MicX Vibrio cholerae sRNA | |
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Secondary structure of MicX sRNA. | |
Identifiers | |
Symbol | MicX |
Rfam | RF01808 |
Other data | |
RNA type | sRNA |
Domain(s) | Vibrio cholerae |
PDB structures | PDBe |
MicX sRNA (formerly known as A10) [1] is a small non-coding RNA found in Vibrio cholerae . [2] It was given the name MicX as it has a similar function to MicA, MicC and MicF in E. coli . [3] MicX sRNA negatively regulates an outer membrane protein (coded for by VC0972) and also a component of an ABC transporter (gene VC0620). [4] These interactions were predicted and then confirmed using a DNA microarray. [2]
MicX was identified through a bioinformatics screen of V. cholerae having been previously predicted. [1] Levels of transcription of this sRNA were compared under several conditions: it was found to be expressed on all tested mediums; richer mediums slightly reduced transcription; repression of certain sigma factors (δS and δE) did not change transcription but it was dramatically reduced in the absence of Hfq protein. [2] This observation is in accordance with other sRNA expression patterns. [5] [6]
The MicX RNA gene overlaps with VCA0943 - a gene coding for a maltose transporter permease - but the ribonuclease RNAase E processes the MicX transcript to create an active and stable form containing only the VCA0943 3′ UTR. [2]
The gene rpoS encodes the sigma factor sigma-38, a 37.8 kD protein in Escherichia coli. Sigma factors are proteins that regulate transcription in bacteria. Sigma factors can be activated in response to different environmental conditions. rpoS is transcribed in late exponential phase, and RpoS is the primary regulator of stationary phase genes. RpoS is a central regulator of the general stress response and operates in both a retroactive and a proactive manner: it not only allows the cell to survive environmental challenges, but it also prepares the cell for subsequent stresses (cross-protection). The transcriptional regulator CsgD is central to biofilm formation, controlling the expression of the curli structural and export proteins, and the diguanylate cyclase, adrA, which indirectly activates cellulose production. The rpoS gene most likely originated in the gammaproteobacteria.
The gene rpoF encodes the sigma factor sigma-28, a protein in Escherichia coli and other species of bacteria. Depending on the bacterial species, this gene may be referred to as sigD or fliA. The protein encoded by this gene has been found to be necessary for flagellum formation.
DicF RNA is a non-coding RNA that is an antisense inhibitor of cell division gene ftsZ. DicF is bound by the Hfq protein which enhances its interaction with its targets. Pathogenic E. coli strains possess multiple copies of sRNA DicF in their genomes, while non-pathogenic strains do not. DicF and Hfq are both necessary to reduce FtsZ protein levels, leading to cell filamentation under anaerobic conditions.
DsrA RNA is a non-coding RNA that regulates both transcription, by overcoming transcriptional silencing by the nucleoid-associated H-NS protein, and translation, by promoting efficient translation of the stress sigma factor, RpoS. These two activities of DsrA can be separated by mutation: the first of three stem-loops of the 85 nucleotide RNA is necessary for RpoS translation but not for anti-H-NS action, while the second stem-loop is essential for antisilencing and less critical for RpoS translation. The third stem-loop, which behaves as a transcription terminator, can be substituted by the trp transcription terminator without loss of either DsrA function. The sequence of the first stem-loop of DsrA is complementary with the upstream leader portion of RpoS messenger RNA, suggesting that pairing of DsrA with the RpoS message might be important for translational regulation. The structures of DsrA and DsrA/rpoS complex were studied by NMR. The study concluded that the sRNA contains a dynamic conformational equilibrium for its second stem–loop which might be an important mechanism for DsrA to regulate the translations of its multiple target mRNAs.
The gcvB RNA gene encodes a small non-coding RNA involved in the regulation of a number of amino acid transport systems as well as amino acid biosynthetic genes. The GcvB gene is found in enteric bacteria such as Escherichia coli. GcvB regulates genes by acting as an antisense binding partner of the mRNAs for each regulated gene. This binding is dependent on binding to a protein called Hfq. Transcription of the GcvB RNA is activated by the adjacent GcvA gene and repressed by the GcvR gene. A deletion of GcvB RNA from Y. pestis changed colony shape as well as reducing growth. It has been shown by gene deletion that GcvB is a regulator of acid resistance in E. coli. GcvB enhances the ability of the bacterium to survive low pH by upregulating the levels of the alternate sigma factor RpoS. A polymeric form of GcvB has recently been identified. Interaction of GcvB with small RNA SroC triggers the degradation of GcvB by RNase E, lifting the GcvB-mediated mRNA repression of its target genes.
The OmrA-B RNA gene family is a pair of homologous OmpR-regulated small non-coding RNA that was discovered in E. coli during two large-scale screens. OmrA-B is highly abundant in stationary phase, but low levels could be detected in exponentially growing cells as well. RygB is adjacent to RygA a closely related RNA. These RNAs bind to the Hfq protein and regulate gene expression by antisense binding. They negatively regulate the expression of several genes encoding outer membrane proteins, including cirA, CsgD, fecA, fepA and ompT by binding in the vicinity of the Shine-Dalgarno sequence, suggesting the control of these targets is dependent on Hfq protein and RNase E. Taken together, these data suggest that OmrA-B participates in the regulation of outer membrane composition, responding to environmental conditions.
Qrr is a non-coding RNA that is thought to be involved in the regulation of quorum sensing in Vibrio species. It is believed that these RNAs, guided by a protein, Hfq, can mediate the destabilisation of the quorum-sensing master regulators LuxR/HapR/VanT mRNAs.
