The Forkhead transcription factor Hcm1 regulates chromosome segregation genes and fills the S-phase gap in the transcriptional circuitry of the cell cycle

Tata, Pramila; Wu, Wei; Miles, Shawna; Noble, William Stafford; Breeden, Linda

doi:10.1101/gad.1450606

Cited by 263 publications

(430 citation statements)

References 85 publications

(112 reference statements)

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“…HTZ1, HHO1, and CSE4 all show cell-cycle-dependent expression (Pramila et al 2006). SBF might play an important role in their regulation because all three genes possess a single predicted high-affinity SBF-binding site (Figure 1, A and C).…”

Section: Sbf and The Timing Of Histone Gene Activationmentioning

confidence: 99%

Regulation of Histone Gene Expression in Budding Yeast

Eriksson¹,

Ganguli²,

Nagarajavel³

et al. 2012

Genetics

116

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We discuss the regulation of the histone genes of the budding yeast Saccharomyces cerevisiae. These include genes encoding the major core histones (H3, H4, H2A, and H2B), histone H1 (HHO1), H2AZ (HTZ1), and centromeric H3 (CSE4). Histone production is regulated during the cell cycle because the cell must replicate both its DNA during S phase and its chromatin. Consequently, the histone genes are activated in late G1 to provide sufficient core histones to assemble the replicated genome into chromatin. The major core histone genes are subject to both positive and negative regulation. The primary control system is positive, mediated by the histone gene-specific transcription activator, Spt10, through the histone upstream activating sequences (UAS) elements, with help from the major G1/S-phase activators, SBF (Swi4 cell cycle box binding factor) and perhaps MBF (MluI cell cycle box binding factor). Spt10 binds specifically to the histone UAS elements and contains a putative histone acetyltransferase domain. The negative system involves negative regulatory elements in the histone promoters, the RSC chromatin-remodeling complex, various histone chaperones [the histone regulatory (HIR) complex, Asf1, and Rtt106], and putative sequence-specific factors. The SWI/SNF chromatin-remodeling complex links the positive and negative systems. We propose that the negative system is a damping system that modulates the amount of transcription activated by Spt10 and SBF. We hypothesize that the negative system mediates negative feedback on the histone genes by histone proteins through the level of saturation of histone chaperones with histone. Thus, the negative system could communicate the degree of nucleosome assembly during DNA replication and the need to shut down the activating system under replication-stress conditions. We also discuss post-transcriptional regulation and dosage compensation of the histone genes.

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Section: Sbf and The Timing Of Histone Gene Activationmentioning

confidence: 99%

Regulation of Histone Gene Expression in Budding Yeast

Eriksson¹,

Ganguli²,

Nagarajavel³

et al. 2012

Genetics

116

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“…We have generated three microarray data sets through the cell cycle with W303 (Pramila et al, 2006), which carries the ssd1-d2 allele,¤ and another data set with an isogenic strain carrying SSD1-V. All four data sets were obtained from cells synchronized with alpha factor and followed through two consecutive cell cycles. We have compared the global transcript profiles across the cell cycle using DiffExp (Bar-Joseph et al, 2003) and find that there are 889 genes (15%) that show significant differences between cells carrying SSD1-V versus ssd1-d.…”

Section: Ssd1-v Affects Transcript Levels Globallymentioning

confidence: 99%

Budding YeastSSD1-VRegulates Transcript Levels of Many Longevity Genes and Extends Chronological Life Span in Purified Quiescent Cells

