Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell RNA-seq for undifferentiated spermatogonia from the testes of control, aged and busulfan-treated C57BL/6 mice

ABSTRACT: GFRa1-GFP positive, Miwi2-tdTom negative and GFRa1-GFP negative, Miwi2-tdTom positive single cells from the testes of 2 adult, 2 aged and 3 busulfan-treated mice were sorted with FACS and cDNA libraries prepared with the SMARTseq2 protocol. Single-cell libraries were sequenced

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Ivalya Ivanova

PROVIDER: E-MTAB-9239 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Bulk RNA-seq for undifferentiated spermatogonia from the testes of control, aged and busulfan-treated C57BL/6 mice

Project description:Samples were prepared from 100 GFRa1-GFP positive, Miwi2-tdTom negative and 100 GFRa1-GFP negative, Miwi2-tdTom positive cells that were sorted with FACS. cDNA libraries were prepared with the SMARTseq2 protocol. Adult, control samples had four biological replicates while the aged and busulfan-treated samples were in triplicate. There were 2 technical replicates per biological sample.

2022-02-28 | E-MTAB-9238 | biostudies-arrayexpress

Affymetrix gene expression array (mouse 2.0) of sorted undifferentiated spermatogonia in inducible Miwi2 knock-out model

Project description:Undifferentiated spermatogonia were sorted from Miwi2Tom/FL; ERT-Cre/+ (Miwi2-iKO) and Miwi2Tom/+; ERT-Cre/+ (Miwi2-CTL) mice injected with tamoxifen two weeks after last tamoxifen injection to understand an impact of acute Miwi2 deletion on spermatogenic homeostasis.

2018-03-21 | E-MTAB-6612 | biostudies-arrayexpress

A MILI-independent piRNA biogenesis pathway empowers partial germline reprogramming.

Project description:In mice, the PIWI-piRNA pathway is essential to re-establish transposon silencing during male germline reprogramming. The cytoplasmic PIWI protein MILI mediates piRNA-guided transposon RNA cleavage as well as piRNA amplification. MIWI2-bound piRNAs and its nuclear localization are proposed to be dependent upon MILI function. Here, we demonstrate the existence of a piRNA biogenesis pathway that in the absence of MILI that sustains partial MIWI2 function and reprogramming activity.

2017-04-25 | E-MTAB-5561 | biostudies-arrayexpress

TEX15 is an essential executor of MIWI2-directed transposon DNA methylation and silencing.

Project description:The PIWI protein MIWI2 and its associated PIWI-interacting RNAs (piRNAs) instruct DNA methylation of young active transposable elements (TEs) in the male germline. Here we show that MIWI2 associates with TEX15 in foetal gonocytes. TEX15 is predominantly a nuclear protein that is not required for piRNA biogenesis but is essential for piRNA-directed TE de novo methylation and silencing. In summary, TEX15 is an essential executor of mammalian piRNA-directed DNA methylation.

2020-06-17 | E-MTAB-9090 | biostudies-arrayexpress

Defective germline reprogramming rewires the spermatogonial transcriptome

Project description:Defective germline reprogramming in Miwi2- and Dnmt3l-deficient mice results in the failure to reestablish transposon silencing, meiotic arrest and progressive loss of spermatogonia. Here we sought to understand the molecular basis for this spermatogonial dysfunction. Through a combination of imaging, conditional genetics and transcriptome analysis, we demonstrate that germ cell elimination in the respective mutants arises due to defective germline reprogramming rather than a function for the respective factors within spermatogonia. In both Miwi2-/- and Dnmt3l-/- spermatogonia the intracisternal-A particle (IAP) family of endogenous retroviruses is de-repressed, but in contrast to meiotic cells DNA damage is not observed. Instead we find that unmethylated IAP promoters rewire the spermatogonial transcriptome by driving expression of neighboring host genes. In summary, defective reprogramming deregulates the spermatogonial transcriptome that may underlie spermatogonial dysfunction.

2018-03-09 | E-MTAB-6202 | biostudies-arrayexpress

A transit amplifying population underpins the efficient regenerative capacity of the testis

Project description:To study the adult population of spermatogonial stem cells marked with the expression of Miwi2, we generated the Miwi2-Tomato reporter knock-in allele. To further explore the molecular identity of Miwi2-TomPos spermatogonia, we performed comparative gene expression analysis between two population hierarchically related, an upstream population of Miwi2-TomHi c-KitNeg spermatogonia and their Miwi2-TomHi c-KitPos descendants. The analysis revealed enrichment for many genes that have been associated with SSC/SPC (Spermatogonial Stem Cells/ Spermatogonial Precursor Cells) phenotype or function.

