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PubMed2000

A four-nucleotide translation enhancer in the 3'-terminal consensus sequence of the nonpolyadenylated mRNAs of rotavirus.

The 5' cap and poly(A) tail of eukaryotic mRNAs work synergistically to enhance translation through a process that requires interaction of the cap-associated eukaryotic initiation factor, eIF-4G, and the poly(A)-binding protein, PABP. Because the mRNAs of rotavirus, and other members of the Reoviridae, contain caps but lack poly(A) tails, their translation may be enhanced through a unique mechanism. To identify translation-enhancement elements in the viral mRNAs that stimulate translation in vivo, chimeric RNAs were prepared that contained an open reading frame for luciferase and the 5' and 3' untranslated regions (UTRs) of a rotavirus mRNA or of a nonviral mRNA. Transfection of the chimeric RNAs into rotavirus-infected cells showed that the viral 3' UTR contained a translation-enhancement element that promoted gene expression. The element did not enhance gene expression in uninfected cells and did not affect the stability of the RNAs. Mutagenesis showed that the conserved sequence GACC located at the 3' end of rotavirus mRNAs operated as an enhancement element. The 3'-GACC element stimulated protein expression independently of the sequence of the 5' UTR, although efficient expression required the RNA to contain a cap. The results indicate that the expression of viral proteins in rotavirus-infected cells is specifically up-regulated by the activity of a novel 4-nt 3' translation enhancer (TE) common to the 11 nonpolyadenylated mRNAs of the virus. The 4-nt sequence of the rotavirus 3' TE represents by far the shortest of any of the sequence enhancers known to stimulate translation.

3' Untranslated Regions↗

PubMed1984

Effect of ethanol, phenol, formamide, dimethyl sulfoxide, paromomycin, and deuterium oxide on the fidelity of translation in a brain cell-free system.

The effects of six different agents (ethanol, phenol, formamide, dimethyl sulfoxide, heavy water, and a misreading-inducing antibiotic, paromomycin) on the activity and the accuracy of poly(U) translation have been compared under a range (2.5-12 mM) of Mg2+ concentrations in a rat brain cell-free system. The effect of most of these agents was remarkably sensitive to the Mg2+ concentration under which the assay was made. Ethanol decreased the fidelity of translation, and the efficiency of ethanol was increased 3-10-fold by higher Mg2+ concentrations. The effect of paromomycin was identical with that of ethanol, despite its very different structure. Formamide, a "RNA denaturant", increased the accuracy of translation under all Mg2+ concentrations tested. Dimethyl sulfoxide, another type of RNA denaturant, decreased the accuracy of translation under all Mg2+ concentrations tested. Phenol increased the accuracy of translation at high Mg2+ concentrations but decreased it at low Mg2+ concentrations. D2O did not change to any appreciable extent the accuracy of translation, at all the Mg2+ concentrations used. There exists a cooperativity between the effects of Mg2+ and ethanol, Mg2+ and paromomycin, and Mg2+ and dimethyl sulfoxide on the fidelity of translation; no such cooperativity was detected between Mg2+ and formamide and between Mg2+ and D2O. The differential effects of dimethyl sulfoxide and formamide are interpreted in terms of their different dielectric constants. The dielectric constant of dimethyl sulfoxide is higher than that of water, while that of formamide is low er.

Animals↗

PubMed1985

Effect of medium hypertonicity on reovirus translation rates. An application of kinetic modeling in vivo.

Translation rates were determined for host and virus mRNAs in reovirus-infected SC-1 cells in hypertonic medium. The effect of low doses of cycloheximide on these translation rates was also measured. The results show that hypertonicity selectively stimulates viral translation relative to host translation. Moreover, in hypertonic medium, host translation is slightly stimulated by low doses of cycloheximide, whereas viral translation is markedly inhibited. This effect of cycloheximide is precisely the opposite to what was previously observed in isotonic media [Walden, W. E., Godefroy-Colburn, T., & Thach, R. E. (1981) J. Biol. Chem. 256, 11739-11746]. It is shown that both these effects of hypertonicity are predicted by the message competition/discrimination model previously described and thus provide support for the applicability of certain aspects of the model to translation rates in vivo.

Animals↗

PubMed2005

Insulin-mediated suppression of apolipoprotein B mRNA translation requires the 5' UTR and is characterized by decreased binding of an insulin-sensitive 110-kDa 5' UTR RNA-binding protein.

