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Data files for manuscript "NAD precursors cycle between host tissues and the gut microbiome"

ABSTRACT: These are the raw mass spec data files for manuscript "NAD precursors cycle between host tissues and the gut microbiome", Karthikeyani Chellappa et al. Check out "Mass Spec data_KEY_Chellappa et al Cell Metabolism_2022.xlsx" for data file arrangement.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Joseph A. Baur

PROVIDER: MSV000090481 | MassIVE | Thu Oct 06 12:25:00 BST 2022

REPOSITORIES: MassIVE

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Publications

NAD precursors cycle between host tissues and the gut microbiome.

Chellappa Karthikeyani K McReynolds Melanie R MR Lu Wenyun W Zeng Xianfeng X Makarov Mikhail M Hayat Faisal F Mukherjee Sarmistha S Bhat Yashaswini R YR Lingala Siddharth R SR Shima Rafaella T RT Descamps Hélène C HC Cox Timothy T Ji Lixin L Jankowski Connor C Chu Qingwei Q Davidson Shawn M SM Thaiss Christoph A CA Migaud Marie E ME Rabinowitz Joshua D JD Baur Joseph A JA

Cell metabolism 20221201 12

Nicotinamide adenine dinucleotide (NAD) is an essential redox cofactor in mammals and microbes. Here we use isotope tracing to investigate the precursors supporting NAD synthesis in the gut microbiome of mice. We find that dietary NAD precursors are absorbed in the proximal part of the gastrointestinal tract and not available to microbes in the distal gut. Instead, circulating host nicotinamide enters the gut lumen and supports microbial NAD synthesis. The microbiome converts host-derived nicoti ...[more]

PMID: 36476934

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GNPS - Data files for manuscript

Project description:These are the raw mass spec data files for manuscript "NAD precursors cycle between host tissues and the gut microbiome", Karthikeyani Chellappa et al. Check out "Mass Spec data_KEY_Chellappa et al Cell Metabolism_2022.xlsx" for data file arrangement.

2022-10-06 | MSV000090481 | GNPS

Data files for manuscript "NAD+ flux is maintained in aged mice"

Project description:These are the data files associated with manuscript "NAD+ flux is maintained in aged mice", McReynolds MR, et al. Please refer to README-raw-data-NADAgedMice-20210802.docx for more details.

2021-08-02 | MSV000087933 | MassIVE

Hidden features of NAD-RNA epitranscriptome in Drosophila life cycle

Project description:Nicotinamide adenine dinucleotide (NAD), a nucleotide-containing metabolite, can be incorporated into the RNA 5’-terminus to result in NAD-capped RNA (NAD-RNA). Since NAD has been heightened as one of the most essential metabolites in cells, its attachment to RNA might indicate a yet-to-be discovered mechanism at the epitranscriptomic level. Here, we design a highly-sensitive method, DO-seq, to capture NAD-RNAs. Using Drosophila, we identify thousands of previously unexplored NAD-RNAs and their dynamics in the fly life cycle, from embryo to adult. We show the evidence that chromosomal clustering might be the structural basis by which co-expression can couple with NAD capping on physically and functionally-linked genes. Furthermore, we note that NAD capping of cuticle genes seems to inversely correlate with gene expression. Combined, we propose NAD-RNA epitranscriptome as a hidden layer of regulation that profoundly impacts biological processes. DO-seq empowers the identification of NAD-capped RNAs, facilitating functional investigation into this modification.

2023-12-21 | GSE228505 | GEO

The RNA-seq for the kidneys injected with cisplatin and NAD precursors.

Project description:To investigate the molecular mechnism of NAD precursors. We then performed gene expression profiling analysis using data obtained from RNA-seq of the kidneys of mice.

2023-02-03 | GSE207587 | GEO

SeaIce, Espegrend, Microscosm, Mnemi

Project description:454 dataset for Hosia, et al. Torstensson et al. Dinasquet et al.

