Transcription premature termination

The 19-mer sequence must not contain four or five consecutive T or A residues, because this would act as a premature termination of transcription signal for the poly III complex. 

There have been many studies that have examined transcription on chromatin templates in vitro. The general sense is that transcription does occur through the nucleosomes, but there is substantial premature termination and repression. An example of earlier experiments in this regard is the work of Wasylyk and Chambon, 1979 [76] in which histones were reconstituted on SV40 form 1 DNA and... 

Eukaryotic DNA contains sequences recognized as termination signals in E. coli, resulting in premature termination of transcription and a truncated protein. Also, there are differences in codon preference affecting translation, which may ultimately... 

There are "nonsense" codes, which do not specify amino acids but specify instructions such as "start" or "stop" transcription or translation. A mutation in such a code might therefore have a profound effect. Alternatively, mutations may give rise to a nonsense code, causing erroneous instructions to be carried out such as the premature termination of a protein. Obviously, mutations of this kind may have a much more profound effect than a single change in an amino acid. 

Hough, C., Kamisue, S., Cameron, C., Notley, C., Tinlin, S., Giles, A. and Lillicrap, D. (2002). Aberrant splicing and premature termination of transcription of the FVIII gene as a cause of severe canine hemophilia A Similarities with the intron 22 inversion mutation in human hemophilia. Thromb. Haemost. 87, 659-665. 

Accordingly, some effort has been devoted to studying the effects of cisplatin on transcription. In vitro experiments with RNA polymerases demonstrated that productive elongation activity was prematurely terminated by the whole spectrum of cisplatin-DNA adducts, but not by the /ran.y-DDP 1,3-intrastrand adducts [150-152], Selective bypass of trans-DDP adducts was also demonstrated in XPA cells, suggesting that repair of the DNA lesions did not contribute to differential transcription inhibition by the platinum compounds [153], In vivo, hormone-induced chromatin remodeling and subsequent transcription from the MMTV promoter was specifically inhibited by cisplatin [154], In this case, platinum adducts seemed to cause a decrease in the DNA binding of one of the transcription factors, NF1. Several chromatin-associated proteins, such as the linker histone protein HI or... 

Fig. 5 NASRE. Wild-type CHRNE generates the normally spliced transcript (a) and the exon 6-skipped transcript (b), because exon 6 carries weak splicing signals. The exon-skipped transcript carries a premature termination codon (PTC) and is degraded by NMD. A 7-nt deletion (arrowhead) in exon 7 generates a PTC in the normally spliced transcript (c) and is degraded by NMD. The deletion resumes the open reading frame from the exon 6-skipped transcript, and the transcript escapes NMD (d)...

Premature termination of transcription before the first structural gene is reached, and... 

In contrast to Xenopus laevis, the maternal histone pool in the mouse one-cell embryo (based on synthetic rates for histones) is probably sufficient for only one to two rounds of DNA replication (Wassarman and Mrozak, 1981). Consistent with such a small histone pool is the observation that poly spermic eggs have the capacity to transform up to three to four sperm nuclei into metaphase chromosomes (Clarke and Masui, 1986) a similar capacity was also determined from experiments that manipulated the cytoplasmic volume by either bisection or cell fusion (Clarke and Masui, 1987). This small pool of maternal histones may hence be insufficient to prevent effectively the assembly of stable basal transcription complexes. Thus, titration of the maternal histone pool by an increase in the mass of DNA due to blasto-mere proliferation may not be a critical factor in regulating the onset of transcription in the mouse embryo and other mammalian eggs this is because the maternal transcription factors may be able to outcompete successfully maternal histones for the newly replicated chromatin. This could, at least in part, account for the early onset of transcription in mammalian embryos ranging from rodents to humans (Telford et al., 1990). Moreover, the lack of arapid S phase in the mouse embryo and other mammalian embryos would permit sufficient time for productively assembled transcription complexes to generate full-length transcripts. In contrast to mammalian embryos, S phase is very short prior to the midblastula transition in Xenopus laevis (Newport and Kirschner, 1982) and hence these rapid rounds of DNA replication could prematurely terminate the transcription of genes for which transcription had initiated. 

Poly (A) and poly (T) (> 3mers) are removed to avoid premature termination of transcription. Poly (G) and poly (C) (> 2mers) and poly (G, C)... 

Choi, D.J., Roth, R.B., Liu, T., Geacintov, N.E., and Sdcchitano, D.A. (1996) Incorrect base insertion and prematurely terminated transcripts during T7 RNA polymerase transcription elongation past benzo[a]pyrenediol epoxide-modified DNA./. Mol. Biol., 264, 213-219. 

The trp operon controls the production of tryptophan biosynthetic enzymes at two levels, depending on the intracellular concentrations of tryptophan. When tryptophan levels are high, Trp repressor-tryptophan complexes are formed and Trp repressor binding to the trp operon inhibits transcription. A second level of control is called attenuation and it involves the premature termination of transcription when TRP-tRNATrp is abundant and a termination structure is formed, resulting in the disengagement of RNA polymerase from the DNA. 

Riboswitch-mediated gene regulation occurs after transcription initiation, as the regulatory element is part of the regulated transcript. In bacteria, preferred modes of regulation are at the levels of premature termination of transcription (referred to as transcriptional attenuation) and translation initiation. Rare examples identified so far in eukaryotic cells affect mRNA stability and splicing. 

These mutant alleles fail to produce receptor proteins cells carrying these mutations do not bind any LDL in saturable fashion. This phenotype arises from point mutations causing premature termination codons early in the protein-coding region, mutations in the promoter region that block transcription, mutations that lead to abnormal splicing and/or instability of the mRNA, and large deletions. 

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