💰 RNA Helicase A - Wikipedia

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DHX9 is an important RNA sensor that is dependent on interferon-beta promoter stimulator (IPS)-1 to sense pathogenic RNA. DHX9 also.


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DHX9 promotes binding of splicing factors to nascent RNA. DHX9 unwinds short RNA–DNA hybrids in vitro, suggesting that it might prevent R-.


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Multifunctional ATP-dependent nucleic acid helicase that unwinds DNA and RNA in a 3' to 5' direction and that plays important roles in many processes, such as.


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DHX9 is an important RNA sensor that is dependent on interferon-beta promoter stimulator (IPS)-1 to sense pathogenic RNA. DHX9 also.


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DHX9 (also known as Nuclear DNA Helicase II (NDH II) and RNA Helicase A (​RHA)) is an NTP-dependent helicase protein capable of unwinding.


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DHX9 is an important RNA sensor that is dependent on interferon-beta promoter stimulator (IPS)-1 to sense pathogenic RNA. DHX9 also.


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In the absence of DHX9, circular RNAs accumulate and transcription and translation are dysregulated—effects that are exacerbated by.


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ATP-dependent RNA helicase A is an enzyme that in humans is encoded by the DHX9 gene. Contents. 1 Function; 2 Interactions; 3 References; 4 Further.


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DHX9, another DEAH-box helicase and a DHX36 paralog, was also reported to bind and resolve rG4s in vitro. In contrast to DHX36, DHX9 can.


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DHX9 (DExH-Box Helicase 9) is a Protein Coding gene. Diseases associated with DHX9 include Werner Syndrome and Pseudopterygium. Among its related.