2017-04-01 | E-MTAB-4828 | biostudies-arrayexpress

SPOCD1 is a novel executor of piRNA-directed DNA methylation that links MIWI2 to the de novo DNA methylation machinery

Project description:In mammals, the acquisition of the germline from the soma provides the germline with an essential challenge, the necessity to erase and reset genomic methylation. In the male germline RNA-directed DNA methylation silences young active transposable elements (TEs). The PIWI protein MIWI2 (PIWIL4) and its associated PIWI-interacting RNAs (piRNAs) are proposed to tether MIWI2 to nascent TE transcripts and instruct DNA methylation. The mechanism by which MIWI2 directs de novo TE methylation is poorly understood but central to the immortality of the germline. Here, we define the interactome of MIWI2 in foetal gonocytes that are undergoing de novo genome methylation and identify a novel MIWI2-associated factor, SPOCD1, that is essential for young TE methylation and silencing. The loss of Spocd1 in mice results in male specific infertility and does not impact on piRNA biogenesis nor localization of MIWI2 to the nucleus. SPOCD1 is a nuclear protein and its expression is restricted to the period of de novo genome methylation. We found SPOCD1 co-purified in vivo with DNMT3L and DNMT3A, components of the de novo methylation machinery as well as constituents of the NURD and BAF chromatin remodelling complexes. We propose a model whereby tethering of MIWI2 to a nascent TE transcript recruits repressive chromatin remodelling activities and the de novo methylation apparatus through its association with SPOCD1. In summary, we have identified a novel and essential executor of mammalian piRNA-directed DNA methylation.

2020-06-01 | E-MTAB-7997 | biostudies-arrayexpress

DNA methylation of yound male wild type and dSpin1 knockout mice

2024-07-22 | E-MTAB-12713 | biostudies-arrayexpress

C19ORF84 connects piRNA and DNA methylation machineries to defend the mammalian germline

Project description:In the male mouse germline, PIWI-interacting RNAs (piRNAs), bound by the PIWI protein MIWI2 (PIWIL4), guide the DNA methylation of young active transposable elements (TEs) through SPOCD1. We identified loss-of-function variants in human SPOCD1 that cause male infertility and defective TE silencing. One SPOCD1 pathogenic allele encodes a truncated protein that lacks the conserved carboxy-terminus. We demonstrated that this deleted region interacts with C19ORF84. In mouse foetal germ cells, the nuclear protein C19ORF84 is required for the association of SPOCD1 with DNMT3L, an essential component of the de novo methylation machinery. In summary, we identified a conserved role for SPOCD1 in safeguarding the continuity of the human germline and discovered C19ORF84, an uncharacterised protein essential for 15 orchestrating piRNA-directed DNA methylation.

2024-02-13 | E-MTAB-11612 | biostudies-arrayexpress

A regulatory role for CHD4 in maintenance of the spermatogonial stem cell pool

Project description:Maintenance and self-renewal of the spermatogonial stem cell (SSC) population is the cornerstone of male fertility. In this manuscript we have identified a key role for the nucleosome remodelling protein Chromodomain Helicase DNA binding protein 4 (CHD4) in regulating SSC function. Gene expression analyses revealed that CHD4 expression is largely restricted to spermatogonia in the mouse testis, and is particularly enriched in SSCs. Using spermatogonial transplantation techniques and RNAi mediated knockdown it was established that loss of Chd4 expression significantly impairs SSC regenerative capacity, resulting in a ~50% reduction in colonisation of recipient testes. A single cell RNA-seq comparison depicted reduced expression of ‘self-renewal’ genes such as Gfra1 and Pten following Chd4 knockdown, along with increased expression of signature progenitor genes, Neurog3 and Dazl. Co-immunoprecipitation analyses demonstrated that CHD4 regulates gene expression in spermatogonia not only though its traditional association with the remodelling complex NuRD, but also via interaction with the GDNF-responsive transcription factor SALL4. Cumulatively, the results of this study depict a previously unappreciated fundamental role for CHD4 in controlling fate decisions in the spermatogonial pool.

2021-06-17 | PXD022066 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data