EC-catalytic subunit dependent erythroid precursor transcriptome
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus domesticus
PROVIDER: GSE167090 | GEO | 2021/05/17
REPOSITORIES: GEO
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Project description:EC-catalytic subunit dependent erythroid precursor transcriptome
| PRJNA702987 | ENA
Project description:We performed mouse single oocyte RNA-seq and bulk oocyte CUT&Tag assays in the current project. In details, SMART-seq based single oocyte RNA-seq was performed at adult GV stage, GV3h stage and MII stage, using control and Dis3 oocyte-speicfic knockout (cKO) oocytes. RiboMinus-seq based single oocyte RNA-seq was performed at adult GV stage using control and Dis3 cKO oocytes, and at p20 GV stage using control, Dis3 cKO, Exosc10 cKO and Dis3/Exosc10 double cKO (dcKO) oocytes. Bulk CUT&Tag of anti-H3K27me3 was done in WT and Dis3 cKO oocytes at adult GV stage, and in WT and Dis3/Exosc10 dcKO oocytes at p20 stage. In addition, CUT&Tag of anti-RNA polymerase II (Ser2+Ser5) was performed in WT and Dis3 cKO oocytes at GV stage. All CUT&Tag experiments share the same rabbit-Igg negative control. All p20 stage oocytes were specified as p20. The non-specified GV oocytes were all adult GV oocytes.
2022-02-11 | GSE196331 | GEO
Project description:Cell-based studies of human ribonucleases traditionally relies on methods that deplete proteins slowly. To assess their immediate roles in nuclear RNA biology, we engineered cells where the 3’->5’ exoribonucleases of the exosome complex, Dis3 and EXOSC10, can be eliminated within 60 minutes. Loss of Dis3 has the greatest impact, causing thousands of enhancer RNAs, intragenic transcripts, promoter upstream transcripts (PROMPTs) and products of premature cleavage and polyadenylation (PCPA) to accumulate. Interestingly, EXOSC10 only targets these substrates when Dis3 is absent, which is explained by its rapid mis-localization to the nucleoplasm following Dis3 loss. Direct detection of EXOSC10 substrates revealed a more specific role in trimming of short 3’ extensions on ribosomal and small nucleolar RNAs. Finally, the 5’-3’ exoribonuclease, Xrn2, has little activity on exosome substrates, but promotes termination following PCPA. Interestingly, Xrn2 is not rate limiting for PROMPT termination providing a distinction between sense and anti-sense transcriptional regulation.
2019-03-06 | GSE120574 | GEO
Project description:Male germ cell meiosis is essential for generating haploid spermatozoa in mice. Here, we investigate the essential role of DIS3 in male germ cell meiosis in mice. Conditional inactivation of DIS3 in spermatocytes with Stra8-cre transgenic mice have severely impaired meiotic progression, which results in defective meiosis and spermatogenesis. RNA-seq analysis reveals that Dis3 deficiency causes significant dysregulation of the expression of transcripts in mutant testes. Meiosis-associated genes are significantly decreased in the absence of DIS3. Therefore, we show that DIS3 ribonuclease plays a critical role in germ cell meiosis during spermatogenesis in mice.
2021-07-16 | GSE180197 | GEO
Project description:The developmentof haematopoietic stem cellsinto mature erythrocytes–erythropoiesis –is a controlled process characterized by cellular reorganisation and drastic reshaping of the proteome landscape.Failure of ordered erythropoiesis isassociated with anaemias and haematological malignancies. Although the ubiquitin (UB) system isa known crucial post-translational regulator in erythropoiesis, how the erythrocyteis reshaped by the UBsystemis poorly understood.Bymeasuringthe proteomiclandscape of in vitrohuman erythropoiesis models, we founddynamic differential expression ofsubunitsof the CTLH E3 ubiquitin ligase complexthat formeddistinctmaturation stage-dependent assemblies of structurally homologous RANBP9-and RANBP10-CTLH complexes.Moreover,protein abundance of CTLH’s cognate E2-conjugating enzyme UBE2H increased during terminal differentiation,which dependedon catalyticallyactive CTLH E3complexes.CRISPR-Cas9 mediated inactivation of all CTLH E3 assemblies by targeting the catalytic subunit MAEA,orUBE2H, triggered spontaneous and accelerated maturationof erythroid progenitor cellsincluding increased heme and haemoglobin synthesis. Thus, the orderly progression of human erythropoiesis is controlled by the assembly of distinct UBE2H-CTLHmodulesfunctioning at different developmental stages.