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In addition to the R-loops that arise as a consequence of perturbed RNA processing, non-pathological R-loops are found throughout the genomes of normal cells 6 , 8. Firstly, treatment of wild-type cells with the transcription inhibitor actinomycin D did not generate the increased RPA foci that were evident in SFPQ-defective cells Supplementary Fig. Data are plotted from three independent experiments. Although defects in pre-mRNA processing leads to the generation of extensive tracts of RNA—DNA hybrids, recent evidence suggests that R-loops, by themselves, do not necessarily cause genomic instability Furthermore, while some R-loops elicit a pathological response in cells, others do not, suggesting that only a subset of R-loops are harmful to cells. You are using a browser version with limited support for CSS. Depletion of SFPQ impairs cell growth. Although excessive R-loops are a feature of cells that are defective in RNA processing, what causes them to form is unclear. Indeed, a variety of proteins have been identified that prevent R-loops from forming. Quantification of FACS data was averaged from three independent experiments. R-loops are stable nucleic acid structures that have important physiological functions, but which also pose a significant threat to genomic stability. Furthermore, we demonstrated that R-loops generated in centromeric DNA, which regulate segregation of chromosomes during mitosis, are also dependent on DHX9 for their formation. These data confirm the importance of the splicing machinery generally and SFPQ, specifically, in preventing the formation of R-loops and promoting genomic stability in cells. Means and s. These data led us to hypothesize that the assembly of splicing factors on nascent RNA strand might be a critical event that prevents R-loops from forming. Lastly, replication stress in SFPQ-depleted cells closely resembled that caused by hydroxyurea, a potent inhibitor of DNA synthesis, which causes replication forks to stall and collapse Supplementary Fig. Firstly, the displaced single-stranded DNA in R-loops is vulnerable to attack from the APOBEC family of cytosine deaminases which, upon further processing by enzymes of the base excision repair pathway, may lead to the generation of single-stranded DNA breaks 9. Input sample and IgG control are also shown. Although perturbations in RNA processing often lead to R-loops that are deleterious for DNA replication and cell growth, R-loops that play a role in normal cell processes are, presumably, not harmful. Although DHX9 has been implicated in many fundamental cellular processes including DNA replication, transcription, and genome stability, its specific biological function remains unclear Moreover, DNA synthesis Fig. In vitro, DHX9 unwinds a variety of nucleic acid structures in reactions that are dependent on ATP hydrolysis 38 , DHX9 helicase activity is required for R-loop formation and growth inhibition. Data are represented as fold enrichment compared to control immunoprecipitations. In another study, mutations in yeast histones were shown to promote the formation of R-loops without inducing DNA damage, indicating that R-loops, per se, do not cause genome instability We found that depletion of XRN2 in human cells also induces R-loops but does not cause replication stress. This supports a model in which it is the retention of RNA Polymerase on chromatin and the concomitant increased transcription—replication collisions that are responsible for pathological replication stress, rather than the generation of R-loops per se.{/INSERTKEYS}{/PARAGRAPH} Together these data strongly argue that, at least some, pathological and non-pathological R-loops are formed through a common mechanism involving DHX9. However, we found, in contrast with a previous study 40 , that depletion of XRN2 induced the generation of R-loops Supplementary Fig. This is supported by several pieces of evidence. Therefore, we next investigated whether the replication stress and impaired cell growth in SFPQ-depleted cells was also linked to the generation of R-loops. Increased R-loops cause replication stress and chromosome fragility and have been associated with diseases such as neurodegeneration and cancer. In normal cells, DHX9 helicase activity promotes the assembly of splicing factors onto nascent RNA and, in the absence of splicing factors, it promotes the formation of R-loops. Homozygous deletion of Sfpq in mice is embryonically lethal Several pieces of evidence indicated that this defect in cell proliferation was caused by impaired DNA synthesis. Data are an average of three independent experiments. The reason for this is not clear. Therefore, we investigated whether the availability of splicing factors affected DHX9 function during transcription and how this might be related to the generation of R-loops. This last point is supported by our experimental evidence showing that DHX9 is required for the binding of splicing factors to nascent RNA as part of the elongating transcription complex. Thirdly, we observed activation of the replication checkpoint as indicated by phosphorylation of Chk1, a substrate of the ATR checkpoint kinase Fig. Cells were transfected with siRNAs targeted to the indicated genes, individually and in combination. This may lead to RNA Pol II becoming trapped on chromatin where it can pose a barrier to DNA replication and increases the likelihood of transcription—replication conflicts. Box and whisker plots display median, upper and lower quartile range with whiskers depicting lowest and highest values. To determine how R-loops form at a specific gene, we used S9. Importantly, replication stress Fig. DHX9 promotes the formation of pathological and non-pathological R-loops. Defects in RNA splicing cause increased R-loops. This led us to two important conclusions. The reasons for this difference are not clear but it is possible that R-loops induced upon treatment with CPT are generated through a different mechanism to those formed as a consequence of impaired RNA processing. We confirmed that these interactions were mediated through RNA by showing that they were diminished in samples treated with RNaseA. It was reported recently that R-loops found at chromosome centromeres cause the local activation