Sentence examples for persistent transcription from inspiring English sources

Basically, we have achieved epigenetic inheritance of a nucleosome-depleted DNA state facilitating persistent transcription in the absence of transcriptional activators in vivo.

Using the yeast PHO5 promoter as a model, we have previously shown that blocking Spt6-mediated histone deposition on to the promoter leads to persistent transcription in the apparent absence of transcriptional activators in vivo.

However, it has been demonstrated that human macrophages support persistent transcription from unintegrated HIV-1 DNA [32] highlighting the role of unintegrated viral DNA.

Next, we asked whether Mediator is required for the persistent transcription that occurs from the nucleosome-depleted PHO5 promoter in the absence of activators.

Interestingly, we reproducibly find that inactivation of Srb4 does not prevent the persistent transcription that occurs in the absence of Spt6).

The post-translational histone modifications examined so far fail to clearly distinguish interphase-only from persistent transcription factor binding sites [ 16, 20], although subtle trends do exist.

This is supported by several reports showing that persistent transcription-blocking lesions trigger somatic growth attenuation in order to switch physiological status from somatic 'growth' to 'maintenance' in an attempt to tolerate persistent transcription-blocking DNA lesions (32, 48).

Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified.

Based on a large body of evidence indicating that persistent transcription-blocking DNA damage cause attenuation of ILS and activation of oxidative stress responses [ 18- 20, 47], it is reasonable to speculate that the transcriptome modulation in the xpa-1 mutant reflects accumulation of transcription blocking DNA lesions.

This persistent PHO5 transcription under repressing conditions in the apparent absence of Spt6 and activators is due to failure to reassemble chromatin on to the PHO5 promoter) [ 13], which enables continued access of the general transcription machinery to the promoter.

Five of these mapped to the second chromosome, as does the Cyclin E gene, which when mutated causes persistent PCNA transcription in the endocycle domains (Duronio and O'Farrell 1995; Sauer et al. 1995).