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CRISPR-Cas9 generated SARM1 knockout and epitope tagged mice reveal no role in transcription, despite confirmation of protein expression in macrophages

ABSTRACT: CRISPR-Cas9 generated SARM1 knockout and epitope tagged mice reveal no role in transcription, despite confirmation of protein expression in macrophages

PROVIDER: PRJNA754436 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15446600_1.fastq.gz	Fastqsanger.gz
	SRR15446600_2.fastq.gz	Fastqsanger.gz
	SRR15446601_1.fastq.gz	Fastqsanger.gz
	SRR15446601_2.fastq.gz	Fastqsanger.gz
	SRR15446602_1.fastq.gz	Fastqsanger.gz

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CRISPR-Cas9 generated SARM1 knockout and epitope tagged mice reveal no role in transcription, despite confirmation of protein expression in macrophages

Project description:The aim of this study was initially to determine the mechanism by which SARM1 regulates Ccl5 expression in murine macrophages. RNA sequencing revealed that the commonly used Sarm1tm1Aidi mouse, generated by targeted gene disruption, harbours passenger genes on chromosome 11 which confound interpretation of differential gene expression. Next-generation SARM1-deficient and epitope-tagged mice generated by CRISPR/Cas9 reveal no broad role for SARM1 in transcription in macrophages or brainstem, despite SARM1 protein expression there.

2021-08-14 | GSE182091 | GEO

HeLa CD4+ cells transfected with epitope-tagged eTat plasmids

Project description:Expression profiles of HeLa CD4+ cells transfected with epitope-tagged eTat plasmid. Cells are treated with nocodazole and hydroxyurea. Keywords: time-course

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HeLa CD4+ transfection with epitope-tagged eTat or parental vector

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Sarm1 knockout prevents type 1 diabetic bone disease in females independent of neuropathy

Project description:Diabetic patients have a high risk of developing skeletal diseases accompanied by diabetic peripheral neuropathy (DPN). In this study, we isolated the role of DPN in skeletal disease with global and conditional knockout models of sterile-α and TIR-motif-containing protein-1 (Sarm1). SARM1, an NADase highly expressed in the nervous system, regulates axon degeneration upon a range of insults, including DPN. Global knockout of Sarm1 prevented DPN, but not skeletal disease, in male mice with type 1 diabetes (T1D). Female wild type mice also developed diabetic bone disease, but without DPN. Unexpectedly, global Sarm1 knockout completely protected female mice from T1D-associated bone suppression and skeletal fragility despite comparable muscle atrophy and hyperglycemia. Global Sarm1 knockout rescued bone health through sustained osteoblast function with abrogation of local oxidative stress responses. This was independent of the neural actions of SARM1, as beneficial effects on bone were lost with neural conditional Sarm1 knockout. This study demonstrates that the onset of skeletal disease occurs rapidly in both male and female mice with T1D completely independent of DPN. In addition, this reveals that clinical SARM1 inhibitors, currently being developed for treatment of neuropathy, may also have benefits for diabetic bone through actions outside of the nervous system.

2024-04-30 | GSE252292 | GEO

Transcription profiling of human HeLa CD4+ cells transfected with epitope-tagged eTat plasmid, or parental plasmid pCep4

Project description:Expression profiles of HeLa CD4+ cells transfected with epitope-tagged eTat plasmid, or parental plasmid pCep4. Cells are unsynchronized and untreated.

