RNA-seq profiling of zinc sulfate-stimulated MFF-1 cells from Siniperca chuatsi
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ABSTRACT:
ORGANISM(S): Siniperca chuatsi
PROVIDER: GSE318615 | GEO | 2026/02/11
REPOSITORIES: GEO
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Project description:RNA-seq profiling of zinc sulfate-stimulated MFF-1 cells from Siniperca chuatsi
| PRJNA1419314 | ENA
Project description:High concenHigh concentration acetic acid in the fermentation medium represses cell growth, metabolism and fermentation efficiency of Saccharomyces cerevisiae, which is widely used for cellulosic ethanol production. Our previous study proved that supplementation of zinc sulfate in the fermentation medium improved cell growth and ethanol fermentation performance of S. cerevisiae under acetic acid stress condition. However, the molecular mechanisms is still unclear. To explore the underlying mechanism of zinc sulfate protection against acetic acid stress, transcriptomic and proteomic analysis were performed. The changed genes and proteins are related to carbon metabolism, amino acid biosynthesis, energy metabolism, vitamin biosynthesis and stress responses. In a total, 28 genes showed same expression in transcriptomic and proteomic data, indicating that zinc sulfate affects gene expression at posttranscriptional and posttranslational levels.tration acetic acid in the fermentation medium represses cell growth, metabolism and fermentation efficiency of Saccharomyces cerevisiae, which is widely used for cellulosic ethanol production. Our previous study proved that supplementation of zinc sulfate in the fermentation medium improved cell growth and ethanol fermentation performance of S. cerevisiae under acetic acid stress condition. However, the molecular mechanisms is still unclear. To explore the underlying mechanism of zinc sulfate protection against acetic acid stress, transcriptomic and proteomic analysis were performed. The changed genes and proteins are related to carbon metabolism, amino acid biosynthesis, energy metabolism, vitamin biosynthesis and stress responses. In a total, 28 genes showed same expression in transcriptomic and proteomic data, indicating that zinc sulfate affects gene expression at posttranscriptional and posttranslational levels.
2022-05-19 | PXD015459 | Pride
Project description:Increased mitochondrial fragmentation drives significant metabolic reprogramming that contributes to tumor progression. We explored the functional role of MFF (Mitochondrial Fission Factor), a key regulator of mitochondrial fragmentation, in the pathobiology of multiple myeloma (MM). MFF was found overexpressed in MM primary samples and cell lines, driving altered mitochondrial dynamics and metabolic reprogramming. MFF silencing inhibited MM cell proliferation, survival, and colony formation in vitro and in vivo. MFF overexpression promoted oxidative phosphorylation (OXPHOS) and a shift towards mitochondrial metabolism, while MFF knockdown favored glycolysis. These metabolic alterations were associated with alterations in lactate intracellular levels. Interestingly, lactate transporter inhibitors, in combination with MFF-targeting strategies, synergistically reduced MM cell viability and overcame proteasome inhibitor (PI) resistance. These findings highlight MFF as a key regulator of mitochondrial dynamics and metabolic adaptation in MM.
2025-11-18 | GSE286009 | GEO
Project description:To determine the physiological roles of zinc in erythroid progenitor cells, cellular zinc was restricted by 50 µM DTPA treatment (a zinc chelator) for 24 hours in differentiating G1E-ER4 cells. G1E-ER4 cells induced for differentiation by beta-estradiol were divided into two groups: control and 50 µM DTPA treatment. A sample from cells untreated with beta-estradiol was also included as an undifferentiated group.
