Topic
Cytoplasmic translation
About: Cytoplasmic translation is a research topic. Over the lifetime, 148 publications have been published within this topic receiving 5269 citations.
Papers published on a yearly basis
Papers
More filters
TL;DR: Cryo-ET was used to visualize previously elusive structures, such as nucleosome chains and the filaments of the nuclear lamina, in situ, which revealed the native structure and organization of the cytoplasmic translation machinery.
Abstract: The molecular organization of eukaryotic nuclear volumes remains largely unexplored. Here we combined recent developments in cryo-electron tomography (cryo-ET) to produce three-dimensional snapshots of the HeLa cell nuclear periphery. Subtomogram averaging and classification of ribosomes revealed the native structure and organization of the cytoplasmic translation machinery. Analysis of a large dynamic structure-the nuclear pore complex-revealed variations detectable at the level of individual complexes. Cryo-ET was used to visualize previously elusive structures, such as nucleosome chains and the filaments of the nuclear lamina, in situ. Elucidation of the lamina structure provides insight into its contribution to metazoan nuclear stiffness.
464 citations
TL;DR: It is demonstrated that cells distinguish a premature termination codon within the β‐globin mRNA from the physiological translation termination codons by a two‐step specification mechanism, and a common principle for nonsense‐mediated decay from yeast to man is proposed.
Abstract: Premature translation termination codons resulting from nonsense or frameshift mutations are common causes of genetic disorders. Complications arising from the synthesis of C-terminally truncated polypeptides can be avoided by 'nonsense-mediated decay' of the mutant mRNAs. Premature termination codons in the beta-globin mRNA cause the common recessive form of beta-thalassemia when the affected mRNA is degraded, but the more severe dominant form when the mRNA escapes nonsense-mediated decay. We demonstrate that cells distinguish a premature termination codon within the beta-globin mRNA from the physiological translation termination codon by a two-step specification mechanism. According to the binary specification model proposed here, the positions of splice junctions are first tagged during splicing in the nucleus, defining a stop codon operationally as a premature termination codon by the presence of a 3' splicing tag. In the second step, cytoplasmic translation is required to validate the 3' splicing tag for decay of the mRNA. This model explains nonsense-mediated decay on the basis of conventional molecular mechanisms and allows us to propose a common principle for nonsense-mediated decay from yeast to man.
404 citations
TL;DR: For the first time, incorporation of labeled amino acids into polypeptides during sperm capacitation is demonstrated, which was completely inhibited by mitochondrial translation inhibitors but not by the cytoplasmic translation inhibitor.
Abstract: It is widely accepted that spermatozoa are translationally silent. The present study demonstrates, for the first time, incorporation of labeled amino acids into polypeptides during sperm capacitation, which was completely inhibited by mitochondrial translation inhibitors but not by the cytoplasmic translation inhibitor. Unlike 80S cytoplasmic ribosomes, 55S mitochondrial ribosomes were present in polysomal fractions, indicating that these ribosomes are actively involved in protein translation in spermatozoa. Inhibition of protein translation significantly reduced sperm motility, capacitation and in vitro fertilization rate. Thus, contrary to the accepted dogma, nuclear genes are expressed as proteins in sperm during their residence in the female reproductive tract until fertilization.
322 citations
TL;DR: A basic theme of this review is that the transcriptionally active nucleoid and the cytoplasmic translation machinery form a structural continuity with the growing cellular envelope and how this dynamic relationship during the cell cycle affects cell polarity and how it leads to cell division.
Abstract: The shape of Escherichia coli is strikingly simple compared to those of higher eukaryotes. In fact, the end result of E. coli morphogenesis is a cylindrical tube with hemispherical caps. It is argued that physical principles affect biological forms. In this view, genes code for products that contribute to the production of suitable structures for physical factors to act upon. After introduction of a physical model, the discussion is focused on the shape-maintaining (peptidoglycan) layer of E. coli. This is followed by a detailed analysis of the structural relationship of the cellular interior to the cytoplasmic membrane. A basic theme of this review is that the transcriptionally active nucleoid and the cytoplasmic translation machinery form a structural continuity with the growing cellular envelope. An attempt has been made to show how this dynamic relationship during the cell cycle affects cell polarity and how it leads to cell division.
290 citations
TL;DR: The results demonstrate that TPI intron 6 functions to position the boundary because it is the 3′-most intron, and the proposed scanning complex may have a greater unwinding capability than the complex that scans for a translation initiation codon.
Abstract: Mammalian cells have established mechanisms to reduce the abundance of mRNAs that harbor a nonsense codon and prematurely terminate translation. In the case of the human triosephosphate isomerase (TPI gene), nonsense codons located less than 50 to 55 bp upstream of intron 6, the 3*-most intron, fail to mediate mRNA decay. With the aim of understanding the feature(s) of TPI intron 6 that confer function in positioning the boundary between nonsense codons that do and do not mediate decay, the effects of deleting or duplicating introns have been assessed. The results demonstrate that TPI intron 6 functions to position the boundary because it is the 3*-most intron. Since decay takes place after pre-mRNA splicing, it is conceivable that removal of the 3*-most intron from pre-mRNA “marks” the 3*-most exon-exon junction of product mRNA so that only nonsense codons located more than 50 to 55 nucleotides upstream of the “mark” mediate mRNA decay. Decay may be elicited by the failure of translating ribosomes to translate sufficiently close to the mark or, more likely, the scanning or looping out of some component(s) of the translation termination complex to the mark. In support of scanning, a nonsense codon does not elicit decay if some of the introns that normally reside downstream of the nonsense codon are deleted so the nonsense codon is located (i) too far away from a downstream intron, suggesting that all exon-exon junctions may be marked, and (ii) too far away from a downstream failsafe sequence that appears to function on behalf of intron 6, i.e., when intron 6 fails to leave a mark. Notably, the proposed scanning complex may have a greater unwinding capability than the complex that scans for a translation initiation codon since a hairpin structure strong enough to block translation initiation when inserted into the 5* untranslated region does not block nonsense-mediated decay when inserted into exon 6 between a nonsense codon residing in exon 6 and intron 6.
289 citations