EC Number   |
General Information |
Reference |
|---|
   3.1.26.12 | evolution |
characterization of the RNase E-PNPase interaction in alpha-proteobacteria, gamma-proteobacteria and cyanobacteria suggests that it arose independently several times during evolution, thus conferring an advantage in control and coordination of RNA processing and degradation |
-, 751598 |
| 3.1.26.12 | malfunction |
absence of RNase E differentially affects the decay of specific mRNAs. Neither the native nor N-terminal extended form of RNase G can restore the growth defect associated with either the rne-1 or rneD1018 alleles even when expressed at very high protein levels. In contrast, two distinct spontaneously derived single amino acid substitutions within the predicted RNase H domain of RNase G, generating the rng-219 and rng-248 alleles, result in complementation of the growth defect associated with various RNase E mutants |
716898 |
| 3.1.26.12 | malfunction |
an NCgl2281 knockout mutant accumulates 5S rRNA precursor molecules. The processing of 16S and 23S rRNA, tRNA, and tmRNA is normal in the mutant cells. Primer extension analysis reveals that the RNase E/G orthologue cleaves at the -1 site of the 5' end of 5S rRNA. Mapping of the 5' and 3' ends of 5S rRNA precursors in NCgl2281 knockout mutant, overview |
-, 713995 |
| 3.1.26.12 | malfunction |
mutations in endoribonucleases RNase E reduce Salmonella virulence capacity. Mutants display an impaired motility, by forming a barely detectable motility ring after 8 h of incubation that remains much smaller than the one formed by the wild type after 24 h of incubation |
729037 |
| 3.1.26.12 | malfunction |
RNAI signals of the DELTA225 mutant lacking the PNPase binding region are similar to those of the wild-type strain. RNAI degradation intermediate accumulates in the DELTA374 mutant lacking the PNPase binding region and protein scaffold domain, which binds to RhlB and enolase, as compared with that in the wild-type strain |
710335 |
| 3.1.26.12 | malfunction |
RNase E deletion or inactivation of temperature-sensitive RNase E protein precludes normal initiation of the SOS response. RNase E-deficient cells remain able to produce RNA and protein during the period when SOS response is inhibited by lack of the enzyme |
730699 |
| 3.1.26.12 | metabolism |
direct entry by RNase E has a major role in bacterial RNA metabolism. Direct entry is mediated by specific unpaired regions that are adjacent to, but not contiguous with, segments cleaved by RNase E. A 5'-monophosphate is not required to activate the catalytic step |
730512 |
| 3.1.26.12 | metabolism |
RNase E-dependent degradation of sinI mRNA from the 5'-end is one of the steps mediating a high turnover of sinI mRNA, which allows the Sin quorum-sensing system to respond rapidly to changes in transcriptional control of N-acyl-homoserine lactone production. RNase E acts on the 5'-untranslated region of sinI independently of the posttranscriptional regulator Hfq |
-, 729937 |
| 3.1.26.12 | metabolism |
the endoribonuclease RNase E of Escherichia coli is an essential enzyme that plays a major role in all aspects of RNA metabolism |
716898 |
| 3.1.26.12 | metabolism |
the enzyme is required for glycolysis |
-, 729924 |
