Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of mitochondrial fission-related genes in mitochondrial morphology and energy metabolism in mouse embryonic stem cells

ABSTRACT: Here we aimed to investigate the function of mitochondrial fission genes in embryonic stem cells (ESCs). Homozygous knockout ESC lines, namely, Fis1-/- , Mff-/- , and Dnm1l-/- ESCs, were generated using the CRISPR-Cas9 system. After then, we analyzed whole genome expression profile for characterizing cellular responses by incomplete mitochondrial fission.

ORGANISM(S): Mus musculus

PROVIDER: GSE148959 | GEO | 2020/04/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

Project description:To explore the function of Mitochondrial Fission 1 (FIS1) in acute myeloid leukemia (AML), we used shRNA to knock down the expression of FIS1 in leukemia cell line MOLM-13 cells and performed RNA-seq experiments to profile transcriptional changes upon FIS1 depletion.

2018-06-01 | GSE114111 | GEO

Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of primary human acute myeloid leukemia (AML) cells

Project description:To explore the function of Mitochondrial Fission 1 (FIS1) in acute myeloid leukemia (AML), we used shRNA to knock down the expression of FIS1 in primary human AML cells and performed RNA-seq experiments to profile global gene expression changes upon FIS1 depletion.

2018-06-01 | GSE114109 | GEO

Carnitine palmitoyltransferase 1A promotes mitochondrial fission by enhancing MFF succinylation in ovarian cancer

Project description:Mitochondria are dynamic organelles that are important for cell growth and proliferation. Dysregulated mitochondrial dynamics are highly associated with the initiation and progression of various cancers, including ovarian cancer. However, the regulatory mechanism underlying mitochondrial dynamics is still not fully understood. Previously, our study showed that carnitine palmitoyltransferase 1A (CPT1A) is highly expressed in ovarian cancer cells and promotes the development of ovarian cancer. Here, we find that CPT1A regulates mitochondrial dynamics and promotes mitochondrial fission in ovarian cancer cells. Our study futher shows that CPT1A regulates mitochondrial fission and function through mitochondrial fission factor (MFF) to promote the growth and proliferation of ovarian cancer cells. Mechanistically, we show that CPT1A promotes succinylation of MFF at lysine 302 (K302), which protects against Parkin-mediated ubiquitin-proteasomal degradation of MFF. Finally, the study shows that MFF is highly expressed in ovarian cancer cells and that high MFF expression is associated with poor prognosis in patients with ovarian cancer. MFF inhibition significantly inhibits the progression of ovarian cancer in vivo. Overall, CPT1A regulates mitochondrial dynamics through MFF succinylation to promote the development of ovarian cancer. Moreover, our findings suggest that MFF is a potential therapeutic target for ovarian cancer.

2023-05-15 | PXD041990 | Pride

Epigenetic dysregulation of the Drp1 binding partners MiD49 and MiD51 increases mitotic mitochondrial fission and promotes pulmonary arterial hypertension: mechanism and therapeutic implications

Project description:Mitotic fission is increased in hyperproliferative, apoptosis-resistant diseases, such as pulmonary arterial hypertension (PAH). PAH’s fissogenic phenotype includes activation of the fission mediator, dynamin related protein 1 (Drp1), which must complex with its adaptor proteins to cause fission. Drp1-induced fission has been therapeutically targeted in experimental PAH. Here we examine the role of two recently discovered, poorly understood, Drp1 adapter proteins, mitochondrial dynamics protein of 49 and 51 kDa (MiD49 and MiD51) in normal vascular cells and explore the role of their dysregulation in the pathogenesis of PAH. MiDs are increased in PAH PASMC. This accelerates Drp1-mediated mitotic fission, which increases cell proliferation and decreases apoptosis. Silencing MiDs (but not Fis1 or MFF) promotes mitochondrial fusion and G1-phase cell cycle arrest through an ERK1/2 and CDK4-dependent mechanism. Augmenting MiDs in normal cells causes fission and recapitulates the PAH phenotype. MiD upregulation results from decreased microRNA-34a-3p (miR-34a-3p) expression. Circulatory miR34a-3p expression is decreased in PAH patients as well as in preclinical models of PAH. Silencing MiDs or augmenting miR-34a-3p regresses experimental PAH. We used microarrays to identify differences in miR expression in pulmonary artery smooth muscle cells (PASMC) taken from either pulmonary arterial hypertension patients or healthy controls

