Format

Send to

Choose Destination
Biophys J. 2014 Jan 21;106(2):479-88. doi: 10.1016/j.bpj.2013.12.011.

Promoter-mediated transcriptional dynamics.

Author information

1
Guangdong Province Key Laboratory of Computational Science, School of Mathematics and Computational Science, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China.
2
Guangdong Province Key Laboratory of Computational Science, School of Mathematics and Computational Science, Sun Yat-Sen University, Guangzhou 510275, People's Republic of China. Electronic address: mcszhtsh@mail.sysu.edu.cn.

Abstract

Genes in eukaryotic cells are typically regulated by complex promoters containing multiple binding sites for a variety of transcription factors, but how promoter dynamics affect transcriptional dynamics has remained poorly understood. In this study, we analyze gene models at the transcriptional regulation level, which incorporate the complexity of promoter structure (PS) defined as transcriptional exits (i.e., ON states of the promoter) and the transition pattern (described by a matrix consisting of transition rates among promoter activity states). We show that multiple exits of transcription are the essential origin of generating multimodal distributions of mRNA, but promoters with the same transition pattern can lead to multimodality of different modes, depending on the regulation of transcriptional factors. In turn, for similar mRNA distributions in the models, the mean ON or OFF time distributions may exhibit different characteristics, thus providing the supplemental information on PS. In addition, we demonstrate that the transcriptional noise can be characterized by a nonlinear function of mean ON and OFF times. These results not only reveal essential characteristics of promoter-mediated transcriptional dynamics but also provide signatures useful for inferring PS based on characteristics of transcriptional outputs.

PMID:
24461023
PMCID:
PMC3907263
DOI:
10.1016/j.bpj.2013.12.011
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center