Insulin has been shown to acutely regulate hepatic apolipoprotein B (apoB) secretion at both translational and post-translational levels; however, mechanisms of apoB mRNA translational control are largely unknown. Recent studies of apoB untranslated regions (UTRs) revealed a potentially important role for cis-trans interactions at the 5' and 3' UTRs. In the present paper, deletion constructs of the UTR regions of apoB revealed that the 5' UTR was necessary and sufficient for insulin to inhibit synthesis of apoB15. Metabolic radiolabeling and in vitro translation experiments in the presence of protease inhibitors confirmed that the effect of insulin on the apoB 5' UTR was translational in nature. Using the nondenaturing electrophoretic mobility shift assay (EMSA), protein-RNA complexes were detected binding to the apoB 5' and 3' UTRs. Denaturing EMSA identified a 110-kDa protein interacting at the 5' UTR. Nondenaturing EMSA determined that insulin altered binding of large protein complexes to the 5' UTR. Binding specificity was determined by competition with both specific and nonspecific competitors. Insulin treatment decreased binding of the 110-kDa protein to the 5' UTR as visualized by EMSA. Absence of insulin increased binding of this trans-acting factor to the 5' UTR by 2-fold. Analysis of the 3' UTR showed no significant insulin-mediated changes in binding of trans-acting factors. We thus propose the existence of a novel RNA-binding insulin-sensitive factor that binds to the 5' UTR and may regulate apoB mRNA translation. Perturbations in hepatic insulin signaling as observed in insulin-resistant states may alter cis-trans interactions at the 5' UTR, leading to alterations in the rate of apoB mRNA translation, thus contributing to apoB-lipoprotein overproduction.

5' Untranslated Regions↗

PubMed2002

Assessing the relative importance of light and the circadian clock in controlling chloroplast translation in Chlamydomonas reinhardtii.

Previous work has shown that transcription of a number of chloroplast-encoded genes, including those for photosynthesis, are under circadian clock control in Chlamydomonas reinhardtii. However, some of these genes encode long-lived mRNAs that are also subject to translational control. Rates of synthesis of the major chloroplast translation products vary dramatically (10-20-fold) during light-dark (LD) cycles, peaking in the light period. To determine whether this pattern reflects circadian clock control, LD-grown cells were shifted to continuous light (LL) and chloroplast protein synthesis monitored by periodic pulse-labeling in the presence of cycloheximide; chloroplast protein synthesis in LD was also examined for comparison. The LD patterns of synthesis of the major polypeptides (including D1, D2, and the large subunit of ribulose-1,5-bisphosphate carboxylase (LS)) were similar to those obtained previously in the absence of cycloheximide. In the LL condition, rates of synthesis of the major chloroplast translation products were high throughout the period examined ( approximately 36 h), fluctuating > 3-fold, although they were generally higher in the subjective light period. LD-grown cells were also shifted to continuous dark (DD) and chloroplast protein synthesis analyzed for approximately 24 h starting from the mid-dark period. There was a gradual decline in synthesis of the major proteins during the first subjective light period, which was followed by a very small peak in synthesis around the second subjective dark --> light transition. RNA blot analysis showed that the mRNAs for D1, D2 and LS were present at high levels during the period of declining translation. These results indicate that with photoautotrophic growth in LD cycles, the illumination conditions per se are more important than the clock in determining chloroplast translation, but the clock may contribute to this regulation. The advantages of controlling translation by a direct light response and transcription primarily by the circadian clock are discussed. Finally, evidence of translational control of elongation factor Tu synthesis was obtained.

Journal Article↗

PubMed2026

Novel CDK-independent function of CDC25 phosphatases in mRNA translation.

Molecular and functional networks driving coordination between cell cycle and mRNA translation remain to be explored. Here, we use mass spectrometry-based proteomics to comprehensively investigate the interactome and phosphoproteome of the cell cycle regulator CDC25A. We identify actors of mRNA regulation, such as RNA-binding proteins and translation factors, as interacting partners of CDC25A. CDC25A overexpression increases global translation, whereas catalytic inactivation or pharmacological inhibition decreases protein synthesis. A Cyclin-Dependent Kinase (CDK) interaction-deficient mutant of CDC25A also enhances translation, indicating a CDK-independent role. Our results further reveal an interplay between CDC25A and CDC25B whereby downregulation of CDC25A leads to compensatory overexpression of CDC25B. The roles of CDC25A and CDC25B in mRNA translation are independent of their roles in the cell cycle, with CDC25A possibly regulating translation elongation and CDC25B rather involved in initiation. In acute myeloid leukemia cells, CDC25A depletion also inhibits translation, suggesting its potential relevance as a therapeutic target. We propose that CDC25 phosphatases might be signaling platforms coordinating cell cycle progression with protein synthesis.

cdc25 Phosphatases↗

PubMed2006

Musashi regulates the temporal order of mRNA translation during Xenopus oocyte maturation.

