Ms1, a novel sRNA interacting with the RNA polymerase core in mycobacteria

Hnilicová, Jarmila; Matějčková, Jitka Jirát; Šiková, Michaela; Pospíšil, Jiří; Halada, Petr; Pánek, Josef; Krásný, Libor

doi:10.1093/nar/gku793

Cited by 36 publications

(75 citation statements)

References 72 publications

(93 reference statements)

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“…controversial (23,56,59), we previously demonstrated its presence and function (15,20,44), and we confirmed its presence by real-time PCR in the present study in mouse liver tissue (data not shown). We acknowledge that several signaling pathways are likely to be involved in this phenomenon.…”

Section: Discussionsupporting

confidence: 87%

Mitigation of autophagy ameliorates hepatocellular damage following ischemia-reperfusion injury in murine steatotic liver

Gupta

Kolachala

Jiang

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ischemia-reperfusion injury (IRI) is a common clinical consequence of hepatic surgery, cardiogenic shock, and liver transplantation. A steatotic liver is particularly vulnerable to IRI, responding with extensive hepatocellular injury. Autophagy, a lysosomal pathway balancing cell survival and cell death, is engaged in IRI, although its role in IRI of a steatotic liver is unclear. The role of autophagy was investigated in high-fat diet (HFD)-fed mice exposed to IRI in vivo and in steatotic hepatocytes exposed to hypoxic IRI (HIRI) in vitro. Two inhibitors of autophagy, 3-methyladenine and bafilomycin A1, protected the steatotic hepatocytes from HIRI. Exendin 4 (Ex4), a glucagon-like peptide 1 analog, also led to suppression of autophagy, as evidenced by decreased autophagy-associated proteins [microtubule-associated protein 1A/1B-light chain 3 (LC3) II, p62, high-mobility group protein B1, beclin-1, and autophagy-related protein 7], reduced hepatocellular damage, and improved mitochondrial structure and function in HFD-fed mice exposed to IRI. Decreased autophagy was further demonstrated by reversal of a punctate pattern of LC3 and decreased autophagic flux after IRI in HFD-fed mice. Under the same conditions, the effects of Ex4 were reversed by the competitive antagonist exendin 9-39. The present study suggests that, in IRI of hepatic steatosis, treatment of hepatocytes with Ex4 mitigates autophagy, ameliorates hepatocellular injury, and preserves mitochondrial integrity. These data suggest that therapies targeting autophagy, by Ex4 treatment in particular, may ameliorate the effects of IRI in highly prevalent steatotic liver.

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Section: Discussionsupporting

confidence: 87%

Mitigation of autophagy ameliorates hepatocellular damage following ischemia-reperfusion injury in murine steatotic liver

Gupta

Kolachala

Jiang

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Differential proteomics suggests roles for 6S-2 in metabolism, an observation probably also applying to other bacterial species (Hoch et al, 2015;Steuten et al, 2014). A related case may be Ms1, a mycobacterial sRNA that interacts with core RNApol (Hnilicova et al, 2015).…”

Section: Protein Sequestratorsmentioning

confidence: 98%

Small RNAs in Bacteria and Archaea

Wagner

Romby

2015

Advances in Genetics

459

245

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“…At least one RNA identified based on its structural similarity to 6S RNA (Ms1 RNA in Mycobacterium smegmatis ) does not bind to the holoenzyme form of RNA polymerase, although it does interact with core RNA polymerase (60, 61). This example serves as a cautionary tale in relying too heavily on secondary structure as the predictor of 6S RNA candidates, but also raises the intriguing possibility that there are additional classes of sRNAs that function through interaction with RNA polymerase using different mechanisms.…”

Section: S Rnas Are Widespread Throughout the Bacterial Kingdommentioning

confidence: 99%

6S RNA, a Global Regulator of Transcription

Wassarman

2018

Microbiol Spectr

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6S RNA is a small RNA regulator of RNA polymerase that is present broadly throughout the bacterial kingdom. Initial functional studies in Escherichia coli revealed that 6S RNA forms a complex with RNA polymerase resulting in regulation of transcription, and cells lacking 6S RNA have altered survival phenotypes. The last decade has focused on deepening the understanding of several aspects of 6S RNA activity including: 1. Addressing questions of how broadly conserved 6S RNAs are in diverse organisms through continued identification and initial characterization of divergent 6S RNAs; 2. The nature of the 6S RNA-RNA polymerase interaction through examination of variant proteins and mutant RNAs, crosslinking approaches, and ultimately a cryo-EM structure; 3. The physiological consequences of 6S RNA function through identification of the 6S RNA-regulon and promoter features that determine 6S RNA sensitivity; 4. The mechanism and cellular impact of 6S RNA-directed synthesis of pRNAs (i.e. pRNA synthesis). Much has been learned about this unusual RNA, its mechanism of action and how it is regulated; yet, much still remains to be investigated, especially regarding potential differences in behavior of 6S RNAs in diverse bacteria.

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Ms1, a novel sRNA interacting with the RNA polymerase core in mycobacteria

Cited by 36 publications

References 72 publications

Mitigation of autophagy ameliorates hepatocellular damage following ischemia-reperfusion injury in murine steatotic liver

Mitigation of autophagy ameliorates hepatocellular damage following ischemia-reperfusion injury in murine steatotic liver

Small RNAs in Bacteria and Archaea

6S RNA, a Global Regulator of Transcription

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