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Dataset | Description | Keywords | Number of Conditions | Reference |
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A common molecular mechanism underlies the role of Mps1 in chromosome biorientation and the spindle assembly checkpoint | The conserved Mps1 kinase corrects improper kinetochore-microtubule attachments, thereby ensuring chromosome biorientation. Yet, its critical targets in this process remain elusive. Mps1 is also involved in the spindle assembly checkpoint (SAC), the surveillance mechanism halting chromosome segregation until biorientation is attained. Its role in SAC activation is antagonized by the PP1 phosphatase and involves phosphorylation of Knl1/Spc105, which recruits Bub1 to kinetochores to promote assembly of SAC effector complexes. A crucial question is whether error correction and SAC activation are part of a single device or separable pathways. Here we characterise a novel yeast mutant, mps1-3, defective in chromosome biorientation and SAC activation. Through an unbiased screen for suppressors, we found that mutations lowering PP1 levels at Spc105 or forced association of Bub1 with Spc105 reinstate both chromosome biorientation and SAC signalling in mps1-3 cells. Our data strongly argue that Mps1-dependent phosphorylation of the Knl1/Spc105 kinetochore scaffold is critical for Mps1 function in both chromosome biorientation and SAC activation, thus supporting the idea that a common sensory apparatus simultaneously elicits error correction and SAC signalling. | genetic interaction | 12 | Benzi G, et al. (2020) PMID:32307893 |
A comprehensive synthetic genetic interaction network governing yeast histone acetylation and deacetylation | Histone acetylation and deacetylation are among the principal mechanisms by which chromatin is regulated during transcription, DNA silencing, and DNA repair | genetic interaction, histone modification | 44 | Lin YY, et al. (2008) PMID:18676811 |
A functional connection between translation elongation and protein folding at the ribosome exit tunnel in Saccharomyces cerevisiae | Proteostasis is a fundamental network of cellular pathways that ensures the optimal concentration and composition of correctly folded proteins within cells in normal and stress conditions. Among key components of this network are the molecular chaperones, which mediate protein folding but also act as modulators of protein synthesis. We have reported on a functional link between translation and de novo folding of proteins in the yeast Saccharomyces cerevisiae by uncovering a specific synthetic-lethal interaction between apparent unrelated mutant variants, the uL3[W255C] variant of the ribosomal protein uL3 and the null mutants of Zuo1 and Ssz1. Zuo1 and Ssz1 are components of the chaperone system named as ribosome-associated complex. Here, we performed a genome-wide analysis of ribosome dynamics by 5PSeq (Pelechano et al. 2015 PMID 2604644) in strains harbouring either wild-type uL3 or mutant uL3[W255C] in the presence or absence of Zuo1 or Ssz1. This method allows the study of ribosome dynamics, by sequencing 5’ phosphorylated mRNA co-translational degradation intermediates. Our results indicate that the rpl3[W255C] mutant is slightly impaired in translation elongation, defect that is significantly enhanced when combined with the deprivation of either Zuo1 or Ssz1. | genetic interaction | 18 | Rodríguez-Galán O, et al. (2021) PMID:33330942 |
A high-resolution protein architecture of the budding yeast genome | The genome-wide architecture of chromatin-associated proteins that maintains chromosome integrity and gene regulation is ill defined. Here we use chromatin immunoprecipitation, exonuclease digestion and DNA sequencing (ChIP–exo/seq) to define this architecture in Saccharomyces cerevisiae. We identify 21 meta-assemblages consisting of roughly 400 different proteins that are related to DNA replication, centromeres, subtelomeres, transposons, and transcription by RNA polymerase (Pol) I, II and III. Replication proteins engulf a nucleosome, centromeres lack a nucleosome, and repressive proteins encompass three nucleosomes at subtelomeric X-elements. We find that most promoters associated with Pol II evolved to lack a regulatory region, having only a core promoter. These constitutive promoters comprise a short nucleosome-free region (NFR) adjacent to a +1 nucleosome, which together bind the transcription-initiation factor TFIID to form a preinitiation complex (PIC). Positioned insulators protect core promoters from upstream events. A small fraction of promoters evolved an architecture for inducibility, whereby sequence-specific transcription factors (ssTFs) create a nucleosome-depleted region (NDR) that is distinct from an NFR. We describe structural interactions among ssTFs, their cognate cofactors and the genome. These interactions include the nucleosomal and transcriptional regulators RPD3-L, SAGA, NuA4, Tup1, Mediator and SWI–SNF. Surprisingly, we do not detect interactions between ssTFs and TFIID, suggesting that such interactions do not stably occur. Our model for gene induction involves ssTFs, cofactors and general factors such as TBP and TFIIB, but not TFIID. By contrast, constitutive transcription involves TFIID but not ssTFs and cofactors. From this, we define a highly integrated network of gene regulation by ssTFs. | transcription, genetic interaction | 1251 | Badjatia N, et al. (2021) PMID:33472084 |