2008-06-14 | E-GEOD-570 | biostudies-arrayexpress

Macrophage depletion blocks congenital SARM1-dependent neuropathy

Project description:Axon loss contributes to many common neurodegenerative disorders. In healthy axons, the axon survival factor NMNAT2 inhibits SARM1, the central executioner of programmed axon degeneration. We identified two rare NMNAT2 missense variants in two brothers afflicted with a progressive neuropathy syndrome. The polymorphisms result in amino acid substitutions, V98M and R232Q, which reduce NMNAT2 NAD+-synthetase activity. We generated a mouse model of the human syndrome and found that Nmnat2V98M/Nmnat2R232Q compound-heterozygous CRISPR mice survive to adulthood but develop progressive motor dysfunction, peripheral axon loss, and macrophage infiltration. These disease phenotypes are all SARM1-dependent. Remarkably, macrophage depletion therapy blocks and reverses neuropathic phenotypes in Nmnat2V98M/R232Q mice, identifying a SARM1-dependent neuroimmune mechanism as a key driver of disease pathogenesis. These findings demonstrate that SARM1 induces an inflammatory neuropathy and highlight the potential of immune therapy to treat this rare syndrome and other neurodegenerative conditions associated with NMNAT2 loss and SARM1 activation.

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A versatile mouse model of epitope-tagged histone H3.3 to study epigenome dynamics

Project description:A versatile mouse model of epitope-tagged histone H3.3 to study epigenome dynamics

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Chip-chip from HeLa S3 expressing epitope-tagged H2Abbd, macroH2A and H2A histones: H2Abbd versus H2A, and macroH2A versus H2A, distributions on 13 regions of the HG18 assembly

Project description:The distribution of histone variants H2Abbd and macroH2A in 13 regions of the HG18 assembly have been studied using a variant of the ChIP-on-Chip technique. HeLa S3 cell lines expressing tagged histones H2A, H2Abbd or macroHA were obtained using retroviral transfer. DNA fractions associated with tagged histones were isolated using a two-step purification procedure that involved affinity chromatography on a column with anti-FLAG antibodies, followed by affinity chromatography on a Ni-agarose column. The obtained genomic DNA samples were analyzed by hybridization with custom NimbleGene genomic microarrays. Two samples. Test sample 1 is HeLa S3 cells expressing epitope-tagged histone H2Abbd and test sample 2 is HeLa S3 cells expressing epitope-tagged histone macroH2A . The control for both test sample 1 and test sample 2 is HeLa S3 expressing epitope-tagged histone H2A. Two copies of each probe per array were made.

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2007-09-28 | E-GEOD-571 | biostudies-arrayexpress

A Conformation specific Nanobody Targeting the NMN-activated State of SARM1

Project description:Upon axonal injury, Sterile alpha (SAM) and Toll/interleukin-1 receptor (TIR) motif containing 1 (SARM1) is activated by nicotinamide mononucleotide (NMN) to deplete NAD and consequently promote the process of axon degeneration (AxD). Currently, only the inactive form of SARM1 in its auto-inhibitory conformation has been resolved. The flexibility of the enzymatically active form of SARM1 has so far precluded its structural determination. To solve the problem, we generated a stabilizing nanobody, Nb-C6, that specifically recognized 30 only the NMN-activated form of SARM1. The conformation specificity was verified by immunoprecipitation and surface plasmon resonance. Fluorescently labeled Nb-C6 could immunostain only the activated SARM1 in cells stimulated with CZ-48, a permeant mimetic of NMN. Expression of Nb-C6 in live cells resulted in stabilization of the active form of the endogenous and exogenous SARM1, producing and elevating cellular levels of cyclic ADP-ribose, a calcium messenger. Cryo-EM of the NMN-activated SARM1 complexed by Nb-C6 showed an octameric structure resembling a “blooming lotus” with the ARM domains bending significantly inward and swinging out together with the TIR domains to form the “petals of the lotus”. Nb-C6 bound to the SAM domain of the activated SARM1 and stabilized its Armadillo repeat motif domain. Analyses using hydrogen-deuterium exchange mass spectrometry (HDX-MS), and cross-linking MS (XL-MS) indicate that the activated SARM1 is highly dynamic and flexible and the neighboring TIRs form dimers via the surface close to one BB loop. The Nanobody is thus a valuable tool for delineating the mechanism of activation of SARM1 in AxD and other cellular processes.

2022-11-29 | PXD033528 | Pride

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