Abstract | Activation of eukaryotic transcription is an intricate process that relies on a multitude of regulatory proteins forming complexes on chromatin. |
Author Summary | Such bursting transcriptional activity has indeed been observed for eukaryotic genes. |
Discussion | In this study, we asked how transcription regulation of conditionally active genes in eukaryotes could be organized so that it is both fast enough, given diffusion limitations, and sensitive enough towards a large number of TFs. |
Discussion | If one were to specify that histone modification is the process that marks the completion of a step in the multi-step process and sensitizes the local chromatin region for the assembly of the next protein complex, this model comes close to the accepted view of transcription activation in eukaryotes [7, 10, 22, 44]. |
Experimental evidence for the ticking mechanism | The ticking mechanism described above is consistent with the wealth of experimental evidence on the role of chromatin covalent-modification and remodelling in regulation of eukaryotic gene transcription [3, 5—7, 9, 10, 22, 44]. |
Introduction | Eukaryotic transcription depends on dozens of proteins, including transcription factors (TFs), chromatin remodellers and RNA polymerase II components [1—7]. |
Introduction | Even though we refer by ‘transcription regulation’ only to regulation of the transcription process itself and not to the regulation of gene expression through transcription, the complexity of eukaryotic transcription regulation is immense. |
Number of proteins in a complex, n | This finding is highly relevant as the number of TF-binding sites actively regulating many eukaryotic genes is readily around ten or more. |
Number of proteins in a complex, n | We will further discuss alternative mechanisms for eukaryotic gene regulation that do not suffer from this limitation. |
Reversible assembly of large protein complexes can take tens of minutes | In summary, our analysis indicates that for many eukaryotic genes mechanism of reversible association of all TFs becomes too slow. |
Revertibility of transcription activation requires a cycle | Our analysis thus far has used criteria of regulatory sensitivity and the speed of regulation of transcription to show that a ‘ticking’ transcription cycle mechanism is an attractive mechanism for eukaryotic genes that are regulated by multiple TFs. |
Author Summary | Our analysis shows how the nature of the two linked properties growth and proliferation can shape eukaryotic cells and eXplain cell size as an emergent rather than regulatory property of this process. |
Introduction | The unicellular eukaryote Saccharomyces cerevisiae can be observed to grow to a ‘critical cell size’ in the G1 phase before committing to passage through the cell cycle [1]. |
Results | We present here an extended version of a minimal eukaryotic cell model that is capable of growth and division (Fig 1A) [32]. |
The model | The model is an extension of a minimal eukaryotic cell model [32]. |
The model | The cell cycle of the model has four transitions, corresponding to the eukaryotic phase transitions (G 1/ S, S/GZ, Gz/M, M/ G1). |
Abstract | Burkholderia pathogenicity relies on protein virulence factors to control and promote bacterial internalization, survival, and replication within eukaryotic host cells. |
Author Summary | Burkholderia species need to manipulate many host processes and pathways in order to establish a successful intracellular infection in eukaryotic host organisms. |
Introduction | This host-adapted bacterium is equipped with an extensive set of mechanisms for invasion and modulation of eukaryotic host-cell environments. |
Summary | Using multiple virulence factors to target eukaryotic-specific mechanisms common to eukaryotic rhizosphere species, B. mallei broadly influences key processes in ubiquitination and cell signaling to modulate and adapt the host-cell environment for its benefit. |