AI Article Synopsis
- The study discusses how Toll-like receptors and various stimuli trigger primary response genes in mammals, emphasizing the role of CpG-island promoters that allow easy activation without needing certain remodeling complexes.
- Low nucleosome occupancy at CpG-island promoters contributes to their independence from SWI/SNF complexes, while non-CpG-island promoters rely on these complexes for stable nucleosome assembly and transcription factor assistance.
- Different stimuli, like serum and tumor necrosis factor-alpha, prefer activating SWI/SNF-independent CpG-island genes, while interferon-beta favors the activation of SWI/SNF-dependent non-CpG-island genes, showcasing the diverse responses to microbial threats.
Article Abstract
We describe a broad mechanistic framework for the transcriptional induction of mammalian primary response genes by Toll-like receptors and other stimuli. One major class of primary response genes is characterized by CpG-island promoters, which facilitate promiscuous induction from constitutively active chromatin without a requirement for SWI/SNF nucleosome remodeling complexes. The low nucleosome occupancy at promoters in this class can be attributed to the assembly of CpG islands into unstable nucleosomes, which may lead to SWI/SNF independence. Another major class consists of non-CpG-island promoters that assemble into stable nucleosomes, resulting in SWI/SNF dependence and a requirement for transcription factors that promote selective nucleosome remodeling. Some stimuli, including serum and tumor necrosis factor-alpha, exhibit a strong bias toward activation of SWI/SNF-independent CpG-island genes. In contrast, interferon-beta is strongly biased toward SWI/SNF-dependent non-CpG-island genes. By activating a diverse set of transcription factors, Toll-like receptors induce both classes and others for an optimal response to microbial pathogens.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712736 | PMC |
| http://dx.doi.org/10.1016/j.cell.2009.04.020 | DOI Listing |
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