of ATR, which regulates phosphorylation of the mitotic regulator protein Aurora B during chromosome segregation 2. This confirms the potential of some R-loops to cause profound replication stress and, more importantly, establishes DHX9 as an important driver of R-loop formation and genomic instability in cells. These too were diminished after knockdown of DHX9 Fig. An increasing number of proteins that function in RNA metabolism have also been shown to contribute to the maintenance of genomic stability Among these are members of the Drosophila Behavior and Human Splicing DBHS family of proteins, which are found in subnuclear bodies called paraspeckles Although DBHS proteins are required for the retention and processing of hyper-edited RNAs, some also play a role in the repair of dsb by homologous recombination and non-homologous end-joining 31 , We focused on one of these, SFPQ splicing factor proline and glutamine rich , and found that it promotes genomic stability by preventing the formation of R-loops. R-loops are found in a broad range of organisms where they function in a variety of cellular processes, including replication of mitochondrial genomes and bacterial plasmids, regulation of chromosome segregation 2 , and immunoglobulin class-switch recombination 3. Using S9. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. Secondly, that by promoting the formation of R-loops, DHX9 contributes to the pathological replication stress caused by perturbations in RNA splicing. A Nature Research Journal. Western blot below shows the level SFPQ protein over time. Our data provide a molecular mechanism for the formation of R-loops that is relevant to neurodegenerative diseases and cancers in which deregulated RNA processing is a feature. We hypothesize that these proteins stabilize the unwound nascent RNA strand, preventing it from forming further secondary structures. Control sample treated with RNaseA is indicated. Our work has now identified DHX9 as a key protein that is required for the formation of, at least, some R-loops and revealed how components of the splicing machinery prevent R-loops from forming by modulating the activity of DHX9 during transcription. This model, described in Fig. Although R-loops are required for normal physiological processes, very little is known about how and why they are generated. Defects in SFPQ cause replication stress. Conversely, in the absence of splicing factors, DHX9 remains associated with the transcription complex where it binds to RNA secondary structures that form in the nascent strand and unwinds them during transcription elongation. To do this, we used S9. We further hypothesized that in normal cells this activity might facilitate the binding of RNA processing proteins, such as splicing factors to nascent RNA. Although R-loops have been shown to play specific roles in normal physiological processes and to accumulate in cells that are defective in RNA metabolism, it is still unclear what causes R-loops to form and whether this requires the activities of specific proteins. Fluorescence intensity of S9. Thirdly, the role of splicing factors and other RNA-binding proteins in preventing R-loop formation is most easily explained if they bind to and stabilize the nascent RNA strand, minimizing its potential to invade DNA duplex. Secondly, regions of transition from single-strand DNA to double-stranded DNA at the extremities of R-loops can be cleaved by proteins of the nucleotide excision repair pathway, generating double-stranded DNA breaks dsb This can lead to stalling and collapse of replication forks and the production of one-ended dsb that are substrates for chromosome translocations 6 , 15 , Given the potential of R-loops to cause genomic instability, the accumulation of these structures in cells must be tightly regulated. In cells, binding of splicing factors to pre-mRNA and the removal of introns occurs concurrently with transcription and is coordinated through interactions between the splicing machinery and the carboxy-terminal domain CTD of RNA Pol II These interactions are regulated through the phosphorylation of the CTD on different serine residues at different stages of transcription Data are depicted as fold enrichment over the control IP. The demonstration by others that proteins involved in RNA splicing and biogenesis of RNP can suppress R-loop formation established an important link between the generation of R-loops and co-transcriptional processing of pre-mRNA 3. Hence, the formation of RNA—DNA hybrids probably begins early in transcription and continues throughout elongation until transcription is terminated. Several other proteins facilitate the removal of R-loops. DHX9 promotes the generation of R-loops. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. In the absence of DHX9, the generation of R-loops in these cells is almost entirely suppressed, restoring DNA synthesis and cell growth. {PARAGRAPH}{INSERTKEYS}Thank you for visiting nature. However, R-loops can pose a significant threat to genomic stability in a variety of ways 7 , 8. Therefore, although pathological and non-pathological R-loops can be formed through a common mechanism involving DHX9, their impact on DNA replication and on genomic instability is probably context-dependent and might also be influenced by other factors. More than cells were counted from each of three independent experiments. Western blot of soluble cytoplasmic and insoluble pellet fractions of nuclear extracts prepared from HeLa cells that were knocked down with siRNAs against the indicated genes. This raised the question, why do some R-loops cause replication stress and genomic instability and others do not? We next addressed the mechanism through which DHX9 promotes R-loop formation. However, it is unclear how these different factors regulate the balance between formation and removal of R-loops to prevent the pathological potential of these stable nucleic acid structures in cells. Our data shed new light on the mechanism through which R-loops are formed and the important role played by splicing factors to prevent R-loop induced replication stress and genomic instability. Exons are depicted as red boxes. In both yeast and human cells, defects in these proteins leads to the accumulation of R-loops and increased DNA damage.