2018-01-31 | GSE108707 | GEO

Oocyte-specific deletion of Eif5 causes apoptosis of mouse oocytes within the early growing follicles by mitochondrial fission defect and DNA damage

Project description:Mutations in several translation initiation factors are closely associated with premature ovarian insufficiency (POI). Here, we demonstrate that the conditional knockout of eukaryotic translation initiation factor 5 (Eif5) in both mouse primordial and growing oocytes resulted in the apoptosis of oocytes within the early growing follicles. The further studies revealed that Eif5 deletion in oocytes downregulated the levels of mitochondrial fission-related proteins (FIS1, MFF, MTFR2 and p-DRP1) and upregulated the levels of the integrated stress response (ISR)-related proteins (SLC7A1, SHMT2 and AARS1) and genes (Atf4, Ddit3 and Fgf21). Consistent with this, Eif5 deletion in oocytes resulted in mitochondrial dysfunction characterized by elongated form, aggregated distribution beneath the oocyte membrane, decreased ATP content and mtDNA copy number, and excessive accumulation of reactive oxygen species (ROS) and mitochondrial superoxide. Meanwhile, Eif5 deletion in oocytes led to a significant increase in the levels of DNAdamageresponse proteins (γH2AX, p-CHK2, and p53) and proapoptotic proteins (PUMA and BAX), as well as a significant decrease in the levels of anti-apoptotic protein BCL-xL. Collectively, these findings indicate that Eif5 deletion in mouse oocytes results in the apoptosis of oocytes within the early growing follicles via mitochondrial fission defect and excessive ROS-induced DNA damage. This study provides new insights into pathogenesis and genetic diagnosis for POI.

2024-08-15 | GSE263785 | GEO

Mitochondrial fusion limits breast cancer metastasis

Project description:Mitochondrial metabolism plays a central role in promoting cancer growth and metastatic progression. The transition between a hyperfused and fragmented mitochondrial network is termed mitochondrial dynamics and is important for many mitochondria-associated functions; however, little is known regarding how this process influences metastasis. Here, we show that breast cancer cells with low metastatic potential exhibit a more fused mitochondrial network compared to highly metastatic breast cancer cells. To examine whether a fused mitochondrial network could impair metastasis, we inhibited mitochondrial fission in metastatic breast cancer cells by individual genetic deletion of three key regulators of mitochondrial fission (Drp1, Fis1 and Mff) or pharmacological intervention using leflunomide, an anti-rheumatic drug. These cells displayed a fused mitochondrial network and limited survival under anoikis conditions, consistent with mitochondrial fusion limiting metastasis. Transcriptomics and metabolomics analyses revealed that mitochondrial fusion causes significant alterations in metabolic pathways and processes related to cell adhesion. Functional bioenergetics assays demonstrated that mitochondrial fusion limited the mitochondrial capacity of cancer cells. Mitochondrial fusion in breast cancer cells had no significant effect on primary tumor growth but almost completely ablated lung metastasis in vivo. Furthermore, the transcriptomics signature associated with enhanced mitochondrial fusion correlated with improved survival in patients with breast cancer. Overall, our findings highlight mitochondrial fusion as a therapeutic opportunity for breast cancer.

2024-09-25 | GSE245216 | GEO

Role of mitochondrial fission-related genes in mitochondrial morphology and energy metabolism in mouse embryonic stem cells

Project description:Role of mitochondrial fission-related genes in mitochondrial morphology and energy metabolism in mouse embryonic stem cells

| PRJNA626620 | ENA

Loss of hepatic DRP1 exacerbates alcoholic hepatitis by inducing megamitochondria and mitochondrial maladaptation

Project description:To investigate the function of mitochondrial fission protein DRP1 in the development of alcoholic liver disease, we generated liver-specific Dnm1l KO mice using Alb-Cre/loxP system. These mice were subjected to Gao-Binge alcohol model. We then performed RNA sequensing analysis using the liver tissue. Gene expression profiling analysis was conducted using data obtained from RNA-seq of 4 different groups.

2022-07-01 | GSE207074 | GEO

APOL1 renal-risk variants induce mitochondrial fission

Project description:APOL1 renal-risk variants induce mitochondrial fission

| PRJNA490827 | ENA

Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

Project description:Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

| PRJNA464347 | ENA