Rewiring of the phosphoproteome executes two meiotic divisions
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion Lumos, Orbitrap Exploris 480
ORGANISM(S): Saccharomyces Cerevisiae (baker's Yeast)
TISSUE(S): Cell Culture
SUBMITTER: 
Adele Marston
LAB HEAD: Adele Marston
PROVIDER: PXD048618 | Pride | 2024-03-21
REPOSITORIES: Pride
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Project description:Gametes are produced via meiosis, a specialized cell division associated with frequent errors which cause birth defects and infertility. Uniquely in meiosis I, homologous chromosomes segregate to opposite poles, usually requiring their linkage by chiasmata, the products of crossover recombination1. The spindle checkpoint delays cell cycle progression until all chromosomes are properly attached to microtubules2 but the steps leading to the capture and alignment of chromosomes on the meiosis I spindle remain poorly understood. In budding yeast meiosis I, Mad2 and Mad3BUBR1 are equally important for spindle checkpoint delay, but biorientation of homologs on the meiosis I spindle requires Mad2, but not Mad3BUBR1 3,4. Here we show that Mad3BUBR1 promotes accurate meiosis I homolog segregation outside its canonical checkpoint role, independently of Mad2. We find that Mad3BUBR1 associates with the TOGL1 domain of Stu1CLASP, a conserved plus-end microtubule protein which is important for chromosome capture onto the spindle. Homologous chromosome pairs that are proficient in crossover formation, but which fail to biorient, rely on Mad3BUBR1-Stu1CLASP to ensure their efficient attachment to microtubules and segregation during meiosis I. Furthermore, we show that Mad3BUBR1-Stu1CLASP are essential to rescue the segregation of mini-chromosomes lacking crossovers. Our findings define a new pathway ensuring microtubule-dependent chromosome capture and demonstrate that spindle checkpoint proteins safeguard the fidelity of chromosome segregation both by actively promoting chromosome alignment and delaying cell cycle progression until this has occurred.
2024-07-18 | PXD048251 | Pride
Project description:The extracellular matrix (ECM) of the ocular trabecular meshwork (TM) builds resistance to aqueous humor outflow, thereby regulating intraocular pressure (IOP). Glaucoma, a leading cause of blindness worldwide, is associated with changes in the ECM of the TM. The elastic modulus indicates glaucomatous TM is more rigid than age-matched normal TM; however, the biomechanical properties of segmental low (LF) and high flow (HF) TM regions in response to elevated pressure, are unknown. In this study, we measured the elastic modulus by atomic force microscopy (AFM) and measured protein expression differences in perfused human TM tissues by proteomics analyses. The elastic modulus of LF regions was 2.3-fold stiffer than HF regions at physiological (1x) pressure, and 7.4-fold or 3.5-fold stiffer than HF regions at elevated (2x) pressure after 24 or 72 hours, respectively. Quantitative proteomics using isobaric tandem mass tags (TMT), multi-notch isolation, high resolution, and extended multiplexing were used to compare protein expression levels between normal, LF, and HF regions at the two pressures. A total of 3730 proteins (2 peptides per protein) were identified from the ECM samples, and 2637 proteins were quantified. Statistically significant ECM proteins over expressed in LF compared with HF regions at 2x, and in HF regions at 1x compared with 2x pressure were determined. A sub-set of ECM proteins, including decorin, TGFβ-induced protein, keratocan, lumican, dermatopontin and thrombospondin 4, were common differential candidates in both comparisons. These data suggest a correlation between the biomechanical properties of TM regions and differential levels of specific ECM proteins in response to elevated pressure.
2018-01-22 | PXD006424 | Pride
Project description:modENCODE_submission_3153 This submission comes from a modENCODE project of Jason Lieb. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The focus of our analysis will be elements that specify nucleosome positioning and occupancy, control domains of gene expression, induce repression of the X chromosome, guide mitotic segregation and genome duplication, govern homolog pairing and recombination during meiosis, and organize chromosome positioning within the nucleus. 126 strategically selected targets include key histone modifications, histone variants, RNA polymerase II isoforms, dosage-compensation proteins, centromere components, homolog-pairing facilitators, recombination markers, and nuclear-envelope constituents. We will integrate information generated with existing knowledge on the biology of the targets, perform ChIP-chip analysis on mutant and RNAi extracts lacking selected target proteins, use extrachromosomal arrays to assess the ability of candidate identified sequence motifs to recruit targets in vivo, identify tissue-specific patterns of selected targets, and create integrated, quantitative models of transcription and whole-chromosome functions. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: Mixed Embryo; Genotype: wild type; Sex: mixed Male and Hermaphrodite population; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: Developmental Stage Mixed Embryo; temp (temperature) 20 degree celsius; Antibody (target is ); Strain N2
2010-12-22 | E-GEOD-26200 | biostudies-arrayexpress
Project description:modENCODE_submission_2970 This submission comes from a modENCODE project of Jason Lieb. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The focus of our analysis will be elements that specify nucleosome positioning and occupancy, control domains of gene expression, induce repression of the X chromosome, guide mitotic segregation and genome duplication, govern homolog pairing and recombination during meiosis, and organize chromosome positioning within the nucleus. 126 strategically selected targets include key histone modifications, histone variants, RNA polymerase II isoforms, dosage-compensation proteins, centromere components, homolog-pairing facilitators, recombination markers, and nuclear-envelope constituents. We will integrate information generated with existing knowledge on the biology of the targets, perform ChIP-chip analysis on mutant and RNAi extracts lacking selected target proteins, use extrachromosomal arrays to assess the ability of candidate identified sequence motifs to recruit targets in vivo, identify tissue-specific patterns of selected targets, and create integrated, quantitative models of transcription and whole-chromosome functions. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: Mixed Embryo; Genotype: wild type; Sex: mixed Male and Hermaphrodite population; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: Developmental Stage Mixed Embryo; temp (temperature) 20 degree celsius; Antibody SDQ4129 Y39G10AR18 (target is Y39G10AR.18); Strain N2
