AI Article Synopsis
- The DREAM complex is crucial for repressing cell-cycle genes in dormant (quiescent) cells, but its mechanism of action is not fully understood.
- Research shows a strong link between the Sin3B protein and the DREAM complex, where Sin3B helps keep these genes turned off during quiescence.
- While disabling Sin3B leads to some gene activation, it doesn’t let cells start dividing again; however, disabling another protein, APC/C, does allow cells lacking Sin3B to re-enter the cell cycle.
Article Abstract
The mammalian DREAM complex is responsible for the transcriptional repression of hundreds of cell-cycle-related genes in quiescence. How the DREAM complex recruits chromatin-modifying entities to aid in its repression remains unknown. Using unbiased proteomics analysis, we have uncovered a robust association between the chromatin-associated Sin3B protein and the DREAM complex. We have determined that genetic inactivation of Sin3B results in the de-repression of DREAM target genes during quiescence but is insufficient to allow quiescent cells to resume proliferation. However, inactivation of APC/C was sufficient for Sin3B cells, but not parental cells, to re-enter the cell cycle. These studies identify Sin3B as a transcriptional corepressor associated with the DREAM complex in quiescence and reveals a functional cooperation between E2F target repression and APC/C in the negative regulation of cell-cycle progression.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6324198 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2018.11.024 | DOI Listing |
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