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We've used systematic and integrative methods to explore multi-omics databases of myogenic differentiation in the search of epigenetic regulatory networks of myogenic differentiation, histone acetylation, and acetyltransferase occupancy in view of distinct chromatin states. In addition, our reports reveal a graphical map of chromatin state expression of residue-specific histone acetylation and concomitant association with histone acetylation and concomitant affiliation with histone acetylation and concomitant differentiation of myoblast differentiation at the start of myoblast differentiation. These datasets can be used to further define the function of muscle-specific regulatory elements governed by other muscle myogenic regulators or signaling molecules.
Source link: https://doi.org/10.1186/s40537-022-00667-3
Pyropia yezoensis, one of the most economically vital marine crops, is one of the red macroalgae. Released archeospores can provide secondary seedling resources in nori raising and be used to establish asexual seeding program. We previously reported that wounds could cause the somatic cells in sectioned Pyropia thalli to grow into a large number of asexual wound-induced spores in a short period. Transcription of RBOH genes was also affected by SAHA, and moreover, ROS signals in cut fragments were attenuated, suggesting that the ROS signaling pathway is closely linked to histone deacetylation. Our results reveal information into the cellular significance of dynatic histone acetylation states in WIS formation in P. yezoensis.
Source link: https://doi.org/10.3389/fpls.2022.1064300
In this research, eleven pkr suppressors were discovered to have mutations in FgSNT1, a component of the Set3C histone deacetylase complex, resulting in the truncation of its C-terminal region. The deletion of the C-terminal 98 aa in FgSNT1 reduced the pkr in growth and H4 acetylation by a factor. The interaction of FgSnt1 with Hdf1 has also increased in the Set3 complex's largest HDAC. No apparent evidence of the Cpk1 catalytic subunit and PKA genes was found in the pkr mutant, which was not inhibited by mutations in FgSNT1. At S443, a conserved PKA-phosphorylation site, Cpk1 directly interacted with the FgSnt1 region of N-terminal area and phosphorylated it. FgSnt1's inhibition binding and suppression of Hdf1 and H4 acetylation may therefore be decreased by phosphorylation at S443 and suppressor mutations, as well as increased FgSnt1's interaction with Hdf1 and H4 acetylation, highlighting a key role of FgSnt1 in crosstalk between cAMP signaling and Set3 complex.
Source link: https://doi.org/10.1371/journal.pgen.1010510
We have found that Tip60-mediated acetylation of SRPK1 is closely linked to chemotherapy sensitivity in this research. Cisplatin induced acetylation in breast cancer cells, but in the corresponding resistant cells, it reduced acetylation but boosted phosphorylation and kinase activity of SRPK1, favoring the splicing of some anti-apoptotic variants. Our analysis, therefore, reveals a key role of SRPK1 in the formation of cisplatin resistance in breast cancer cells and identifies a potential therapeutic route for overcoming chemotherapy resistance.
Source link: https://doi.org/10.1038/s42003-020-0983-4
Abstract: About 70% of human breast tumors are estrogen receptor positive, estrogen and ERu03b1 are key factors in breast cancer formation, with estrogen and ERu03b1 being omitted. Endocrine therapy has been shown to be a highly therapeutic approach by disrupting the ERu03b1 signaling pathway. We found a way by which Transcription Start Site -associated histone H3K27 acetylation signals the Super Elongation Complex to regulate transcriptional elongation of the ESR1 gene. Depletion of AFF4 by siRNA or CRISPR/Cas9 dramatically reduces the expression of ESR1 and its target genes, thus inhibiting breast cancer cell proliferation.
Source link: https://doi.org/10.1038/s42003-020-0898-0
We show that early in several types of Drosophila ND models such as Parkinson's Disease, Huntingtonu2019s Disease, and Amyotrophic Lateral Sclerosis, we found that, similar to AD, early disruption of Tip60 HAT/HDAC2 balance, as well as concomitant epigenetic repression of common Tip60 target neuroplasticity genes occurs early in some forms of Drosophila ND models such as Parkinson's Disease and Amyo Repressed neuroplasticity genes enrichment of Tip60 and epigenetic acetylation signatures at all gene loci tested, with some genes displaying inappropriate HDAC2 repressor enrichment. Multiple NDs are experiencing increasing Tip60 HAT levels, specifically in the mushroom body learning and memory center.
Source link: https://doi.org/10.1038/s41598-020-75035-3
Here we describe a novel configuration of Scc2 with pre-engaged cohesin and reveal dynamic conformations of the cohesin/Scc2 complex in the loading reaction. We show that Smc3 acetylation blocks the association of Scc2 with a pre-engaged cohesin by mocking Scc2's communication with Smc3's head by mocking Scc2's interaction with Smc3's head. Lastly, we show that ATP binding forces the cohesin/Scc2 complex to clamp DNA by encouraging the interaction of Scc2 and Smc3 coiled coils.
Source link: https://doi.org/10.1101/2022.12.04.519023
This research sought to determine the role of FBXL10 in epithelial-mesenchymal transition and breast cancer metastasis, as well as metastasis of breast cancer, and sought to determine the molecular mechanisms involved in this process. Functional experiments in vitro demonstrated that FBXL10 inhibited breast cancer cell proliferation and invasion of breast cancer cells by blocking E-cadherin expression and inducing EMT. SNAI1's CDH1-repressor activity on breast cancer cells was also promoted by the company's transcriptional repression activity. Further, FBXL10 played a key role in the deacetylation of SNAI1 by facilitating the interaction between SNAI1 and HDAC1, a key acetylase of SNAI1. In addition, mouse models were also used to determine the effect of FBXL10 on breast cancer lung metastasis in vivo. FBXL10 acted as a pro-metastatic cause of breast cancer by suppressing the expression of E-cadherin and inducing EMT.
Source link: https://doi.org/10.1038/s41420-021-00722-7
Abstract Cellular metabolism is one of the key factors to control epigenetic environment in various cells, including immune cells, embryonic stem cells, and hair follicle stem cells. Dermal papilla cells collaborate with epithelial stem cells to orchestrate hair formation, orchestrating hair formation. In the absence of low glucose and glycolysis inhibitors, we observed a decrease of signature genes associated with hair induction by DP. Interestingly, high glucose can cause the expression of hair inductive genes and elongation of hair shaft. In vitro, hair follicles can be generated by active DP to produce hair follicles. This finding may be useful in the establishment and maintenance of active DP.
Source link: https://doi.org/10.1038/s41598-020-61824-3
Abstract Background Mitochondrial dysfunction is a common pathogenic condition in acute kidney injury. Methods The protein level of GCN5L1 was determined by western blot assay, according to its research. The renal injury of AKI mice was shown by the amounts of creatinine and urea nitrogen, as well as the pathological changes of renal tissue. We found that GCN5L1 was highly expressed in vivo and in vitro, as well as renal tubules specific knockdown of GCN5L1 that may be able to safely attenuate mitochondrial dysfunction in AKI-induced mitochondrial dysfunction. Moreover, acetylated proteomics showed that acetylated TFAM was highly elevated in AKI mice's kidney, alerting us that TFAM might be an acetylating substrate of GCN5L1. We established that GCN5L1 could acetylate TFAM at its K76 site and later reduced its binding to TOM70, lowering TFAM imports into mitochondrial and mitochondrial biogenesis, which is shown by mechanistically. GCN5L1 and acetylated TFAM were positively related to disease severity, according to clinical studies.
Source link: https://doi.org/10.1186/s12967-022-03782-0
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