Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE24686
PROVIDER: PRJNA132255 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Splicing regulatory networks are essential components of eukaryotic gene expression programs, yet little is known about how they are integrated with transcriptional regulatory networks into coherent gene expression programs. Here we define the MER1 splicing regulatory network and examine its role in the gene expression program during meiosis in budding yeast. Mer1p splicing factor promotes splicing of just four pre-mRNAs. All four Mer1p-responsive genes also require Nam8p for splicing activation by Mer1p, however other genes require Nam8p but not Mer1p, exposing an overlapping meiotic splicing network controlled by Nam8p. MER1 mRNA and three of the four Mer1p substrate pre-mRNAs are induced by the transcriptional regulator Ume6p. This unusual arrangement delays expression of Mer1p-responsive genes relative to other genes under Ume6p control. Products of Mer1p-responsive genes are required for initiating and completing recombination, and for activation of Ndt80p, the transcriptional network that controls subsequent steps in the program. Thus the MER1 splicing regulatory network mediates the dependent relationship between the UME6 and NDT80 transcriptional regulatory networks in the meiotic gene expression program. This work reveals how splicing regulatory networks can be interlaced with transcriptional regulatory networks in eukaryotic gene expression programs. This SuperSeries is composed of the SubSeries listed below.
2011-04-05 | GSE24686 | GEO
Project description:Despite its streamlined genome, there are important examples of regulated RNA splicing in Saccharomyces cerevisiae. One of the most striking is the regulated splicing of meiotic transcripts, part of the dramatic reprogramming of gene expression upon meiotic onset. Here we show a crucial role for the chromatin remodeler Snf2, part of the Swi/Snf complex in meiotic regulation of splicing. We find that the complex affects meiotic splicing in several ways. First, meiosis-specific expression of the splicing activator Mer1 is Swi/Snf dependent, involves precise timing of acetylation of histone H3K9 at the MER1 locus, and changes in the acetylation state of Snf2. Additionally, Swi/Snf abundance regulates meiosis-specific downregulation of ribosomal protein encoding RNAs, leading to the redistribution of spliceosomes from this abundant class of intron-containing RNAs to meiotic transcripts. This regulation is achieved by rapid downregulation of the Snf2 protein. Taken together these data reveal that the Swi/Snf complex coordinates a cascade of events to direct the regulated splicing of meiotic genes, establishing it as a master regulator of meiotic splicing in S. cerevisiae.
2017-04-20 | GSE94404 | GEO
Project description:Here we studied the budding yeast Lachancea kluyveri, a cousin of the model Saccharomyces cerevisiae, in order to try to understand the mechanism responsible for the absence of meiotic recombination on its almost entire sex chromosome (Brion et al. 2017). We performed meiotic DSB mapping using CC-seq (Gittens 2019). Briefly, we observed a distribution of meiotic DSBs mainly in gene promoters as in S. cerevisiae and a depletion within Lakl0C-left (the 1 Mb long domain on the sex chromosome with no meiotic recombination). Also, we noted a poor conservation of DSB hotspots strength between L. kluyveri and S. cerevisiae.
2024-03-18 | GSE237706 | GEO
Project description:To investigate the relationship between chromatin organization and meiotic processes, we used Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE) to map open chromatin during the transition from mitosis to meiosis in the budding yeast Saccharomyces cerevisiae.
2009-07-01 | GSE16163 | GEO
Project description:To better understand the gene regulatory mechanisms that program developmental processes, we carried out simultaneous, genome-wide measurements of mRNA, translation and protein through meiotic differentiation in budding yeast.
2018-01-02 | MSV000081874 | MassIVE
Project description:In Saccharomyces cerevisiae, most ribosomal proteins are produced from duplicated genes. These nearly identical protein pairs are expressed at varying levels, with one ‘major paralog’ usually predominating. The minor paralog is highly transcribed but held in check through reduced intron removal, but the mechanism and purpose of this copy-specific repression remains unclear. In this study, we searched for proteins that achieve copy-specific expression by acting through the intron of the minor paralog of the model duplicated small ribosomal subunit protein S9 genes. By mass spectrometry and gene deletion we demonstrate that the transcription factors Rim101 and Taf14 bind to the intron and inhibit the splicing of the minor RPS9 paralog. RPS9A is then specifically de-repressed during meiosis to ensure optimal expression of meiotic genes and efficient sporulation. Our results reveal a new regulatory paradigm where transcriptional factors can also modulate splicing rates to optimize the expression of duplicated ribosomal protein genes.
2024-12-20 | PXD050249 | Pride
Project description:The Spo11-generated double-strand breaks (DSBs) that initiate meiotic recombination are non-randomly distributed across the genome. Here, we use S1Seq mapping to map the distribution of meiotic DSBs in spo11 mutant strains of Saccharomyces cerevisiae.
2020-05-12 | GSE150313 | GEO
Project description:The Spo11-generated double-strand breaks (DSBs) that initiate meiotic recombination are non-randomly distributed across the genome. Here, we use Spo11-oligonucleotide complexes to map the distribution of meiotic DSBs in a spo11 mutant strain of Saccharomyces cerevisiae.
2020-05-12 | GSE150314 | GEO
Project description:Changes in gene regulation rapidly accumulate between species and may contribute to reproductive isolation through misexpression of genes in interspecific hybrids. Hybrid misexpression, defined by expression levels outside the range of both parental species, is thought to be a result of cis- and trans-acting regulatory changes that interact in the hybrid, or arise from changes in the relative abundance of various tissues or cell types due to defects in developmental. Here, we show that misexpressed genes in a sterile interspecific Saccharomyces yeast hybrid result from a heterochronic shift in the timing of the normal meiotic gene expression program. By tracking nuclear divisions, we find that S. cerevisiae initiates meiosis earlier than its closest known relative, S. paradoxus, yet both species complete meiosis at the same time. Although the hybrid up- and down-regulates genes in a similar manner to both parents, the hybrid meiotic program occurs earlier than both parents. The timing shift results in a heterochronic pattern of misexpression throughout meiosis I and the beginning of meiosis II. Coincident with the timing of misexpression, we find an increase in the relative abundance of opposing cis and trans-acting changes and compensatory changes, as well as a transition from predominantly trans-acting to cis-acting expression divergence over the course of meiosis. However, misexpression does not appear to be a direct consequence of cis- and trans-acting regulatory divergence. Our results demonstrate that hybrid misexpression in yeast results from a heterochronic shift in the meiotic gene expression program. We analyzed three biological replicates of the parental yeast strains, S. cerevisiae and S. paradoxus, and four replicates of their hybrid over four developmental time points. Two hybrid replicates contain MATa from S. cerevisiae and MATalpha from S. paradoxus. The other two hybrid replicates are reciprocal crosses. The developmental time points are T0, which serves as a control, and is the moment cells enter sporulation media. M1 is the beginning of meiosis I. M1/M2 is the overlap of the end of meiosis I and the beginning of meiosis II. M2 is the end of meiosis II.
2013-10-31 | E-GEOD-51809 | biostudies-arrayexpress
Project description:The Spo11-generated double-strand breaks (DSBs) that initiate meiotic recombination are non-randomly distributed across the genome. Here, we use Spo11-oligonucleotide complexes, a byproduct of DSB formation, to map the distribution of meiotic DSBs in pch2 and sir2 mutant strains of Saccharomyces cerevisiae.
2018-11-25 | GSE122882 | GEO