The RprA RNA gene encodes a 106 nucleotide regulatory non-coding RNA. Translational regulation of the stationary phase sigma factor RpoS is mediated by the formation of a double-stranded RNA stem-loop structure in the upstream region of the rpoS messenger RNA, occluding the translation initiation site. Clones carrying rprA increased the translation of RpoS. As with DsrA, RprA is predicted to form three stem-loops. Thus, at least two small RNAs, DsrA and RprA, participate in the positive regulation of RpoS translation. RprA also appears to bind to the RpoS leader. RprA is non-essential. Wasserman et al. demonstrated that this RNA is bound by the Hfq protein. Binding to Hfq alters the conformation of RprA. In the presence of Hfq the stability of RprA is influenced by the osmolarity of the cell, this is dependent on the endoribonuclease RNase E.
RyhB RNA is a 90 nucleotide RNA that down-regulates a set of iron-storage and iron-using proteins when iron is limiting; it is itself negatively regulated by the ferric uptake repressor protein, Fur.
SgrS is a 227 nucleotide small RNA that is activated by SgrR in Escherichia coli during glucose-phosphate stress. The nature of glucose-phosphate stress is not fully understood, but is correlated with intracellular accumulation of glucose-6-phosphate. SgrS helps cells recover from glucose-phosphate stress by base pairing with ptsG mRNA and causing its degradation in an RNase E dependent manner. Base pairing between SgrS and ptsG mRNA also requires Hfq, an RNA chaperone frequently required by small RNAs that affect their targets through base pairing. The inability of cells expressing sgrS to create new glucose transporters leads to less glucose uptake and reduced levels of glucose-6-phosphate. SgrS is an unusual small RNA in that it also encodes a 43 amino acid functional polypeptide, SgrT, which helps cells recover from glucose-phosphate stress by preventing glucose uptake. The activity of SgrT does not affect the levels of ptsG mRNA of PtsG protein. It has been proposed that SgrT exerts its effects through regulation of the glucose transporter, PtsG.
The MicA RNA is a small non-coding RNA that was discovered in E. coli during a large scale screen. Expression of SraD is highly abundant in stationary phase, but low levels could be detected in exponentially growing cells as well.
In molecular biology the ArcZ RNA is a small non-coding RNA (ncRNA). It is the functional product of a gene which is not translated into protein. ArcZ is an Hfq binding RNA that functions as an antisense regulator of a number of protein coding genes.
The sroB RNA is a non-coding RNA gene of 90 nucleotides in length. sroB is found in several Enterobacterial species but its function is unknown. SroB is found in the intergenic region on the opposite strand to the ybaK and ybaP genes. SroB is expressed in stationary phase. Experiments have shown that SroB is a Hfq binding sRNA.
The Hfq protein encoded by the hfq gene was discovered in 1968 as an Escherichia coli host factor that was essential for replication of the bacteriophage Qβ. It is now clear that Hfq is an abundant bacterial RNA binding protein which has many important physiological roles that are usually mediated by interacting with Hfq binding sRNA.
An Hfq binding sRNA is an sRNA that binds the bacterial RNA binding protein called Hfq. A number of bacterial small RNAs which have been shown to bind to Hfq have been characterised . Many of these RNAs share a similar structure composed of three stem-loops. Several studies have expanded this list, and experimentally validated a total of 64 Hfq binding sRNA in Salmonella Typhimurium. A transcriptome wide study on Hfq binding sites in Salmonella mapped 126 Hfq binding sites within sRNAs. Genomic SELEX has been used to show that Hfq binding RNAs are enriched in the sequence motif 5′-AAYAAYAA-3′. Genome-wide study identified 40 candidate Hfq-dependent sRNAs in plant pathogen Erwinia amylovora. 12 of them were confirmed by Northern blot.
VrrA is a non-coding RNA that is conserved across all Vibrio species of bacteria and acts as a repressor for the synthesis of the outer membrane protein OmpA. This non-coding RNA was initially identified from Tn5 transposon mutant libraries of Vibrio cholerae and its location within the bacterial genome was mapped to the intergenic region between genes VC1741 and VC1743 by RACE analysis.
Bacterial small RNAs (sRNA) are small RNAs produced by bacteria; they are 50- to 500-nucleotide non-coding RNA molecules, highly structured and containing several stem-loops. Numerous sRNAs have been identified using both computational analysis and laboratory-based techniques such as Northern blotting, microarrays and RNA-Seq in a number of bacterial species including Escherichia coli, the model pathogen Salmonella, the nitrogen-fixing alphaproteobacterium Sinorhizobium meliloti, marine cyanobacteria, Francisella tularensis, Streptococcus pyogenes, the pathogen Staphylococcus aureus, and the plant pathogen Xanthomonas oryzae pathovar oryzae. Bacterial sRNAs affect how genes are expressed within bacterial cells via interaction with mRNA or protein, and thus can affect a variety of bacterial functions like metabolism, virulence, environmental stress response, and structure.
FnrS RNA is a family of Hfq-binding small RNA whose expression is upregulated in response to anaerobic conditions. It is named FnrS because its expression is strongly dependent on fumarate and nitrate reductase regulator (FNR), a direct oxygen availability sensor.
Mycobacterium tuberculosis contains at least nine small RNA families in its genome. The small RNA (sRNA) families were identified through RNomics – the direct analysis of RNA molecules isolated from cultures of Mycobacterium tuberculosis. The sRNAs were characterised through RACE mapping and Northern blot experiments. Secondary structures of the sRNAs were predicted using Mfold.
In molecular biology, Vibrio cholerae ToxT activated RNAs are small RNAs which are produced by the bacterium Vibrio cholerae. They are regulated by the transcriptional activator ToxT and may play a role in V. cholerae virulence. Two ToxT activated RNAs have been described: TarA and TarB.