2023-03-11 | PXD031992 | Pride
Project description:The repair of DNA double strand breaks (DSBs) has recently been shown to depend not only on protein function but also on RNA. In particular, the processing of a long damage-induced RNA into small damage induced RNAs (diRNAs) has been a focus of interest. Given that the RNA exosome has been shown in Drosophila and human cells to participate in DSB repair, we investigated whether the catalytic components EXOSC10 and DIS3 have a function in diRNA biogenesis in human cells.
2019-04-10 | GSE113109 | GEO
Project description:Erythropoiesis is a tightly controlled process. Although human and murine erythropoiesis are grossly similar, several aspects of these processes present significant differences. We have performed a label free quantification of proteins expressed during murine erythroid differentiation of primary cells with the aim to compare human and murine differentiations. Furthermore, we also analyzed the proteome of three murine cell lines, MEDEP, G1ER and Friend cells, to determine their similarities with the proteome of primary cells.
2020-05-26 | PXD009384 | Pride
Project description:A time course study to assess the intracellular metabolic changes of progenitors isolated from stress erythropoiesis expansion culture.
2021-12-05 | ST002009 | MetabolomicsWorkbench
Project description:Preeclampsia (PE) has been associated with placental dysfunction, resulting in foetal hypoxia, accelerated erythropoiesis and increased erythroblast count in the umbilical cord blood (UCB). Although the detailed effects remain unknown, placental dysfunction can also cause inflammation, nutritional and oxidative stress in the fetus that can affect erythropoiesis. Here, we compared the expression of surface adhesion molecules and erythroid differentiation capacity of UCB hematopoietic stem/ progenitor cells (HSPCs), UCB erythroid profiles along with transcriptome and proteome of these cells between male and female foetuses from PE and normotensive pregnancies. While no significant differences were observed in UCB HSPC migration/ homing and in vitro erythroid colony differentiation, the UCB HSPC transcriptome and the proteomic profile of the in vitro differentiated erythroid cells differed between PE vs normotensive samples. Accordingly, despite absence of significant differences in the UCB erythroid populations in male or female foetuses from PE or normotensive pregnancies, transcriptional changes were observed during erythropoiesis, particularly affecting male foetuses. Pathway analysis suggested deregulation in mTORC1/AMPK signaling pathways controlling cell cycle, differentiation and protein synthesis. These results associate PE with transcriptional and proteomic changes in foetal HSPCs and erythroid cells that may underlie the higher erythroblast count in the UCB in PE.
2019-06-20 | PXD010364 | Pride
Project description:Suppression of programmed cell death is critical for the final maturation of red blood cells and depends largely on the anti-apoptotic effects of EpoR-STAT5-Bcl-x(L) signaling. As the major eukaryotic serine/threonine phosphatase, protein phosphatase 2A (PP2A) regulates multiple cellular processes, including apoptosis. However, whether PP2A plays a role in preventing erythroid cells from undergoing apoptosis remains to be elucidated. We conditionally inactivated the catalytic subunit ? of PP2A (PP2Ac?), which is the predominant form of PP2Ac, during early embryonic hematopoiesis. Loss of PP2Ac? in hematopoietic cells perturbed definitive erythropoiesis characterized by fetal liver atrophy, reduced Ter119(+) cell number, abnormal expression patterns of molecular markers, less colony formation, and a reduction in definitive globin expression. Levels of erythropoiesis-promoting cytokines and initial seeding with hematopoietic progenitors remained unchanged in PP2Ac?(TKO) fetal livers. We noted impaired expansion of the fetal erythroid compartment, which was associated with increased apoptosis of committed erythroid cells. Mechanistically, PP2Ac? depletion markedly reduced Tyr(694) phosphorylation of STAT5 and expression of Bcl-x(L). Unexpectedly, PP2Ac?-deficient embryos did not manifest any early embryonic vascular defects. Collectively, these data provide direct loss-of-function evidence demonstrating the importance of PP2Ac? for the survival of committed erythroid cells during fetal liver erythropoiesis.
| S-EPMC3081176 | biostudies-literature