Qin

et al. 2009

MBoC

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Ssd1 is an RNA-binding protein that affects literally hundreds of different processes and is polymorphic in both wild and lab yeast strains. We have used transcript microarrays to compare mRNA levels in an isogenic pair of mutant (ssd1-d) and wild-type (SSD1-V) cells across the cell cycle. We find that 15% of transcripts are differentially expressed, but there is no correlation with those mRNAs bound by Ssd1. About 20% of cell cycle regulated transcripts are affected, and most show sharper amplitudes of oscillation in SSD1-V cells. Many transcripts whose gene products influence longevity are also affected, the largest class of which is involved in translation. Ribosomal protein mRNAs are globally down-regulated by SSD1-V. SSD1-V has been shown to increase replicative life span¤ and we show that SSD1-V also dramatically increases chronological life span (CLS). Using a new assay of CLS in pure populations of quiescent prototrophs, we find that the CLS for SSD1-V cells is twice that of ssd1-d cells. INTRODUCTIONSsd1 is an RNA-binding protein (Uesono et al., 1997;Hogan et al., 2008) that can be distinguished from the hundreds of other RNA-binding proteins by its unusual properties. First of all, ssd1 is highly pleiotropic. This locus has at least nine different names because of its having been identified in genetic screens for its effect on minichromosome stability, stress tolerance, membrane trafficking, and cell wall integrity, among other things Kosodo et al., 2001;Vannier et al., 2001;Reinke et al., 2004). Systematic global screens have identified ϳ200 genes that show genetic or physical interactions with Ssd1 (Reguly et al., 2006). These genes show a striking enrichment (Hong et al., 2008) for posttranslational modifiers (p ϭ 10 Ϫ14 ), including 19 kinases and nine histone deacetylases, and genes involved in the cell cycle and cell morphogenesis (p ϭ 10 Ϫ8 ). ssd1 mutants display sensitivity to high osmolarity, caffeine, fungicides¤ and numerous other compounds, which suggests a role for this protein in the maintenance of cell wall integrity (Ibeas et al., 2001;Parsons et al., 2004), but its mechanism of action remains obscure.Despite, or perhaps because of, its impact on so many different cellular functions, SSD1 is a common site of variation in both laboratory strains and natural populations of budding yeast (Wheeler et al., 2003). One possible explanation is that SSD1-V, which encodes the full-length "wildtype" protein, reduces the virulence of Saccharomyces cerevisiae in one mouse model (Wheeler et al., 2003), but SSD1-V is critical in Candida (Gank et al., 2008) and several fungal pathogens of plants for evading their hosts' defense systems (Tanaka et al., 2007). In most cases, genetic interactions with SSD1-V are positive, whereas the premature termination alleles (ssd1-d) cause lethality or a more extreme phenotype. One important exception is the RAM signaling pathway mutants, tao3 (Du and Novick, 2002), and cbk1 (Tong et al., 2001;Jorgensen et al., 2002), whose loss of function is lethal if the SSD1-V a...

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“…40), as well as Hcm1 (ref. 41). Finally, we tested the effect of Ndd1 and Cdh1 m11 on mRNA levels of HOF1, a CLB2 cluster gene whose protein is not degraded by the APC/C 42 .…”

Section: Resultsmentioning

confidence: 99%

“…Cin8, which is also periodically transcribed by Hcm1 (ref. 41) and degraded by the APC/C Cdh1 also loses its periodicity on APC/C Cdh1 inactivation 49 .…”

Section: Discussionmentioning

confidence: 99%

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Degradation of Ndd1 by APC/CCdh1 generates a feed forward loop that times mitotic protein accumulation

et al. 2015

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Ndd1 activates the Mcm1-Fkh2 transcription factor to transcribe mitotic regulators. The anaphase-promoting complex/cyclosome activated by Cdh1 (APC/C Cdh1 ) mediates the degradation of proteins throughout G1. Here we show that the APC/C Cdh1 ubiquitinates Ndd1 and mediates its degradation, and that APC/C Cdh1 activity suppresses accumulation of Ndd1 targets. We confirm putative Ndd1 targets and identify novel ones, many of them APC/C Cdh1 substrates. The APC/C Cdh1 thus regulates these proteins in a dual manner-both pretranscriptionally and post-translationally, forming a multi-layered feedforward loop (FFL). We predict by mathematical modelling and verify experimentally that this FFL introduces a lag between APC/C Cdh1 inactivation at the end of G1 and accumulation of genes transcribed by Ndd1 in G2. This regulation generates two classes of APC/C Cdh1 substrates, early ones that accumulate in S and late ones that accumulate in G2. Our results show how the dual state APC/C Cdh1 activity is converted into multiple outputs by interactions between its substrates.

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The Forkhead transcription factor Hcm1 regulates chromosome segregation genes and fills the S-phase gap in the transcriptional circuitry of the cell cycle

Cited by 263 publications

References 85 publications

Regulation of Histone Gene Expression in Budding Yeast

Regulation of Histone Gene Expression in Budding Yeast

Budding YeastSSD1-VRegulates Transcript Levels of Many Longevity Genes and Extends Chronological Life Span in Purified Quiescent Cells

Degradation of Ndd1 by APC/CCdh1 generates a feed forward loop that times mitotic protein accumulation

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