| PRJEB7907 | ENA

A viral ADP-ribosyltransferase attaches RNA chains to host proteins

Project description:The mechanisms by which viruses hijack their host’s genetic machinery are of enormous current interest. One mechanism is adenosine diphosphate (ADP) ribosylation, where ADP-ribosyltransferases (ARTs) transfer an ADP-ribose fragment from the ubiquitous co-factor nicotinamide adenine dinucleotide (NAD) to acceptor proteins (Cohen and Chang, 2018). When bacteriophage T4 infects Escherichia coli, three different ARTs reprogram the host’s transcriptional and translational apparatus (Koch et al., 1995; Tiemann et al., 2004). Recently, NAD was identified as a 5’-modification of cellular RNA molecules in bacteria and higher organisms (Cahova et al., 2015; Chen et al., 2009; Jiao et al., 2017). Here, we report that a bacteriophage T4 ART ModB accepts not only NAD but also NAD-RNA as substrate, thereby covalently linking entire RNA chains to acceptor proteins in an “RNAylation” reaction. This enzyme specifically RNAylates its host protein targets, ribosomal proteins rS1 and rL2, at arginine residues and prefers NAD-RNA over NAD. RNAylation of specific ribosomal proteins decreases ribosome activity. We identify specific E. coli and T4 phage RNAs, which are RNAylated to rS1 in vivo.T4 phages expressing an inactive mutant of ModB show a decreased burst size and a decelerated lysis of E. coli during T4 infection. Our findings not only challenge the established views of the phage replication cycle but also reveal a distinct biological role of NAD-RNA, namely activation of the RNA for enzymatic transfer. Our work exemplifies the first direct connection between RNA modification and post-translational protein modification. As ARTs play important roles far beyond viral infections (Fehr et al., 2020), RNAylation may have far-reaching implications.

2023-05-26 | PXD038075 | Pride

A viral ADP-ribosyltransferase attaches RNA chains to host proteins

2023-05-30 | PXD041714 | Pride

SPAAC-NAD-seq, a sensitive and accurate method to profile NAD+-capped transcripts

Project description:We developed a Copper-free, strain-promoted azide-alkyne cycloaddition reaction (SPAAC) to capture NAD-RNAs without RNA degradation. We examined the specificity of CuAAC and SPAAC reactions towards NAD+ vs. m7G, and found that both prefer NAD+ but also act on m7G. We show that m7G-capped RNA can be immuno-depleted, allowing for the specific identification of NAD-RNA via the SPAAC reaction and sequencing, which we name SPAAC-NAD-seq. Subjecting Arabidopsis RNA to both the original NAD captureSeq and SPAAC-NAD-seq, we found that more NAD+-capped RNA was identified by the latter, particularly those with low abundance. This led to the discovery of new gene ontology terms such as starch biosynthsis, intracellular protein transport and response to cadmium stress associated with genes that produce NAD-RNA. Furthermore, reads were uniformly distributed along gene bodies, which suggested that SPAAC-NAD-seq retained full-length sequence information. SPAAC-NAD-seq enables specific and efficient discovery of NAD-RNA in prokaryotes, and when combined with m7G-RNA depletion, in eukaryotes.

2021-04-14 | GSE162114 | GEO

SNP search in NAD+ resistent Streptococcus pneumoniae

Project description:To gain deeper insights into antibacterial mechanisms of NAD+ and bacterial adaptation, we generated and sequenced NAD+ resistant clones of Spn. For this purpose, Spn was cultivated in liquid medium with increasing concentrations (50 µM to 5 mM) of NAD+. After six passages, bacteria were plated on blood agar supplemented with 500 µM NAD+ and three clones were picked

2023-06-11 | E-MTAB-12644 | biostudies-arrayexpress

NAD+ precursors prolong survival and improve cardiac phenotypes in a mouse model of Friedreich’s Ataxia

Project description:Friedreich’s ataxia (FRDA) is a progressive disorder caused by insufficient expression of frataxin, which plays a critical role in assembly of iron-sulfur centers in mitochondria. Individuals are cognitively normal, but display a loss of motor coordination and cardiac abnormalities. Many ultimately succumb to heart failure. Administration of nicotinamide adenine dinucleotide (NAD+) precursors has shown promise in mitochondrial myopathy and rodent models of heart failure, including mice lacking frataxin in cardiomyocytes. We studied mice with systemic knockdown of frataxin (shFxn), which display motor deficits and early mortality with cardiac hypertrophy. Hearts in these mice do not “fail” per se but become hyperdynamic with small chamber sizes. Data from an ongoing natural history study indicate that hyperdynamic hearts are observed in young individuals with FRDA, suggesting that the mouse model could reflect early pathology. Administering nicotinamide mononucleotide or riboside to shFxn mice increases survival, modestly improves cardiac hypertrophy, and limits increases in ejection fraction. Mechanistically, most of the transcriptional and metabolic changes induced by frataxin knockdown are insensitive to NAD+ precursor administration, but glutathione levels are increased suggesting improved antioxidant capacity. Overall, our findings indicate that NAD+ precursors are modestly cardioprotective in this model of Friedreich’s Ataxia and warrant further investigation.

2024-08-28 | GSE271798 | GEO

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