AI Article Synopsis
- Cbf11 and Cbf12 are CSL transcription factors in fission yeast that influence cell-cycle progression, yet their specific roles and target genes are not fully understood.
- By analyzing gene expression and CSL-DNA interactions, researchers found that manipulating these proteins affects the expression of stress-response and cell-cycle genes, leading to cell-cycle defects.
- Cbf11 operates in response to nutrient levels and shows direct regulation over lipid metabolism genes, with its absence causing notable decreases in storage lipid droplets.
Article Abstract
Background: Cbf11 and Cbf12, the fission yeast CSL transcription factors, have been implicated in the regulation of cell-cycle progression, but no specific roles have been described and their target genes have been only partially mapped.
Methodology/principal Findings: Using a combination of transcriptome profiling under various conditions and genome-wide analysis of CSL-DNA interactions, we identify genes regulated directly and indirectly by CSL proteins in fission yeast. We show that the expression of stress-response genes and genes that are expressed periodically during the cell cycle is deregulated upon genetic manipulation of cbf11 and/or cbf12. Accordingly, the coordination of mitosis and cytokinesis is perturbed in cells with genetically manipulated CSL protein levels, together with other specific defects in cell-cycle progression. Cbf11 activity is nutrient-dependent and Δcbf11-associated defects are mitigated by inactivation of the protein kinase A (Pka1) and stress-activated MAP kinase (Sty1p38) pathways. Furthermore, Cbf11 directly regulates a set of lipid metabolism genes and Δcbf11 cells feature a stark decrease in the number of storage lipid droplets.
Conclusions/significance: Our results provide a framework for a more detailed understanding of the role of CSL proteins in the regulation of cell-cycle progression in fission yeast.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4569565 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0137820 | PLOS |
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