The <i>HTL1</i> gene (YCR020W‐b) of <i>Saccharomyces cerevisiae</i> is necessary for growth at 37°C, and for the conservation of chromosome stability and fertility

Lanzuolo, Chiara; Ederle, Sara; Pollice, Alessandra; Russo, Francesco; Storlazzi, Aurora; Pulitzer, John F.

doi:10.1002/yea.778

Cited by 13 publications

(29 citation statements)

References 20 publications

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“…Heterozygous htl1⌬::TRP1 diploids were induced to sporulate, and haploid segregants were dissected. Tryptophan prototrophy cosegregated with temperature sensitivity for growth at or above 34°C, consistent with the previous report by Lanzuolo et al (25). As anticipated, the htl1⌬ mutants were capable of growth on glycerol-containing medium (Fig.…”

Section: Resultssupporting

confidence: 91%

“…To elucidate the nature of the second pathway branch and to identify novel targets of Pkc1, we conducted a screen for mutations that displayed additive growth defects with a pkc1 ts mutation. Here we report the isolation of HTL1, a gene previously reported to be required for genomic stability and for growth at elevated temperatures (25). We demonstrate that HTL1 is important for cell cycle progression.…”

mentioning

confidence: 71%

“…The remaining two mutants (DL2822 and DL2823) were both rescued by plasmids (designated A3 and A4, respectively) containing overlapping fragments from the right arm of chromosome 3, with PET18, MAK31, HTL1, and HSP30 in common. Deletion analysis of these plasmids revealed that the smallest segment allowing sectoring of strains DL2822 and DL2823 at 23°C and growth at 37°C was a 527-bp EcoRV-HindIII fragment containing only HTL1/YCR020W-B (named HTL for high temperature lethal [25]) (Fig. 1A).…”

Section: Resultsmentioning

confidence: 99%

“…Previously described PET18 mutants (28) resulted from spontaneous deletions of greater than 10 kb from the right arm of chromosome 3 (43). Such mutants are temperature sensitive due to loss of HTL1 (25) and unable to grow on nonfermentable carbon sources. The latter phenotype is known to result from loss of function of another, as yet unidentified gene within the deleted region (25).…”

Section: Resultsmentioning

confidence: 99%

“…Such mutants are temperature sensitive due to loss of HTL1 (25) and unable to grow on nonfermentable carbon sources. The latter phenotype is known to result from loss of function of another, as yet unidentified gene within the deleted region (25). We found that like the previously described mutants, strains DL2822 and DL2823 were unable to grow on rich medium containing glycerol as the sole carbon source (Fig.…”

Section: Resultsmentioning

confidence: 99%

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HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae

Romeo

Angus-Hill

Sobering

et al. 2002

Molecular and Cellular Biology

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RSC is an essential chromatin remodeling complex in Saccharomyces cerevisiae that performs central roles in transcriptional regulation and cell cycle progression. Here we identify Htl1 as a novel factor that associates with the RSC complex both physically and functionally. We isolated HTL1 through a genetic screen for mutants that displayed additive growth defects with a conditional mutation in the protein kinase C gene (PKC1), which has been suggested through genetic connections to interact functionally with RSC. Several lines of evidence connect HTL1 to RSC function. First, an htl1⌬ mutant displayed temperature-sensitive growth and a G 2 /M cell cycle arrest at restrictive temperatures, a phenotype similar to that of strains with conditional mutations in essential RSC components. Second, we isolated RSC3, which encodes a component of the RSC complex, as a dosage suppressor of the htl1⌬ growth arrest. Third, an htl1⌬ mutant displayed additive growth defects with conditional rsc3 alleles. Fourth, overexpression of HTL1 suppressed the growth defect of a strain with a conditional mutation in another RSC component, RSC8. Finally, we demonstrate that Htl1 is a nuclear protein that can associate in vivo with a fraction of the RSC complex. We propose that an RSC-Htl1 complex acts coordinately with protein kinase C to regulate the G 2 /M transition.

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Section: Resultssupporting

confidence: 91%

mentioning

confidence: 71%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae

Romeo

Angus-Hill

Sobering

et al. 2002

Molecular and Cellular Biology

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Accurate repair of non‐cohesive, double strand breaks in Saccharomyces cerevisiae: enhancement by homology‐assisted end‐joining

Moscariello

Florio

Pulitzer

2010

Yeast

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Although the joining of blunt ends in yeast by non-homologous end joining (NHEJ) is reported to be inefficient in comparison to cohesive-end joining (Boulton and Jackson, 1996), we find that efficiency varies greatly, depending on strain, growth phase and sequence. In particular, the levels of efficiency of recircularization of a plasmid linearized by non-cohesive cleavage is augmented to that of cohesive end joining if the cleavage cut site is flanked by sequences present in the genome. We call this enhancement 'homology-assisted end joining' (HAEJ), which depends on components of the NHEJ repair pathway and, in some cases, on components of the homologous recombination (HR) pathway and on Htl1 a component of the remodels structure of chromatin (RSC) complex. The homologous genome sequences are not used as templates for repair DNA synthesis, but may facilitate end-to-end collision and ligation by providing a track for guided diffusion.

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The defects in cell wall integrity and G₂–M transition of the ∆htl1 mutant are interconnected

Wang¹,

Cheng²

2011

Yeast

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The Saccharomyces cerevisiae RSC (remodel the structure of chromatin) complex is involved in functions associated with the transcriptional regulation, cell cycle progression, DNA damage repair and cell wall integrity. Here we investigate the cellular functioning of HTL1, which encodes a non-essential subunit of the RSC complex. The results show that the Δhtl1 mutant displays a characteristic defect in cell wall integrity, and the phenotype of the Δhtl1 cells, which include the cell wall defect, temperature sensitivity and ploidy increase, are rescued by the osmotic stabilizer sorbitol but not by overexpression of PKC1, the signalling kinase important for the cell wall biogenesis and stress response. In addition, the expression level of Slt2p, the MAP kinase downstream of the cell wall integrity pathway, is upregulated in Δhtl1 cells. Furthermore, the mitotic arrest of the Δhtl1 mutant is moderated by 1 M sorbitol and deletion of SLT2. The present findings suggest that HTL1 may play a role that is different from other RSC components in terms of cell wall integrity and the G 2 -M transition. The results also suggest that the defects in cell wall integrity and the G 2 -M transition of the Δhtl1 mutant are interconnected.

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The HTL1 gene (YCR020W‐b) of Saccharomyces cerevisiae is necessary for growth at 37°C, and for the conservation of chromosome stability and fertility

Cited by 13 publications

References 20 publications

HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae

HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae

Accurate repair of non‐cohesive, double strand breaks in Saccharomyces cerevisiae: enhancement by homology‐assisted end‐joining

The defects in cell wall integrity and G₂–M transition of the ∆htl1 mutant are interconnected

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The HTL1 gene (YCR020W‐b) of Saccharomyces cerevisiae is necessary for growth at 37°C, and for the conservation of chromosome stability and fertility

Cited by 13 publications

References 20 publications

HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae

HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae

Accurate repair of non‐cohesive, double strand breaks in Saccharomyces cerevisiae: enhancement by homology‐assisted end‐joining

The defects in cell wall integrity and G2–M transition of the ∆htl1 mutant are interconnected

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The defects in cell wall integrity and G₂–M transition of the ∆htl1 mutant are interconnected