Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An isogenic pair of Escherichia coli strains, one carrying an rnc+ and the other an rnc- allele (a mutation which reduces the level of ribonuclease III), was compared. The rnc- strain fails to grow at very elevated temperatures (for E. coli) while the rnc+ strain does grow exponentially. Assaying the residual RNase III like activity in extracts of the rnc- strain at different pHs and at different temperatures suggested that this residual RNase III like activity is not due to RNase III. This raised the possibility that the rnc- strain is devoid of any RNase III activity in the cell. Comparing the decay of newly synthesized RNA and functional decay of beta-galactosidase mRNA in such strains revealed that in both strains these parameters proceed in similar rates, which suggests that RNase III is not involved in the metabolism of mRNA. During carbon starvation preexisting total RNA, as well as 23S and 16S rRNA, decay faster in the rnc- strain, thus eliminating the possibility that RNase III is the endoribonuclease which initiates the decay of rRNA during starvation (Kaplan and Apirion, 1975a).
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PMID:Consequences of losing ribonuclease III on the Escherichia coli cell. 77 91

Stability of RNA was tested in strains of Escherichia coli carrying single, double, or triple mutations in the RNA processing enzymes RNase III, RNase E and RNase P. Tests were carried out for total pulse labeled RNA, beta-galactosidase mRNA and for the decay of preexisting RNA during carbon starvation. Decay of RNA was measured at permissive and nonpermissive temperatures, and in no case were significant differences between mutants and non-mutant strains found. Therefore, we conclude that the three processing enzymes; RNase III, E and P do not contribute significantly to turnover of RNA IN Escherichia coli.
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PMID:Decay of RNA in RNA processing mutants of Escherichia coli. 615 28

Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.
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PMID:Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae. 1598 63

bolA is a sigma(S)-dependent Escherichia coli morphogene involved in the general cellular adaptation to stress and cell division. In this report it is shown that endoribonuclease RNase III acts as a post-transcriptional modulator of bolA expression under carbon starvation conditions. Unexpectedly RNase III positively regulates bolA1p mRNA levels and stabilities. This effect is also observed when sulA, bfr, uspA and uspB transcripts were analyzed. RNase III is furthermore shown to be necessary for the normal expression of sigma(S), ensuring normal levels of rpoS mRNA and sigma(S) protein under glucose starvation. Since sigma(S) controls a complex regulon of stress-response genes, RNase III is proposed as possible modulator of bacterial cell response to stress.
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PMID:Adaptation to carbon starvation: RNase III ensures normal expression levels of bolA1p mRNA and sigma(S). 1630 17

Nonsense-mediated mRNA decay (NMD) eliminates transcripts carrying premature translation termination codons, but the role of NMD on yeast unspliced pre-mRNA degradation is controversial. Using tiling arrays, we show that many unspliced yeast pre-mRNAs accumulate in strains mutated for the NMD component Upf1p and the exonuclease Xrn1p. Intron identity and suboptimal splicing signals resulting in weak splicing were found to be important determinants in NMD targeting. In the absence of functional NMD, unspliced precursors accumulate in the cytoplasm, possibly in P-bodies. NMD can also complement RNase III-mediated nuclear degradation of unspliced RPS22B pre-mRNAs, degrades most unspliced precursors generated by a 5' splice site mutation in RPS10B, and limits RPS29B unspliced precursors accumulation during amino acid starvation. These results show that NMD has a wider impact than previously thought on the degradation of yeast-unspliced transcripts and plays an important role in discarding precursors of regulated or suboptimally spliced transcripts.
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PMID:Widespread impact of nonsense-mediated mRNA decay on the yeast intronome. 1869 68

The human opportunistic pathogen Staphylococcus aureus produces numerous small regulatory RNAs (sRNAs) for which functions are still poorly understood. Here, we focused on an atypical and large sRNA called RsaC. Its length varies between different isolates due to the presence of repeated sequences at the 5' end while its 3' part is structurally independent and highly conserved. Using MS2-affinity purification coupled with RNA sequencing (MAPS) and quantitative differential proteomics, sodA mRNA was identified as a primary target of RsaC sRNA. SodA is a Mn-dependent superoxide dismutase involved in oxidative stress response. Remarkably, rsaC gene is co-transcribed with the major manganese ABC transporter MntABC and, consequently, RsaC is mainly produced in response to Mn starvation. This 3'UTR-derived sRNA is released from mntABC-RsaC precursor after cleavage by RNase III. The mature and stable form of RsaC inhibits the synthesis of the Mn-containing enzyme SodA synthesis and favors the oxidative stress response mediated by SodM, an alternative SOD enzyme using either Mn or Fe as co-factor. In addition, other putative targets of RsaC are involved in oxidative stress (ROS and NOS) and metal homeostasis (Fe and Zn). Consequently, RsaC may balance two interconnected defensive responses, i.e. oxidative stress and metal-dependent nutritional immunity.
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PMID:RsaC sRNA modulates the oxidative stress response of Staphylococcus aureus during manganese starvation. 3150 67