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Cyclin interactome - Quantitative proteomics reveals the basis for the biochemical specificity of the cell-cycle machinery

ABSTRACT: Quantitative analysis of the Cyclin-A interactome during the cell cycle

INSTRUMENT(S): LTQ FT, instrument model

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hela Cell

SUBMITTER: Mark Collins

PROVIDER: PRD000407 | Pride | 2011-09-05

REPOSITORIES: pride

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			Action	DRS
	PRIDE_Exp_Complete_Ac_16858.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_16858.pride.mztab.gz	Mztab
	PRIDE_Exp_Complete_Ac_16858.xml.gz	Xml
	PRIDE_Exp_Complete_Ac_16859.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_16859.pride.mztab.gz	Mztab

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Publications

Quantitative proteomics reveals the basis for the biochemical specificity of the cell-cycle machinery.

Pagliuca Felicia Walton FW Collins Mark O MO Lichawska Agata A Zegerman Philip P Choudhary Jyoti S JS Pines Jonathon J

Molecular cell 20110801 3

Cyclin-dependent kinases comprise the conserved machinery that drives progress through the cell cycle, but how they do this in mammalian cells is still unclear. To identify the mechanisms by which cyclin-cdks control the cell cycle, we performed a time-resolved analysis of the in vivo interactors of cyclins E1, A2, and B1 by quantitative mass spectrometry. This global analysis of context-dependent protein interactions reveals the temporal dynamics of cyclin function in which networks of cyclin-c ...[more]

PMID: 21816347

Similar Datasets

Quantitative proteomics reveals the basis for the biochemical specificity of the cell-cycle machinery.

Project description:Cyclin-dependent kinases comprise the conserved machinery that drives progress through the cell cycle, but how they do this in mammalian cells is still unclear. To identify the mechanisms by which cyclin-cdks control the cell cycle, we performed a time-resolved analysis of the in vivo interactors of cyclins E1, A2, and B1 by quantitative mass spectrometry. This global analysis of context-dependent protein interactions reveals the temporal dynamics of cyclin function in which networks of cyclin-cdk interactions vary according to the type of cyclin and cell-cycle stage. Our results explain the temporal specificity of the cell-cycle machinery, thereby providing a biochemical mechanism for the genetic requirement for multiple cyclins in vivo and reveal how the actions of specific cyclins are coordinated to control the cell cycle. Furthermore, we identify key substrates (Wee1 and c15orf42/Sld3) that reveal how cyclin A is able to promote both DNA replication and mitosis.

| S-EPMC3332305 | biostudies-literature

Toxoplasma gondii Cyclin-4 Interactome

Project description:Toxoplasma endodyogeny is governed by a set of Cdk-related kinases (Crk). In this study we investigated TgCrk4 and its cyclin partner TgCyc4. This complex regulates many cell cycle related processes at the G2 phase. To beter undestand the funtion of the TgCrk4/TgCyc4 complex we analyzed the interactome of TgCyc4.

2024-06-16 | PXD043994 | Pride

Budding yeast relies on qualitative G1 cyclin specificity to couple cell cycle progression with morphogenetic development

Project description:Two models have been put forward for cyclin-dependent kinase (Cdk) control of the cell cycle. In the qualitative model, cell cycle events are ordered by distinct substrate specificities associated with successive waves of G1, S and mitotic cyclins. Alternatively, the gradual quantitative rise of Cdk activity from G1 phase to mitosis could lead to ordered substrate phosphorylation at sequential thresholds. Here, we study the relative contributions of qualitative and quantitative Cdk control in the budding yeast S. cerevisiae. S-phase cyclins can be replaced by a single mitotic cyclin, albeit at the cost of reduced fitness. The single cyclin can in addition replace G1 cyclins to support ordered cell cycle progression, fulfilling key predictions of the quantitative model. However, single-cyclin cells fail to polarize or grow buds and thus cannot sustain proliferation. Our results suggest that budding yeast has become dependent on G1 cyclin specificity to couple cell cycle progression to essential morphogenetic events.

