most abundant and differential modification found in RNAs ranging in size from 50 to 90 nucleotides, predominantly tRNAs, and that it correlates with greater testicular Dnmt2 methyltransferase expression. Injection of sperm small RNA fractions from MTX-treated males into normal fertilized eggs generated cranial cartilage defects in the offspring. Overall, our data suggest that paternal MTX exposure alters sperm sncRNAs expression and modifications that may contribute to developmental defects in their offspring.CSIC: I+D_2020_43

Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border

The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the Notch1 locus, and the spatiotemporal expression of Notch1 and its downstream target gene Bmp4 were expanded in the NPB. Cell fate analysis on folate deficient embryos revealed a significant increase in the number of cells coexpressing both neural (SOX2) and NPB (PAX7) markers, which may represent an enhancing effect in the cellular potential of those progenitors. Taken together, our findings propose a model where the RFC1 deficiency drives methylation changes in specific genomic regions that are correlated with a dysregulation of pathways involved in early development such as Notch1 and BMP4 signaling. These changes affect the potency of the progenitors residing in the juncture of the neural plate and NPB territories, thus driving them to a primed state.</jats:p

Image3_Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border.TIFF

The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the Notch1 locus, and the spatiotemporal expression of Notch1 and its downstream target gene Bmp4 were expanded in the NPB. Cell fate analysis on folate deficient embryos revealed a significant increase in the number of cells coexpressing both neural (SOX2) and NPB (PAX7) markers, which may represent an enhancing effect in the cellular potential of those progenitors. Taken together, our findings propose a model where the RFC1 deficiency drives methylation changes in specific genomic regions that are correlated with a dysregulation of pathways involved in early development such as Notch1 and BMP4 signaling. These changes affect the potency of the progenitors residing in the juncture of the neural plate and NPB territories, thus driving them to a primed state.</p

Table2_Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border.XLSX

The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the Notch1 locus, and the spatiotemporal expression of Notch1 and its downstream target gene Bmp4 were expanded in the NPB. Cell fate analysis on folate deficient embryos revealed a significant increase in the number of cells coexpressing both neural (SOX2) and NPB (PAX7) markers, which may represent an enhancing effect in the cellular potential of those progenitors. Taken together, our findings propose a model where the RFC1 deficiency drives methylation changes in specific genomic regions that are correlated with a dysregulation of pathways involved in early development such as Notch1 and BMP4 signaling. These changes affect the potency of the progenitors residing in the juncture of the neural plate and NPB territories, thus driving them to a primed state.</p

Image2_Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border.TIFF

The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the Notch1 locus, and the spatiotemporal expression of Notch1 and its downstream target gene Bmp4 were expanded in the NPB. Cell fate analysis on folate deficient embryos revealed a significant increase in the number of cells coexpressing both neural (SOX2) and NPB (PAX7) markers, which may represent an enhancing effect in the cellular potential of those progenitors. Taken together, our findings propose a model where the RFC1 deficiency drives methylation changes in specific genomic regions that are correlated with a dysregulation of pathways involved in early development such as Notch1 and BMP4 signaling. These changes affect the potency of the progenitors residing in the juncture of the neural plate and NPB territories, thus driving them to a primed state.</p

Table1_Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border.XLSX

The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the Notch1 locus, and the spatiotemporal expression of Notch1 and its downstream target gene Bmp4 were expanded in the NPB. Cell fate analysis on folate deficient embryos revealed a significant increase in the number of cells coexpressing both neural (SOX2) and NPB (PAX7) markers, which may represent an enhancing effect in the cellular potential of those progenitors. Taken together, our findings propose a model where the RFC1 deficiency drives methylation changes in specific genomic regions that are correlated with a dysregulation of pathways involved in early development such as Notch1 and BMP4 signaling. These changes affect the potency of the progenitors residing in the juncture of the neural plate and NPB territories, thus driving them to a primed state.</p

Image1_Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border.TIFF

The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the Notch1 locus, and the spatiotemporal expression of Notch1 and its downstream target gene Bmp4 were expanded in the NPB. Cell fate analysis on folate deficient embryos revealed a significant increase in the number of cells coexpressing both neural (SOX2) and NPB (PAX7) markers, which may represent an enhancing effect in the cellular potential of those progenitors. Taken together, our findings propose a model where the RFC1 deficiency drives methylation changes in specific genomic regions that are correlated with a dysregulation of pathways involved in early development such as Notch1 and BMP4 signaling. These changes affect the potency of the progenitors residing in the juncture of the neural plate and NPB territories, thus driving them to a primed state.</p

Image4_Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border.TIFF

The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the Notch1 locus, and the spatiotemporal expression of Notch1 and its downstream target gene Bmp4 were expanded in the NPB. Cell fate analysis on folate deficient embryos revealed a significant increase in the number of cells coexpressing both neural (SOX2) and NPB (PAX7) markers, which may represent an enhancing effect in the cellular potential of those progenitors. Taken together, our findings propose a model where the RFC1 deficiency drives methylation changes in specific genomic regions that are correlated with a dysregulation of pathways involved in early development such as Notch1 and BMP4 signaling. These changes affect the potency of the progenitors residing in the juncture of the neural plate and NPB territories, thus driving them to a primed state.</p