2025-11-19 | GSE310207 | GEO
Project description:Zinc is a common metal in most ambient particulate matter (PM), and has been proposed to be a causative component in PM-induced adverse cardiovascular health effects. Zinc is also an essential metal and has the potential to induce many physiological and nonphysiological changes. Most toxicological studies employ high levels of zinc. We hypothesized that subchronic inhalation of environmentally relevant levels of zinc would cause cardiac changes in healthy rats. To address this question, healthy male WKY rats (12 wks age) were exposed via nose only inhalation to filtered air or 10, 30 or 100 ug/m3 of aerosolized Zn in sulfate form, 5 h/d, 3 d/wk for 16 wks. Necropsies occurred 48 h after the last exposure to ensure effects were due to chronic exposure rather than the last exposure. No significant changes were observed in neutrophil or macrophage count, total lavageable cells, or enzyme activity levels (lactate dehydrogenase, n-acetyl ?-D-glucosaminidase, ?-glutamyl transferase) in bronchoalveolar lavage fluid, indicating minimal pulmonary effect. In the heart, cytosolic glutathione peroxidase activity decreased, while mitochondrial ferritin levels increased and succinate dehydrogenase activity decreased, suggesting a mitochondria-specific effect. Although no cardiac pathology was seen, cardiac gene array analysis indicated changes in genes involved in cell signaling, a pattern concordant with known zinc effects. These data indicate that inhalation of zinc at environmentally relevant levels may induce cardiac effects. While changes are small in healthy rats, these may be especially relevant in individuals with pre-existent cardiovascular disease. Keywords: dose response
2008-09-22 | GSE11091 | GEO
Project description:To investigate the effect of mitochondrial fission factor (MFF) on oocyte competence and female fertility using an oocyte-specific Mff knockout mouse model. Oocyte-specific Mff deficiency hindered oocyte maturation and early embryonic development via regulation of mitochondrial dynamics, resulting in female subfertility. What is known already: Emerging studies have demonstrated that mitochondrial dynamics play a vital role in oocyte maturation and early embryo development. MFF is one of the crucial proteins regulating mitochondrial dynamics. Our previous studies have indicated that Mff is necessary for oocyte competence and fertility using a global Mff knockout mouse model. However, further investigation is needed to determine whether the deletion of Mff in oocytes could affect oocyte competence and early embryonic development by regulating mitochondrial dynamics.The Mfffl/fl; Gdf9-Cre mice consistently exhibited reduced fertility with a significant decrease in litter size, number of litters per female, and number of pups per female compared to the Mfffl/fl mice. The numbers of GV oocytes, ovulated oocytes and 2-cell embryos were significantly lower in the Mfffl/fl; Gdf9-Cre mice. The blastocyst (32.32% vs. 68.44%, p<0.05) embryo development rate per 2-cell embryos was also significantly lower. In vitro maturation revealed that of Mfffl/fl; Gdf9-Cre GV oocytes had significantly lower rates of GV break-down and polar body extrusion . The ratios of aberrant spindle and misaligned chromosomesin ovulated oocytes from Mfffl/fl; Gdf9-Cre mice were significantly increased. In terms of mitochondrial dynamics, the mitochondrial size and the ratio of abnormal mitochondrial distribution (unevenly aggregated) in Mfffl/fl; Gdf9-Cre oocytes significantly elevated. This study found that the Mff played a crucial role in oocyte maturation and early embryonic development. These results shed light on the important role played by MFF in ensuring proper mitochondrial dynamics in oocytes and underscore the significance of this protein in female fertility. This study provides insights into potential therapeutic targets for infertility and related diseases in humans.
2026-01-01 | GSE285731 | GEO
Project description:Melanosomes are lysosome-related organelles that produce and accumulate melanin. Their biogenesis begins with the trafficking of melanogenic proteins from the endo-lysosomal system into non-pigmented vacuoles derived from endosomes. Subsequently, melanosome maturation is regulated by their association with mitochondria and requires the export and recycling of unneeded cargo via tubular carriers and fission, the mechanisms of which are unknown. Here we show that the outer mitochondrial membrane protein mitochondrial fission factor (MFF) is actively released from mitochondria to melanosomes. We found MFF on melanosomes at different stages of maturation and early melanosome fission sites. Upon downregulation of MFF, but not DRP1, early melanosomes enlarged, intracellular melanin accumulated and melanosome lumen catabolism increased. The MFF interactome in melanocytes posited a role for a complex network of cytoskeletal factors in its activity. Inhibition of actin nucleation was sufficient to restore the effects of MFF silencing on melanosomes. Our data unveil an extramitochondrial role for MFF in the regulation of melanosome morphology and maturation that, independently of DRP1, is supported by actin polymerization and nucleation factors.
2026-03-20 | PXD052198 | Pride
Project description:The project aimmed to characterize the proteomic response of the human pathogenic fungus Histoplasma capsulatum to zinc poor environment. For that yeast cells were incubated in two conditions: zinc replete (with 20uM fo zinc sulfate) and zinc depleted (suppplemented with diethylenetriaminepentaacetic acid. Finaly teh proteins regulaed by zinc availability were identified.
2020-10-21 | PXD022039 | Pride
Project description:This project aims to investigate the proteomic responses of Aeromonas hydrophila to 100 μg/mL zinc sulfate (ZnSO4) treatment for 8 hours compared to an untreated control. Cultured bacterial samples were subjected to quantitative proteomic analysis using LC-MS/MS-based techniques, including protein extraction, tryptic digestion, and label-free quantification. Differentially expressed proteins were identified to characterize molecular mechanisms underlying zinc stress adaptation.
2025-05-16 | PXD063998 |
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