2021-08-23 | PXD022757 | Pride

Cyclin Specificity Governs Centrosomal Cyclin/CDK Localisation and is Necessary for the G2/M Transition

Project description:In eukaryotes, cyclin/CDK complexes drive cells through DNA replication and mitosis, establising cell cycle temporal order. The fission yeast S. pombe is able to function with a single cyclin/CDK complex, with cell cycle order emerging from differential substrate sensitivities to CDK activity. What influence cyclin specificity has upon the cell cycle in this situation is currently unknown. Here we show that in a system that is reliant on a single cyclin for both the G1/S and G2/M transition, cyclin specificity is not needed for the G1/S transition, but instead is required for the G2/M transition and correct localisation of cyclin/CDK to the yeast centrosome equivalent, the SPB. This loss of centrosome localisation was also seen in human cells expressing mutant Cyclin B1, suggesting conservation of function. In fission yeast, although interphase centrosomal localisation is lost, mitotic SPB localisation remains. This hitherto unknown second localisation method is dependent on Polo kinase, suggesting a finer spatiotemporal control of cyclin/CDK during cell cycle progression than previously known. Thus, cyclin specificity is intrinsically twinned with spatial control of cyclin/CDK, and we suggest that this regulation may be conserved through evolution.

2019-05-27 | PXD011987 | Pride

Gene expression change in cyclin D1 -/- retinas in comparison to wildtype.

Project description:Cyclin D1 belongs to the core cell cycle machinery1, and it is frequently overexpressed in human cancers2. The full repertoire of cyclin D1 functions in normal development and in cancer cells is currently unknown. To address this question, here we introduce a novel approach that allows one to determine the set of cyclin D1-interacting proteins (D1 “interactome”) and cyclin D1-bound genomic fragments (D1 “cistrome”) in essentially any mouse organ, at any point of development or at any stage of cancer progression. Using this approach, we detected several novel tissue-specific interactors of cyclin D1. A significant number of these partners represent proteins involved in transcription. We show, using genome-wide location analysis3, that cyclin D1 occupies promoters of a very large number of genes in the developing mouse, where it binds in close proximity to transcription start sites. Bioinformatics analyses of cyclin D1-bound genomic segments in the developing embryo revealed DNA recognition sequences for several transcription factors. By querying SAGE libraries4, promoter CpG content5 and gene expression profiles of cyclin D1-null organs, we demonstrate that cyclin D1 binds promoters of highly expressed genes, and that it functions to activate or to repress gene expression in vivo. Analyses of cyclin D1 transcriptional targets reveal that cyclin D1 contributes to cell proliferation by upregulating genes required for S-phase entry and progression. Hence, cyclin D1 plays a broad transcriptional regulatory function in vivo during normal mouse development.

2010-01-29 | GSE13635 | GEO

ZBTB33 (Kaiso) Differentially Regulates Cell Cycle Through cyclin D1 and cyclin E1 in a Cell Specific Manner [RNA-seq]