2012-04-22 | E-GEOD-37488 | biostudies-arrayexpress
Project description:modENCODE_submission_3151 This submission comes from a modENCODE project of Jason Lieb. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The focus of our analysis will be elements that specify nucleosome positioning and occupancy, control domains of gene expression, induce repression of the X chromosome, guide mitotic segregation and genome duplication, govern homolog pairing and recombination during meiosis, and organize chromosome positioning within the nucleus. Our 126 strategically selected targets include key histone modifications and histone variants. We will integrate information generated with existing knowledge on the biology of the targets and perform ChIP-chip analysis on mutant and RNAi extracts lacking selected target proteins. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Keywords: CHIP-chip EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: Mixed Embryo; Genotype: wild type; Sex: mixed Male and Hermaphrodite population; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: Developmental Stage Mixed Embryo; temp (temperature) 20 degree celsius; Antibody AB2621 H3K79me3:361576 (target is H3K79me3); Strain N2
2011-03-09 | E-GEOD-27778 | biostudies-arrayexpress
Project description:modENCODE_submission_3204 This submission comes from a modENCODE project of Jason Lieb. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The focus of our analysis will be elements that specify nucleosome positioning and occupancy, control domains of gene expression, induce repression of the X chromosome, guide mitotic segregation and genome duplication, govern homolog pairing and recombination during meiosis, and organize chromosome positioning within the nucleus. Our 126 strategically selected targets include key histone modifications and histone variants. We will integrate information generated with existing knowledge on the biology of the targets and perform ChIP-chip analysis on mutant and RNAi extracts lacking selected target proteins. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Keywords: CHIP-chip EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: Mixed Embryo; Genotype: wild type; Sex: mixed Male and Hermaphrodite population; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: Developmental Stage Mixed Embryo; temp (temperature) 20 degree celsius; Antibody AB3594 H3K79me2:346021 (target is H3K79me2); Strain N2
2011-03-09 | E-GEOD-27780 | biostudies-arrayexpress
Project description:Crossing over between homologs is critical for the stable segregation of chromosomes during the first meiotic division. S. cerevisiae Mer3 (HFM1 in mammals) is a SF2 helicase and member of the ZMM group of proteins, that facilitates the formation of the majority of crossovers during meiosis. Here we describe the structural organisation of Mer3 and using AlphaFold modelling and XL-MS we further characterise the previously described interaction with Mlh1-Mlh2. We find that Mer3 also forms a previously undescribed complex with the recombination regulating factors Top3 and Rmi1 and that this interaction is competitive with Sgs1BLM helicase in a phospho-dependent manner. Using in vitro reconstituted D-loop assays we show that Mer3 inhibits the anti-recombination activity of Sgs1 helicase, but only in the presence of Dmc1. Thus we provide a mechanism whereby Mer3 interacts with a network of proteins to protect Dmc1 derived D-loops from dissolution.
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Project description:This SuperSeries is composed of the following subset Series: GSE32016: Autoantibody Epitope Spreading in the Pre-Clinical Phase Predicts Progression to Rheumatoid Arthritis [ANALYTE: ANTIGEN] GSE32019: Autoantibody Epitope Spreading in the Pre-Clinical Phase Predicts Progression to Rheumatoid Arthritis [ANALYTE: Cytokine or chemokine] Refer to individual Series
2011-09-09 | E-GEOD-32021 | biostudies-arrayexpress
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2011-03-09 | E-GEOD-27782 | biostudies-arrayexpress
Project description:Rheumatoid arthritis is a prototypical autoimmune arthritis affecting nearly 1% of the world population and is a significant cause of worldwide disability. Though prior studies have demonstrated the appearance of RA-related autoantibodies years before the onset of clinical RA, the pattern of immunologic events preceding the development of RA remains unclear. To characterize the evolution of the autoantibody response in the preclinical phase of RA, we used a novel multiplex autoantigen array to evaluate development of the anti-citrullinated protein antibodies (ACPA) and to determine if epitope spread correlates with rise in serum cytokines and imminent onset of clinical RA. To do so, we utilized a cohort of 81 patients with clinical RA for whom stored serum was available from 1-12 years prior to disease onset. We evaluated the accumulation of ACPA subtypes over time and correlated this accumulation with elevations in serum cytokines. We then used logistic regression to identify a profile of biomarkers which predicts the imminent onset of clinical RA (defined as within 2 years of testing). We observed a time-dependent expansion of ACPA specificity with the number of ACPA subtypes. At the earliest timepoints, we found autoantibodies targeting several innate immune ligands including citrullinated histones, fibrinogen, and biglycan, thus providing insights into the earliest autoantigen targets and potential mechanisms underlying the onset and development of autoimmunity in RA. Additionally, expansion of the ACPA response strongly predicted elevations in many inflammatory cytokines including TNF-?, IL-6, IL-12p70, and IFN-?. Thus, we observe that the preclinical phase of RA is characterized by an accumulation of multiple autoantibody specificities reflecting the process of epitope spread. Epitope expansion is closely correlated with the appearance of preclinical inflammation, and we identify a biomarker profile including autoantibodies and cytokines which predicts the imminent onset of clinical arthritis. A total of 556 human sera were profiled using multiplex cytokine and chemokine assays. The cohort was comprised of 80 patients with clinical RA for whom stored serum was available from 1-10 years prior to disease onset and 78 control subjects without RA matched to cases based on age, gender, race, region of assignment, and time of serum sampling.
2011-09-09 | E-GEOD-32019 | biostudies-arrayexpress