Hog1 Targets Whi5 and Msa1 Transcription Factors To Downregulate Cyclin Expression upon Stress

González-Novo, Alberto; Jiménez, Javier; Clotet, Josep; Nadal-Ribelles, Mariona; Cavero, Santiago; Nadal, Eulàlia de; Posas, Francesc

doi:10.1128/mcb.01279-14

Cited by 42 publications

(54 citation statements)

References 59 publications

(87 reference statements)

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“…Msa1 and Msa2 also associate with Ste12 and Tec1 to bind and activate two genes involved in pseudohyphal development (van der Felden, et al 2014). In osmotic stress, Msa1 and Whi5 are phosphorylated by Hog1 kinase and this leads to inhibition of SBF targets (Gonzalez-Novo, et al 2015). These observations suggest that Msa1 and Msa2 are involved in coordinating cell division and development in response to environmental changes.…”

Section: Novel Quiescence-specific Regulators Of G1/s Genesmentioning

confidence: 99%

A common strategy for initiating the transition from proliferation to quiescence

Miles

Breeden

2016

Curr Genet

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Development, tissue renewal and long term survival of multi-cellular organisms is dependent upon the persistence of stem cells that are quiescent, but retain the capacity to re-enter the cell cycle to self-renew, or to produce progeny that can differentiate and re-populate the tissue. Deregulated release of these cells from the quiescent state, or preventing them from entering quiescence, results in uncontrolled proliferation and cancer. Conversely, loss of quiescent cells, or their failure to re-enter cell division, disrupts organ development and prevents tissue regeneration and repair. Understanding the quiescent state and how cells control the transitions in and out of this state is of fundamental importance. Investigations into the mechanics of G1 arrest during the transition to quiescence continue to identify striking parallels between the strategies used by yeast and mammals to regulate this transition. When cells commit to a stable but reversible arrest, the G1/S genes responsible for promoting S phase must be inhibited. This process, from yeast to humans, involves the formation of quiescence-specific complexes on their promoters. In higher cells these so-called DREAM complexes of E2F4/DP/RBL/MuvB recruit the highly conserved histone deacetylase HDAC1, which leads to local histone deacetylation and repression of S phase-promoting transcripts. Quiescent yeast cells also show pervasive histone deacetylation by the HDAC1 counterpart Rpd3. In addition, these cells contain quiescence-specific regulators of G1/S genes: Msa1 and Msa2, which can be considered components of the yeast equivalent of the DREAM complex. Despite a lack of physical similarities, the goals and the strategies used to achieve a reversible transition to quiescence are highly conserved. This motivates a detailed study of this process in the simple model organism: budding yeast.

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Section: Novel Quiescence-specific Regulators Of G1/s Genesmentioning

confidence: 99%

A common strategy for initiating the transition from proliferation to quiescence

Miles

Breeden

2016

Curr Genet

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“…Our data suggests that this G1/S arrest occurs through crosstalk to the Hog1 pathway, since downregulation of SBF/MBF target genes and initial cell cycle arrest do not occur in hog1D cells. This Hog1-dependent arrest likely occurs through a combination of its effect on transcription and its ability to upregulate Cdk1 inhibitors, as previously described (Bellí et al, 2001;Chang et al, 2017;Escoté et al, 2004;González-Novo et al, 2015).…”

Section: Discussionmentioning

confidence: 56%

“…Remarkably, we find that CN downregulates targets of multiple cell cycle TFs through distinct mechanisms. We find that CN blocks expression of G1/S genes by stimulating the activity of the stress-activated MAPK Hog1, an established inhibitor of G1/S TFs (Bellí et al, 2001;González-Novo et al, 2015). In contrast, CN inactivates G2/M TFs through both Hog1-dependent and -independent mechanisms.…”

Section: Introductionmentioning

confidence: 80%

“…Together CN and Hog1 promote widespread changes in the expression of cell cycle-regulated genes (Figure 7). The concurrent activation of these pathways triggers an immediate downregulation of several clusters of cell cycle genes within 10 minutes of CaCl2 treatment: Hog1 mediates inactivation of SBF and MBF to downregulate G1/S genes (Bellí et al, 2001;González-Novo et al, 2015), CN dephosphorylates and inactivates the S-phase TF Hcm1 (Arsenault et al, 2015), and CN and Hog1 both contribute to Swe1 activation, which results in dephosphorylation of G2/M TFs Ndd1 and Fkh2. After approximately 20 minutes, inactivation of these TFs is reinforced as CN functions to maintain Hog1 activation, and levels of Fkh2 and Ndd1 proteins decrease through a Hog1-dependent pathway.…”

Section: Discussionmentioning

confidence: 99%

“…In budding yeast, the stress-activated MAPK Hog1 has two roles in controlling entry into S phase. Hog1 both inhibits the SBF and MBF TF complexes that drive expression of G1/S genes (Bellí et al, 2001;González-Novo et al, 2015), and increases levels of the Cdk1 inhibitors Sic1 and Cip1, which inhibit G1 cyclin/Cdk complexes and block entry into S phase (Chang et al, 2017;Escoté et al, 2004).…”

Section: Cn Activates the Sapk Hog1 To Downregulate G1/s Genesmentioning

confidence: 99%

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The coordinate actions of calcineurin and Hog1 mediate the response to cellular stress through multiple nodes of the cell cycle network

et al. 2019

Preprint

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Upon exposure to environmental stressors, cells transiently arrest the cell cycle while they adapt and restore homeostasis. A challenge for all cells is to distinguish between diverse stress signals and coordinate the appropriate adaptive response with cell cycle arrest. Here we investigate the role of the stress-activated phosphatase calcineurin (CN) in this process and show that CN utilizes multiple pathways to control the cell cycle. Upon activation, CN inhibits transcription factors (TFs) that regulate the G1/S transition through activation of the stress-activated MAPK Hog1. In contrast, CN inactivates G2/M TFs through a combination of Hog1-dependent and -independent mechanisms. These findings demonstrate that CN and Hog1 act in a coordinated manner at multiple nodes of the cell cycle-regulatory network to rewire gene expression and arrest cells in response to stress. Our results suggest that crosstalk between CN and stress-activated MAPKs helps cells tailor their adaptive responses to specific stressors.

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How Do Yeast and Other Fungi Recognize and Respond to Genome Perturbations?

Skoneczna

Król

Skoneczny

2018

Stress Response Mechanisms in Fungi

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Hog1 Targets Whi5 and Msa1 Transcription Factors To Downregulate Cyclin Expression upon Stress

Cited by 42 publications

References 59 publications

A common strategy for initiating the transition from proliferation to quiescence

A common strategy for initiating the transition from proliferation to quiescence

The coordinate actions of calcineurin and Hog1 mediate the response to cellular stress through multiple nodes of the cell cycle network

How Do Yeast and Other Fungi Recognize and Respond to Genome Perturbations?

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