Spatial regulation of the Start repressor Whi5

Taberner, Francisco J.; Quilis, Inma; Igual, J. Carlos

doi:10.4161/cc.8.18.9621

Cited by 47 publications

(72 citation statements)

References 50 publications

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“…Msn5 is the karyopherin responsible for the nuclear export of cell cycle transcription factors Swi6, Whi5 and Swi5 [52][53][54] or of other cell cycle regulators like the CKI inhibitor Far1 or the since our results indicate that Kap60 and Cse1 are involved in the transport of Cln1 and Cln2. On the other hand, the nuclear import of a multiprotein complex could depend on the reconstitution of an NLS by residues from different subunits of the complex.…”

Section: Wwwlandesbiosciencecom Cell Cycle 3125mentioning

confidence: 80%

“…The minimal NES identified in some of the Msn5 cargoes often involves long protein regions of approximately 100 amino acids. 53,55,57,58 This is also the case for Cln2. The nuclear export mediated by Msn5 often requires the phosphorylation of the cargo proteins in critical residues.…”

Section: Methodsmentioning

confidence: 86%

“…The nuclear export mediated by Msn5 often requires the phosphorylation of the cargo proteins in critical residues. 53,[57][58][59] Interestingly, it has been suggested that Cln2 phosphorylation by Cdc28 may regulate its localization, since the mutant version of Cln2 at Cdc28 phosphorylation sites shows a nuclear accumulation of the cyclin. 14 This could suggest that nuclear export is enhanced upon the phosphorylation of Cln2.…”

Section: Methodsmentioning

confidence: 99%

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Molecular basis of the functional distinction between Cln1 and Cln2 cyclins

Quilis

Igual²

2012

Cell Cycle

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Section: Wwwlandesbiosciencecom Cell Cycle 3125mentioning

confidence: 80%

Section: Methodsmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

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Molecular basis of the functional distinction between Cln1 and Cln2 cyclins

Quilis

Igual²

2012

Cell Cycle

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“…Standard PCR-based gene-replacement methods were used to obtain the indicated deletions, C-terminal translational fusions to GFP and mCherry, or transcriptional fusions to the GAL1 promoter at the respective chromosomal loci. To analyse Whi5-deficient cells, we used a GFP fusion of the N-terminal fragment of Whi5 (whi5N) unable to inhibit the G1/S transition but still subject to cell-cycleregulated export 46 .…”

Section: Methodsmentioning

confidence: 99%

“…4b) or expressing whi5N (Fig. 4c), which produces an N-terminal fragment of Whi5 unable to inhibit the G1/S transition but still subject to cell-cycle-regulated export 46 . A priori, we expected that smaller cells at Start could be obtained by decreasing either k, the slope inherent to the sizer mechanism that defines the linear growth rate dependency, or V 0 , the minimal volume at Start for a cell with a growth rate approaching zero.…”

Section: Cell Size At Start Is Dictated By Volume Growth Rate In G1mentioning

confidence: 99%

The critical size is set at a single-cell level by growth rate to attain homeostasis and adaptation

et al. 2012

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Budding yeast cells are assumed to trigger start and enter the cell cycle only after they attain a critical size set by external conditions. However, arguing against deterministic models of cell size control, cell volume at start displays great individual variability even under constant conditions. Here we show that cell size at start is robustly set at a single-cell level by the volume growth rate in G1, which explains the observed variability. We find that this growth-rate-dependent sizer is intimately hardwired into the start network and the Ydj1 chaperone is key for setting cell size as a function of the individual growth rate. mathematical modelling and experimental data indicate that a growth-rate-dependent sizer is sufficient to ensure size homeostasis and, as a remarkable advantage over a rigid sizer mechanism, it reduces noise in G1 length and provides an immediate solution for size adaptation to external conditions at a population level.

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Prolyl isomerases in gene transcription

Hanes

2015

Biochimica et Biophysica Acta (BBA) - General Subjects

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Background Peptidyl-prolyl isomerases (PPIases) are enzymes that assist in the folding of newly-synthesized proteins and regulate the stability, localization, and activity of mature proteins. They do so by catalyzing reversible (cis-trans) rotation about the peptide bond that precedes proline, inducing conformational changes in target proteins. Scope of Review This review will discuss how PPIases regulate gene transcription by controlling the activity of (1) DNA-binding transcription regulatory proteins, (2) RNA polymerase II, and (3) chromatin and histone modifying enzymes. Major Conclusions Members of each family of PPIase (cyclophilins, FKBPs, and parvulins) regulate gene transcription at multiple levels. In all but a few cases, the exact mechanisms remain elusive. Structure studies, development of specific inhibitors, and new methodologies for studying cis/trans isomerization in vivo represent some of the challenges in this new frontier that merges two important fields. General Significance Prolyl isomerases have been found to play key regulatory roles in all phases of the transcription process. Moreover, PPIases control upstream signaling pathways that regulate gene-specific transcription during development, hormone response and environmental stress. More broadly, although transcription is often rate-limiting in the production of enzymes and structural proteins, post-transcriptional modifications are also critical, and PPIases play key roles here as well (see other reviews in this issue).

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Spatial regulation of the Start repressor Whi5

Cited by 47 publications

References 50 publications

Molecular basis of the functional distinction between Cln1 and Cln2 cyclins

Molecular basis of the functional distinction between Cln1 and Cln2 cyclins

The critical size is set at a single-cell level by growth rate to attain homeostasis and adaptation

Prolyl isomerases in gene transcription

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