Project description:The emerging correlation between aberrant DNA methylation patterns leading to transcriptional responses that promote and progress many cancers has prompted an interest in discerning the associated regulatory mechanisms. ZBTB33 (also known as Kaiso) is a specialized transcription factor that selectively recognizes mCpG-containing sites as well as a sequence-specific DNA target (termed the KBS) utilizing three Cys2His2 zinc fingers. Increasing reports link ZBTB33 overexpression and transcriptional activities with metastatic potential and poor prognosis, though the specific cellular consequences appear to be dependent on disease phenotype. There is currently little mechanistic insight into how various cellular phenotypes are then able to harness the transcriptional capabilities of ZBTB33 to differentially promote and progress the disease state. Here we have mechanistically interrogated the cell cycle responses mediated by the transcriptional activities of ZBTB33 in two different cell lines. Utilizing a series of ZBTB33 depletion and overexpression studies, we have determined that in HeLa cells ZBTB33 directly occupies the promoter regions of cyclin D1 and cyclin E1 in a KBS and methyl-specific manner, respectively, inducing increased proliferation by promoting RB1 hyper-phosphorylation, allowing for E2F transcriptional activity that coordinates an accelerated G1- to S-phase transition. Conversely, in HEK293 cells ZBTB33 indirectly regulates Cyclin E abundance resulting in reduced RB1 phosphorylation, decreased E2F activity and a decelerated transition through G1-phase. Thus, we have identified a novel mechanism by which ZBTB33 directly mediates the highly coordinated cyclin D1/cyclin E1/RB1/E2F signaling pathway controlling the passage through the G1-phase restriction point and accelerating cellular proliferation in a cancer cell line.

2017-01-30 | GSE81781 | GEO

ZBTB33 (Kaiso) Differentially Regulates Cell Cycle Through cyclin D1 and cyclin E1 in a Cell Specific Manner [BiSulfite-seq]

2017-01-30 | GSE81779 | GEO

Progesterone Receptor–Cyclin D1 Complexes Induce Cell Cycle–Dependent Transcriptional Programs in Breast Cancer Cells

Project description:The progesterone receptor (PR) and its coactivators are direct targets of activated cyclin-dependent kinases (CDKs) in response to peptide growth factors, progesterone, and deregulation of cell cycle inhibitors. Herein, using the T47D breast cancer model, we probed mechanisms of cell cycle-dependent PR action. In the absence of exogenous progestin, the PR is specifically phosphorylated during the G2/M phase. Accordingly, numerous PR target genes are cell cycle regulated, including HSPB8, a heat-shock protein whose high expression is associated with tamoxifen resistance. Progestin-induced HSPB8 expression required cyclin D1 and was insensitive to antiestrogens but blocked by antiprogestins or inhibition of specificity factor 1 (SP1). HSPB8 expression increased with or without ligand when cells were G2/M synchronized or contained high levels of cyclin D1. Knockdown of PRs abrogated ligand-independent HSPB8 expression in synchronized cells. Notably, PRs and cyclin D1 copurified in whole-cell lysates of transiently transfected COS-1 cells and in PR-positive T47D breast cancer cells expressing endogenous cyclin D1. PRs, cyclin D1, and SP1 were recruited to the HSPB8 promoter in progestin-treated T47D breast cancer cells. Mutation of PR Ser345 to Ala (S345A) or inhibition of CDK2 activity using roscovitine disrupted PR/cyclin D1 interactions with DNA and blocked HSPB8 mRNA expression. Interaction of phosphorylated PRs with SP1 and cyclin D1 provides a mechanism for targeting transcriptionally active PRs to selected gene promoters relevant to breast cancer progression. Understanding the functional linkage between PRs and cell cycle regulatory proteins will provide keys to targeting novel PR/cyclin D1 cross talk in both hormone-responsive disease and HSPB8-high refractory disease with high HSPB8 expression.

2014-02-27 | GSE46715 | GEO

ZBTB33 (Kaiso) Differentially Regulates Cell Cycle Through cyclin D1 and cyclin E1 in a Cell Specific Manner

Project description:ZBTB33 (Kaiso) Differentially Regulates Cell Cycle Through cyclin D1 and cyclin E1 in a Cell Specific Manner

| PRJNA322535 | ENA

Cyclin K and cyclin D1b are oncogenic in myeloma cells

Project description:To study the oncogenic potential of cyclin D1b in the context of mature B cells we generated several cell clones derived from LP-1 MM cell line expressing either cyclin D1b, Myc or cyclin K oncogenes. Transcriptomic analysis allowed us to describe several mechanisms of cyclin D1b- and K-mediated oncogenesis.

2010-04-23 | GSE15497 | GEO

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