A strict temporal order of maternal mRNA translation is essential for meiotic cell cycle progression in oocytes of the frog Xenopus laevis. The molecular mechanisms controlling the ordered pattern of mRNA translational activation have not been elucidated. We report a novel role for the neural stem cell regulatory protein, Musashi, in controlling the translational activation of the mRNA encoding the Mos proto-oncogene during meiotic cell cycle progression. We demonstrate that Musashi interacts specifically with the polyadenylation response element in the 3' untranslated region of the Mos mRNA and that this interaction is necessary for early Mos mRNA translational activation. A dominant inhibitory form of Musashi blocks maternal mRNA cytoplasmic polyadenylation and meiotic cell cycle progression. Our data suggest that Musashi is a target of the initiating progesterone signaling pathway and reveal that late cytoplasmic polyadenylation element-directed mRNA translation requires early, Musashi-dependent mRNA translation. These findings indicate that Musashi function is necessary to establish the temporal order of maternal mRNA translation during Xenopus meiotic cell cycle progression.

3' Untranslated Regions↗

PubMed2004

Pharmacological-based translational induction of transgene expression in mammalian cells.

In the quest for the development of pharmacological switches that control gene expression, no system has been reported that regulates at the translational level. To permit small-molecule control of transgene translation, we have constructed a farnesyl transferase inhibitor-responsive translation initiation factor. This artificial protein is a three-component chimaera consisting of the ribosome recruitment core of the eIF4G1 eukaryotic translation initiation factor, the RNA-binding domain of the R17 bacteriophage coat protein and the plasma membrane localization CAAX motif of farnesylated H-Ras. This membrane-delocalized translation factor is inactive unless liberated in the cytosol. Farnesyl transferase inhibitor FTI-277 prevents the membrane association of the CAAX motif and thus increases the cytoplasmic levels of the eIF4G fusion protein, which is then capable of inducing translation of the second cistron of a bicistronic messenger RNA containing an R17-binding site in its intercistronic space. Such direct translational control by farnesyl transferase inhibitors provides a system for fast, graded and reversible regulation of transgene expression.

Alkyl and Aryl Transferases↗

PubMed1998

Growth-dependent and PKC-mediated translational regulation of the upstream stimulating factor-2 (USF2) mRNA in hematopoietic cells.

Upstream stimulating factor (USF2) is a basic helix-loop-helix leucine zipper transcription factor, which is found in most tissues. A critical role for USF2 in cellular proliferation has been proposed based on its importance in the regulation of various cyclins and P53 and its capability to antagonize c-myc. In this paper we report that IL-3, which is a major growth factor for mast cells, induces USF2 protein synthesis in murine mast cells (MC-9). Surprisingly, it does not significantly affect the level of USF2 mRNA in these cells at any of the time points tested. Using polysomal fractionation and RNA analysis we then demonstrated that this translational regulation is mostly the result of increased USF2 translational efficiency. Moreover, protein kinase C (PKC) inhibitors prevented both the induction of USF2 protein synthesis and the increase in USF2 translational efficiency in IL-3-activated mast cells. Two other hematopoietic cell lines were used to determine whether the translational regulation of USF2 is of a more general nature: mouse lymphosarcoma cells whose proliferation is inhibited by dexamethasone; and mouse erythroleukemia cells that differentiate upon exposure to hexamethylen bisacetamide. In both cell types, USF2 translation was repressed in the non-dividing cells. This strongly implies that USF2 is translationally repressed in quiescent hematopoietic cells. Considering the proposed role of USF in proliferation it seems that translational regulation of USF2 might have an important role in cellular growth.

Animals↗

PubMed2004

The role of translation in neoplastic transformation from a pathologist's point of view.