An inducible CRISPR-interference library for genetic interrogation of Saccharomyces cerevisiae biology | Genome-scale CRISPR interference (CRISPRi) is widely utilized to study cellular processes in a variety of organisms. To date, a genome-wide CRISPRi library, optimized for targeting the Saccharomyces cerevisiae genome, has not been presented. Here, we have generated a comprehensive, inducible CRISPRi library, based on spacer design rules optimized for yeast. We have validated this library for genome-wide interrogation of gene function across a variety of applications, including accurate discovery of haploinsufficient genes and identification of enzymatic and regulatory genes involved in adenine and arginine biosynthesis. The comprehensive nature of the library also revealed refined spacer design parameters for transcriptional repression, including location, nucleosome occupancy and nucleotide features. CRISPRi screens using this library can identify genes and pathways with high precision and low false discovery rate across a variety of experimental conditions, enabling rapid and reliable genome-wide assessment of genetic function and interactions in S. cerevisiae. | genetic interaction | 20 | Momen-Roknabadi A, et al. (2020) PMID:33247197 |
Ash1 and Tup1 Dependent Repression of the Saccharomyces cerevisiae HO promoter Requires Activator-Dependent Nucleosome Eviction | Transcriptional regulation of the Saccharomyces cerevisiae HO gene is highly complex, requiring a balance of multiple activating and repressing factors to ensure that only a few transcripts are produced in mother cells within a narrow window of the cell cycle. Here, we show that the Ash1 repressor associates with two DNA sequences that are usually concealed within nucleosomes in the HO promoter and recruits the Tup1 corepressor and the Rpd3 histone deacetylase, both of which are required for full repression in daughters. Genome-wide ChIP identified greater than 200 additional sites of co-localization of these factors, primarily within large, intergenic regions from which they could regulate adjacent genes. Most Ash1 binding sites are in nucleosome depleted regions (NDRs), while a small number overlap nucleosomes, similar to HO. We demonstrate that Ash1 binding to the HO promoter does not occur in the absence of the Swi5 transcription factor, which recruits coactivators that evict nucleosomes, including the nucleosomes obscuring the Ash1 binding sites. In the absence of Swi5, artificial nucleosome depletion allowed Ash1 to bind, demonstrating that nucleosomes are inhibitory to Ash1 binding. The location of binding sites within nucleosomes may therefore be a mechanism for limiting repressive activity to periods of nucleosome eviction that are otherwise associated with activation of the promoter. Our results illustrate that activation and repression can be intricately connected, and events set in motion by an activator may also ensure the appropriate level of repression and reset the promoter for the next activation cycle. | genetic interaction | 12 | Parnell EJ, et al. (2020) PMID:33382702 |
Basis of Specificity for a Conserved Promiscuous Chromatin Remodeling Protein | This SuperSeries is composed of the SubSeries listed below. | genetic interaction | 72 | Donovan DA, et al. (2021) PMID:33576335 |
Basis of Specificity for a Conserved Promiscuous Chromatin Remodeling Protein [ChIP-Seq] | We propose an interacting barrier mechanism for cooperation between Isw2-related proteins and sequence-specific DNA binding factors. | genetic interaction | 11 | Donovan DA, et al. (2021) PMID:33576335 |
Basis of Specificity for a Conserved Promiscuous Chromatin Remodeling Protein [Mnase-seq] | We propose an interacting barrier mechanism for cooperation between Isw2-related proteins and sequence-specific DNA binding factors. | genetic interaction | 49 | Donovan DA, et al. (2021) PMID:33576335 |
Basis of Specificity for a Conserved Promiscuous Chromatin Remodeling Protein [RNA-Seq] | We propose an interacting barrier mechanism for cooperation between Isw2-related proteins and sequence-specific DNA binding factors. | genetic interaction | 12 | Donovan DA, et al. (2021) PMID:33576335 |