AI Article Synopsis

  • Interferon-beta mRNA displays significant variability in expression levels among primary human dendritic cells infected by Newcastle disease virus, ranging from a few to thousands of copies.
  • Analysis reveals that the distribution of mRNA expression follows a power law, suggesting a broader variation compared to a standard Gaussian distribution.
  • A model of stochastic gene regulation, including transcriptional pulsing, is proposed, aligning well with observed patterns in mRNA distribution during infections, indicating a complex regulatory mechanism at play.

Article Abstract

Interferon-beta (IFNB1) mRNA shows very large cell-to-cell variability in primary human dendritic cells infected by Newcastle disease virus, with copy numbers varying from a few to several thousands. Analysis of data from the direct measurement of the expression of this gene in its natural chromatin environment in primary human cells shows that the distribution of mRNA across cells follows a power law with an exponent close to -1, and thus encompasses a range of variation much more extensive than a Gaussian. We also investigate the single cell levels of IFNB1 mRNA induced by infection with Texas influenza A mutant viruses, which vary in their capacity to inhibit the signaling pathways responsible for activation of this gene. Here as well we observe power-law behavior for the distribution of IFNB1 mRNA, albeit over a truncated range of values, with exponents similar to the one for cells infected by Newcastle disease virus. We propose a model of stochastic enhanceosome and preinitiation complex formation that incorporates transcriptional pulsing. Analytical and numerical results show good agreement with the observed power laws, and thus support the existence of transcriptional pulsing of an unmodified, intact gene regulated by a natural stimulus.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756378PMC
http://dx.doi.org/10.1016/j.bpj.2009.05.067DOI Listing

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