Increased cell proliferation, which is a hallmark of aggressive malignant neoplasms, requires a general increase in protein synthesis and a specific increase in the synthesis of replication-promoting proteins. Transient increase in the general protein synthesis rate, as well as preferential translation of specific mRNAs coding for growth promoting proteins (e.g. cyclin D1), takes place during normal mitogenic response. A number of extensively studied growth signal transduction pathways (Ras, PI3K, MAPK, mTOR-dependent pathways) activate the function and expression of various components of the translational machinery. In abnormal situations, constitutive activation of signal transduction pathways (e.g. oncogenic activation of Ras or Myc) leads to continuous upregulation of key elements of translational machinery. On the other hand, tumor suppressor genes (p53, pRb) downregulate ribosomal and tRNA synthesis, and their inactivation results in uncontrolled production of these translational components. During recent years, a significant effort has been dedicated to determining whether expression of translation factors is increased in human tumors using clinical biopsy specimens. The results of these studies indicate that expression of particular translation initiation factors is not always increased in human neoplasms. The pattern of expression is characteristic for a particular tumor type. For example, eIF-4E is usually increased in bronchioloalveolar carcinomas but not in squamous cell carcinomas of the lung. Interestingly, in certain highly proliferative and aggressive neoplasms (e.g. squamous cell carcinoma of the lung, melanoma), the expression of eIF-4E is barely detectable. These findings suggest that mechanisms for increasing general protein synthesis in various neoplasms differ significantly. Finally, the possibility of qualitative alterations in the translational machinery, rather than a simple increase in the activity of its components, is discussed along with the possibility of targeting those qualitative differences for tumor therapy.

Animals↗

PubMed2005

To replicate or not to replicate: achieving selective oncolytic virus replication in cancer cells through translational control.

To ensure that their mRNAs are translated and that the viral proteins necessary for assembling the next generation of infectious progeny are produced, viruses must effectively seize control of the translational machinery within their host cells. In many cases, the ability to productively engage host translational components can determine if a given cell type can support viral replication, illustrating the critical importance of this task in the viral life cycle. Failure to interface properly with the host translational apparatus can compromise the productive growth cycle, resulting in an abortive infection and radically restricting viral replication. Not only have viruses become facile at commandeering this machinery, they are also particularly adept at manipulating cellular translation control pathways for their own ends. In this review, the mechanisms by which numerous viruses manipulate host translational control circuits are discussed. Furthermore, particular attention is devoted to understanding how interfering with the ability of a virus to properly regulate translation in its host can be exploited to generate oncolytic strains that selectively replicate in cancer cells.

Eukaryotic Initiation Factor-2↗

PubMed2006

The identification of an internal ribosomal entry site in the 5'-untranslated region of p53 mRNA provides a novel mechanism for the regulation of its translation following DNA damage.

The tumor suppressor p53 plays a crucial role in maintaining the genetic integrity of the cell and in suppressing cell transformation. Its cellular levels are usually low and rise substantially in response to DNA damage. Although research on p53 induction following DNA damage has mainly focused on the post-translational modification of p53 by Mdm2, it is known that protein translation also contributes to p53 induction. However, the mechanisms underlying translational regulation of the p53 protein in response to DNA damage are still poorly understood. We show that p53 synthesis increases dramatically in MCF-7 cells treated with etoposide. Interestingly, this increase is accompanied by an increase in the association of the translation initiation factor eIF-4E with its binding protein 4E-BP1, an inhibitor of cap-dependent protein translation. We further identified an internal ribosomal entry site (IRES) located in the 5'-untranslated region of the p53 transcript, that is capable of driving the cap-independent translation of a downstream cistron encoding Firefly luciferase in a dicistronic expression vector. Moreover, we found that the activity of the IRES element increases in response to etoposide-induced DNA damage in MCF-7 cells. These findings provide a novel mechanism for the regulation of p53 translation in response to DNA damage.

5' Untranslated Regions↗

PubMed2006

Decreased expression of eukaryotic initiation factor 3f deregulates translation and apoptosis in tumor cells.

