Chapter 2 Biosynthesis and Function of Queuine and Queuosine tRNAs

Kersten, H.; Kersten, W.

doi:10.1016/s0301-4770(08)61488-8

Cited by 38 publications

(28 citation statements)

References 59 publications

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“…High amounts of free q-base are found in embryonic cells and tissues and in some solid tumors (3). To answer the question as to whether intracellular accumulation of the q-base is associated with the transformed phenotype of mammalian tumor cells, we analysed the intracellular concentration of q in five other transformed cell lines that were supplemented with 300 nM q-base.…”

Section: Resultsmentioning

confidence: 99%

“…Although the presence of Q-tRNAs is not vital for mammals and other eukaryotes (3,7), the q-base and/or Q-tRNAs participate in the fine-tuning of many cellular functions such as differentiation (8,9), the control of the aerobic/anaerobic energy metabolism (3,10), the management of hypoxic stress (11,12), the regulation of protein synthesis (13) especially during re-entry of cells into the cell cycle (11), the adaptive regulation of cell proliferation to the metabolic predisposition (14), and the modulation of signal transduction pathways (15,16). Moreover, the q-base is essential for the adaptive regulation of cell proliferation to aerobiosis or hypoxia in HeLa cells (14).…”

Section: Introductionmentioning

confidence: 99%

“…Tumor cells frequently contain considerable amounts of tRNAGUN (Q-deficient tRNA), whereas a complete conversion to tRNAsQUN is found in normal terminally differentiated somatic cells (2,3). Characteristic fluctuations in the extent to which tRNAsGUN are converted to tRNASQUN also occur during differentiation (8).…”

Section: Introductionmentioning

confidence: 99%

“…Apparently, availability of the substrate q is not the limiting factor, because q was found in tumor cells in sufficient amounts, while a significant portion of the tRNAs remained Q-deficient (3). Increased amounts ofpteridines in tumor cells-competitive inhibitors of the eukaryotic TGTmay be connected to hypomodification of Q-tRNAs (3). It was described that the TGT enzyme needs oxygen for maximal activity (10), suggesting that hypoxia may be a reason for the lack ofTGT activity in tumor cells.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, we described that the q-base is not inserted into tRNA in hypoxically grown HeLa cells under conditions where serum factors become depleted from the culture medium (12 (3) in an atmosphere of 95% air and 5% CO2 (aerobic conditions corresponding to 21% oxygen content). To create hypoxic conditions, cells were grown in an incubator in which the oxygen content was reduced to 7% by replacement ofthe atmosphere with nitrogen.…”

Section: Introductionmentioning

confidence: 99%

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Involvement of protein kinase C in the control of tRNA modification with queuine in HeLa cells

Langgut

Reisser

1995

Nucl Acids Res

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Involvement of protein kinase C in the control of tRNA modification with queuine in HeLa cells

Langgut

Reisser

1995

Nucl Acids Res

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Possible involvement of queuine in regulation of cell proliferation

2007

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An increase in cell number is one of the most prominent characteristics of cancer cells. This may be caused by an increase in cell proliferation or decrease in cell death. Queuine is one of the modified base which is found at first anticodon position of specific tRNAs. It is ubiquitously present throughout the living system except mycoplasma and yeast. The tRNAs of Q-family are completely modified to Q-tRNAs in terminally differentiated somatic cells, however hypomodification of Q-tRNA is closely associated with cell proliferation and malignancy. Queuine participates at various cellular functions such as regulation of cell proliferation, cell signaling and alteration in the expression of growth associated proto-oncogenes. Like other proto-oncogenes bcl2 is known to involve in cell survival by inhibiting apoptosis. Queuine or Q-tRNA is suggested to inhibit cell proliferation but the mechanism of regulation of cell proliferation by queuine or Q-tRNA is not well understood. Therefore, in the present study regulation in cell proliferation by queuine in vivo and in vitro as well as the expression of cell death regulatory protein Bcl2 are investigated. For this DLAT cancerous mouse, U87 cell line and HepG2 cell line are treated with different concentrations of queuine and the effect of queuine on cell proliferation and apoptosis are studied. The results indicate that queuine down regulates cell proliferation and expression of Bcl2 protein, suggesting that queuine promotes cell death and participates in the regulation of cell proliferation.

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The Q-base of asparaginyl-tRNA is dispensable for efficient −1 ribosomal frameshifting in eukaryotes

Marczinke

Hagervall

Brierley

2000

Journal of Molecular Biology

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The frameshift signal of the avian coronavirus infectious bronchitis virus (IBV) contains two cis-acting signals essential for efficient frameshifting, a heptameric slippery sequence (UUUAAAC) and an RNA pseudoknot structure located downstream. The frameshift takes place at the slippery sequence with the two ribosome-bound tRNAs slipping back simultaneously by one nucleotide from the zero phase (U UUA AAC) to the -1 phase (UUU AAA). Asparaginyl-tRNA, which decodes the A-site codon AAC, has the modified base Q at the wobble position of the anticodon (5' QUU 3') and it has been speculated that Q may be required for frameshifting. To test this, we measured frameshifting in cos cells that had been passaged in growth medium containing calf serum or horse serum. Growth in horse serum, which contains no free queuine, eliminates Q from the cellular tRNA population upon repeated passage. Over ten cell passages, however, we found no significant difference in frameshift efficiency between the cell types, arguing against a role for Q in frameshifting. We confirmed that the cells cultured in horse serum were devoid of Q by purifying tRNAs and assessing their Q-content by tRNA transglycosylase assays and coupled HPLC-mass spectroscopy. Supplementation of the growth medium of cells grown either on horse serum or calf serum with free queuine had no effect on frameshifting either. These findings were recapitulated in an in vitro system using rabbit reticulocyte lysates that had been largely depleted of endogenous tRNAs and resupplemented with Q-free or Q-containing tRNA populations. Thus Q-base is not required for frameshifting at the IBV signal and some other explanation is required to account for the slipperiness of eukaryotic asparaginyl-tRNA.

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Chapter 2 Biosynthesis and Function of Queuine and Queuosine tRNAs

Cited by 38 publications

References 59 publications

Involvement of protein kinase C in the control of tRNA modification with queuine in HeLa cells

Involvement of protein kinase C in the control of tRNA modification with queuine in HeLa cells

Possible involvement of queuine in regulation of cell proliferation

The Q-base of asparaginyl-tRNA is dispensable for efficient −1 ribosomal frameshifting in eukaryotes

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