Cell cycle-specific expression of the SWI4 transcription factor is required for the cell cycle regulation of HO transcription.

Breeden, Linda; Mikesell, Glen

doi:10.1101/gad.5.7.1183

Cited by 80 publications

(65 citation statements)

References 34 publications

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“…It appears that the CTSl gene is transcribed during a-factor arrest, although it is possible that a-factor stabilizes previously synthesized CTSl mRNA. HO and CTSl regulation are similar in that mRNA accumulation is substantially reduced during the first cell cycle following release from a-factor arrest Breeden and Mikesell 1991). HO and CTSl differ with repect to cell-type regulation.…”

Section: Ctsl Is Cell Cycle Regulatedmentioning

confidence: 71%

“…These two regulatory pathways, SWI5 activation of HO and ACE2 activation of CTSl, show a number of common features: The transcription factor gene is expressed in G2, the transcription factor shows cell cycle-dependent cellular localization, and the target gene is expressed late in Gj. The SWI4 and SWI6 genes are required for expression of both HO and CTSl, as well as the G^ cyclins of yeast (Breeden and Mikesell 1991;Nasmyth and Dirick 1991;Ogas et al 1991). Although these two regulatory pathways reflect the same pattern, they are clearly distinct pathways.…”

Section: Genes and Developmentmentioning

confidence: 99%

“…The same aliquots of cells were used in this experiment and in the experiment shown in Fig. 2 regulation of HO (Stern et al 1984;Breeden and Nasmyth 1987;Breeden and Mikesell 1991). SWI4 and SWIS are components of a cell cycle-regulated DNAbinding activity and are also transcriptional activators of the Gi cyclins of yeast, CLNl, CLN2, and HSC26 (Andrevy^s and Herskowitz 1989;Nasmyth and Dirick 1991;Ogas et al 1991).…”

Section: + -+ -Ace2mentioning

confidence: 99%

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Parallel pathways of gene regulation: homologous regulators SWI5 and ACE2 differentially control transcription of HO and chitinase.

Dohrmann¹,

Butler²,

Tamai³

et al. 1992

Genes Dev.

220

246

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Two independent pathways oJ transcriptional regulation that show functional homology have been identified in yeast. It has been demonstrated previously that SWI5 encodes a zinc finger DNA-binding protein whose transcription and cellular localization both are cell cycle regulated. We show that ACE2, whose zinc finger region is nearly identical to that of SWI5, shows patterns of cell cycle-regulated transcription and nuclear localization similar to those seen previously for SMTIS. Despite their similarities, SWI5 and ACE2 function in separate pathways of transcriptional regulation. SWI5 is a transcriptional activator of the HO endonuclease gene, whereas ACE2 is not. In contrast, ACE2 is a transcriptional activator of the CTSl gene (which encodes chitinase), whereas SWI5 is not. An additional parallel between the SWI5/HO pathway and the ACE2/CTS1 pathway is that HO and CTSl both are cell cycle regulated in the same way, and HO and CTSl both require the SWI4 and SWr6 transcriptional activators. Overproduction of either SWI5 or ACE2 permits transcriptional activation of the target gene from the other pathway, suggesting that the DNA-binding proteins are capable of binding in vivo to promoters that they do not usually activate. Chimeric SWI5/ACE2 protein fusion experiments suggest that promoter specificity resides in a domain distinct from the zinc finger domain.

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Section: Ctsl Is Cell Cycle Regulatedmentioning

confidence: 71%

Section: Genes and Developmentmentioning

confidence: 99%

Section: + -+ -Ace2mentioning

confidence: 99%

See 1 more Smart Citation

Parallel pathways of gene regulation: homologous regulators SWI5 and ACE2 differentially control transcription of HO and chitinase.

Dohrmann¹,

Butler²,

Tamai³

et al. 1992

Genes Dev.

220

246

View full text Add to dashboard Cite

show abstract

“…SBF contains two subunits, Swi4 and Swi6. In the absence of Swi6, Swi4 can act as a weaker activator for the target genes (26). The model predicts that a partially active SBF would reduce both the firing frequency and amplitude.…”

Section: Discussionmentioning

confidence: 99%

Stochastic expression and epigenetic memory at the yeast HO promoter

Zhang¹,

Yoon²,

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Eukaryotic gene regulation usually involves sequence-specific transcription factors and sequence-nonspecific cofactors. A large effort has been made to understand how these factors affect the average gene expression level among a population. However, little is known about how they regulate gene expression in individual cells. In this work, we address this question by mutating multiple factors in the regulatory pathway of the yeast HO promoter (HOpr) and probing the corresponding promoter activity in single cells using time-lapse fluorescence microscopy. We show that the HOpr fires in an "on/off" fashion in WT cells as well as in different genetic backgrounds. Many chromatin-related cofactors that affect the average level of HO expression do not actually affect the firing amplitude of the HOpr; instead, they affect the firing frequency among individual cell cycles. With certain mutations, the bimodal expression exhibits short-term epigenetic memory across the mitotic boundary. This memory is propagated in "cis" and reflects enhanced activator binding after a previous "on" cycle. We present evidence that the memory results from slow turnover of the histone acetylation marks.

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“…All rich (YEP) and minimal (YC) media, growth conditions, and alpha factor synchronizations were as described before (6). Cultures used for elutriation were grown in YC-Ura glucose media and then inoculated into YEPD media and grown to an optical density at 600 nm of 2.5 to 3.…”

Section: Methodsmentioning

confidence: 99%

Rad53 Checkpoint Kinase Phosphorylation Site Preference Identified in the Swi6 Protein of Saccharomyces cerevisiae

Sidorova

Breeden

2003

Molecular and Cellular Biology

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Rad53 of Saccharomyces cerevisiae is a checkpoint kinase whose structure and function are conserved among eukaryotes. When a cell detects damaged DNA, Rad53 activity is dramatically increased, which ultimately leads to changes in DNA replication, repair, and cell division. Despite its central role in checkpoint signaling, little is known about Rad53 substrates or substrate specificity. A number of proteins are implicated as Rad53 substrates; however, the evidence remains indirect. Previously, we have provided evidence that Swi6, a subunit of the Swi4/Swi6 late-G 1 -specific transcriptional activator, is a substrate of Rad53 in the G 1 /S DNA damage checkpoint. In the present study we identify Rad53 phosphorylation sites in Swi6 in vitro and demonstrate that at least one of them is targeted by Rad53 in vivo. Mutations in these phosphorylation sites in Swi6 shorten but do not eliminate the Rad53-dependent delay of the G 1 -to-S transition after DNA damage. We derive a consensus for Rad53 site preference at positions ؊2 and ؉2 (؊2/؉2) and identify its potential substrates in the yeast proteome. Finally, we present evidence that one of these candidates, the cohesin complex subunit Scc1 undergoes DNA damage-dependent phosphorylation, which is in part dependent on Rad53.

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Cell cycle-specific expression of the SWI4 transcription factor is required for the cell cycle regulation of HO transcription.

Cited by 80 publications

References 34 publications

Parallel pathways of gene regulation: homologous regulators SWI5 and ACE2 differentially control transcription of HO and chitinase.

Parallel pathways of gene regulation: homologous regulators SWI5 and ACE2 differentially control transcription of HO and chitinase.

Stochastic expression and epigenetic memory at the yeast HO promoter

Rad53 Checkpoint Kinase Phosphorylation Site Preference Identified in the Swi6 Protein of Saccharomyces cerevisiae

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