The eukaryotic initiation factor 3f (eIF3f) is the p47 subunit of the multi-subunit eIF3 complex. eIF3 plays an important role in translation initiation. In the present study, we investigate the biological function of eIF3f in translation and apoptosis in tumor cells. We demonstrated for the first time that eIF3f is downregulated in most human tumors using a cancer profiling array and confirmed by real-time reverse transcription PCR in melanoma and pancreatic cancer. Overexpression of eIF3f inhibits cell proliferation and induces apoptosis in melanoma and pancreatic cancer cells. Silencing of eIF3f protects melanoma cells from apoptosis. We further investigated the biological function of eIF3f. In vitro translation studies indicate that eIF3f is a negative regulator of translation and that the region between amino acids 170 and 248 of eIF3f is required for its translation regulatory function. Ectopic expression of eIF3f inhibits translation and overall cellular protein synthesis. Ribosome profile and ribosomal RNA (rRNA) fragmentation assays revealed that eIF3f reduces ribosomes, which may be associated with rRNA degradation. We propose that eIF3f may play a role in ribosome degradation during apoptosis. These data provide critical insights into the cellular function of eIF3f and in linking translation initiation and apoptosis.

Apoptosis↗

PubMed2003

Translation and restandardization of an instrument: the Early Infant Temperament Questionnaire.

AIMS OF THE STUDY: To test the psychometric properties of a Danish translation of the Early Infant Temperament Questionnaire (EITQ) and to establish standards for scoring the questionnaire. RATIONALE: The general aim was to create a translation that remained close to the original version, was meaningful for the Danish participants, and had acceptable psychometric properties. BACKGROUND: Patterns of temperament can be discerned early in life and tend to persist over time and across situations. For the past 50 years, temperament has been studied by theorists, clinicians and nurse clinicians to predict behaviour, discover interventions that prevent serious behaviour disturbances, and help parents understand the implications of their child's temperament. Thomas and Chess's conceptualization of temperament in nine categories was the framework for the development of the English-language EITQ. Research methods. The translation followed a stepwise process of translation, back translation and consensus. A convenience sample of 204 Danish mothers with 1-4-month old infants completed the translated questionnaire and a demographic questionnaire in 1999. RESULTS: Alpha coefficients for the nine subscales ranged from 0.59 to 0.82. All alpha coefficients were comparable to or higher than those reported on the original United States standardization study. There were statistically significant differences between reported United States mean scores and those in the Danish sample. DISCUSSION: The psychometric properties of the Danish translation are equal to or better than those reported for the United States study. Differences in mean scores or most subscales point to the need to create Danish profiles for scoring. CONCLUSIONS: The Danish version of the EITQ has acceptable reliability and is ready for use in Denmark.

Denmark↗

PubMed1997

Escherichia coli RNase III (rnc) autoregulation occurs independently of rnc gene translation.

Control of mRNA stability is an established means of regulating gene expression. However, the detailed mechanisms by which such control is achieved are only now emerging. In particular, there remains a question about the involvement of translation. Escherichia coli ribonuclease III (RNase III) negatively autoregulates expression of its own gene (rnc) approximately 10-fold, by cleaving the untranslated leader and initiating approximately 10-fold more rapid decay of the rnc mRNA, after which RNase III plays no further role. Here, we define the mechanism of this control further. Mutations that increase rnc gene translation abolish autoregulation by increasing the stability of the RNase III-cleaved transcript RNA approximately 10-fold, with no effect on the uncleaved species. Mutations that decrease translation destabilize the rnc mRNA in the presence or absence of RNase III. In so doing, they reveal a pathway of rnc transcript decay distinct from the RNase III-dependent pathway. Stability of a 'mini-rnc' transcript containing the rnc leader and only the first two codons of the rnc gene is unaffected by decreased translation, presumably because sequences required for this pathway were removed. Importantly, this mini-rnc transcript is regulated normally by RNase III. Moreover, rnc transcripts synthesized in vitro do not decay in cell-free extracts lacking ribosomes, unless they are first cleaved by RNase III. These two results show that RNase III cleavage can initiate rnc transcript decay independently of rnc gene translation, unambiguously establishing that control of mRNA decay need not involve changes in translation. How rnc gene translation is optimized for efficient autoregulation will also be discussed.

Base Sequence↗

PubMed1998

An AUG initiation codon, not codon-anticodon complementarity, is required for the translation of unleadered mRNA in Escherichia coli.

We determined the in vivo translational efficiency of 'unleadered' lacZ compared with a conventionally leadered lacZ with and without a Shine-Dalgarno (SD) sequence in Escherichia coli and found that changing the SD sequence of leadered lacZ from the consensus 5'-AGGA-3' to 5'-UUUU-3' results in a 15-fold reduction in translational efficiency; however, removing the leader altogether results in only a twofold reduction. An increase in translation coincident with the removal of the leader lacking a SD sequence suggests the existence of stronger or novel translational signals within the coding sequence in the absence of the leader. We examined, therefore, a change in the translational signals provided by altering the AUG initiation codon to other naturally occurring initiation codons (GUG, UUG, CUG) in the presence and absence of a leader and find that mRNAs lacking leader sequences are dependent upon an AUG initiation codon, whereas leadered mRNAs are not. This suggests that mRNAs lacking leader sequences are either more dependent on perfect codon-anticodon complementarity or require an AUG initiation codon in a sequence-specific manner to form productive initiation complexes. A mutant initiator tRNA with compensating anticodon mutations restored expression of leadered, but not unleadered, mRNAs with UAG start codons, indicating that codon-anticodon complementarity was insufficient for the translation of mRNA lacking leader sequences. These data suggest that a cognate AUG initiation codon specifically serves as a stronger and different translational signal in the absence of an untranslated leader.

Anticodon↗

PubMed2001

Translation at higher than an optimal level interferes with coupling at an intercistronic junction.

In pairs of adjacent genes co-transcribed on bacterial polycistronic mRNAs, translation of the first coding region frequently functions as a positive factor to couple translation to the distal coding region. Coupling efficiencies vary over a wide range, but synthesis of both gene products at similar levels is common. We report the results of characterizing an unusual gene pair, in which only about 1% of the translational activity from the upstream gene is transmitted to the distal gene. The inefficient coupling was unexpected because the upstream gene is highly translated, the distal initiation site has weak but intrinsic ability to bind ribosomes, and the AUG is only two nucleotides beyond the stop codon for the upstream gene. The genes are those in the filamentous phage IKe genome, which encode the abundant single-stranded DNA binding protein (gene V) and the minor coat protein that caps one tip of the phage (gene VII). Here, we have used chimeras between the related phage IKe and f1 sequences to localize the region responsible for inefficient coupling. It mapped upstream from the intercistronic region containing the gene V stop codon and the gene VII initiation site, indicating that low coupling efficiency is associated with gene V. The basis for inefficient coupling emerged when coupling efficiency was found to increase as gene V translation was decreased below the high wild-type level. This was achieved by lowering the rate of elongation and by decreasing the efficiency of suppression at an amber codon within the gene. Increasing the strength of the Shine-Dalgarno interaction with 16S rRNA at the gene VII start also increased coupling efficiency substantially. In this gene pair, upstream translation thus functions in an unprecedented way as a negative factor to limit downstream expression. We interpret the results as evidence that translation in excess of an optimal level in an upstream gene interferes with coupling in the intercistronic junction.

Bacteriophage IKe↗

PubMed2002

Post-transcriptional mechanisms control catalase synthesis during its light-induced turnover in rye leaves through the availability of the hemin cofactor and reversible changes of the translation efficiency of mRNA.

The enzyme catalase is light-sensitive. In leaves, losses caused by photoinactivation are replaced by new enzyme and the rate of de novo synthesis must be rapidly and flexibly attuned to fluctuating light conditions. In mature rye leaves, post-transcriptional mechanisms were shown to control the rate of catalase synthesis. The amount of the leaf catalase (CAT-1) transcript did not increase with light intensity, but was even higher after dark exposure of light-grown leaves. Initiation was apparently not limiting translation in the dark, as the association of the Cat1 mRNA with polysomes did not change notably under different light conditions. By analysing the translation of catalase polypeptides in cell-free systems with poly(A)+ RNA from leaves or with mRNA transcribed from a Cat1-containing cDNA clone, two mechanisms of post-transcriptional control were identified. First, translation of catalase depended on the presence of hemin. In leaves, the availability of hemin may signal the extent of catalase degradation as the hemin of the inactivated enzyme is recycled. Second, the translation efficiency of the Cat1 transcripts was reversibly modulated in a dose-dependent manner by the light intensity to which leaves were exposed, prior to extraction. The Cat1 mRNA from light-exposed leaves was translated much more efficiently than mRNA from dark-exposed leaves. The increase of its translation activity in vivo was not blocked by cordycepin but was suppressed by methylation inhibitors, indicating a reversible modification of pre-existing mRNA by methylation. Translation of in vitro synthesized Cat1 mRNA required a methylated cap (m7GpppG), but was virtually below detection when it contained an unmethylated cap (GpppG).

Catalase↗