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Analysis of EYA3 phosphorylation by Src kinase

ABSTRACT: Data-dependent nLC-MS/MS analysis of EYA3 phosphorylation by Src protein tyrosine kinase

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Aura Elena Ionescu

LAB HEAD: Stefan Eugen Szedlacsek

PROVIDER: PXD016520 | Pride | 2019-12-17

REPOSITORIES: Pride

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			Action	DRS
	OR9_20150907_ACL_AI_1_Eya3D311N_Src_ATP_0h_repeat1.raw	Raw
	OR9_20150907_ACL_AI_1_Eya3D311N_Src_ATP_0h_repeat1_10mcv.msf	Msf
	OR9_20150907_ACL_AI_1_Eya3D311N_Src_ATP_0h_repeat2.raw	Raw
	OR9_20150907_ACL_AI_1_Eya3D311N_Src_ATP_0h_repeat2_10mcv.msf	Msf
	OR9_20150907_ACL_AI_1_Eya3D311N_Src_ATP_0h_repeat3.raw	Raw

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Publications

Analysis of EYA3 Phosphorylation by Src Kinase Identifies Residues Involved in Cell Proliferation.

Ionescu Aura E AE Mentel Mihaela M Munteanu Cristian V A CVA Sima Livia E LE Martin Eliza C EC Necula-Petrareanu Georgiana G Szedlacsek Stefan E SE

International journal of molecular sciences 20191213 24

Eyes absent (EYA) are non-thiol-based protein tyrosine phosphatases (PTPs) that also have transcriptional co-activator functions. Their PTP activity is involved in various pathologies. Recently, we demonstrated that Src tyrosine kinase phosphorylates human EYA3 by controlling its subcellular localization. We also found EYA3's ability to autodephosphorylate, while raising the question if the two opposing processes could be involved in maintaining a physiologically adequate level of phosphorylatio ...[more]

PMID: 31847183

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Multiple functions for Eya3 in mammalian organism

Project description:The important function of Eya (eyes absent) in eye development of D.melanogaster is well known, the function of its mammalian orthologs Eya1-4 is only partially understood. Yet, no phenotype for Eya2 and Eya3 in humans or mouse have been described. In our study we analysed new Eya-deficient mouse model generated by insertional mutagenesis. Expression analysis of Eya3 by in-situ hybridizations and β-Gal-staining revealed a broad expression of the gene throughout development, e.g. in brain, eyes, branchial arches, somites and limbs. This diverse expression pattern suggests pleiotropic effects of Eya3 in mammalian organisms. In contrast to D. melanogaster, a close examination of the eye by various methods did not show any obvious ocular defects in mutant animals. A broad phenotypical characterization of homozygous mutants displayed decreased body weight and body length. Additionally, behavioral changes as a educed forward locomotor activity and altered exploratory behaviour were identified. A significant reduction of forelimb grip strength and an impairment of cardiac processes in Eya3-/- mice suggest a role for Eya3 in muscle development and heart function. Our results implicate that Eya3 plays various roles outside the eye with effects particularly on heart and muscle function in the mouse. Keywords: Eya3-deficient mice, cDNA microarrays, brain, heart, muscle

2008-12-17 | GSE9999 | GEO

Multiple functions for Eya3 in mammalian organism

Project description:The important function of Eya (eyes absent) in eye development of D.melanogaster is well known, the function of its mammalian orthologs Eya1-4 is only partially understood. Yet, no phenotype for Eya2 and Eya3 in humans or mouse have been described. In our study we analysed new Eya-deficient mouse model generated by insertional mutagenesis. Expression analysis of Eya3 by in-situ hybridizations and M-NM-2-Gal-staining revealed a broad expression of the gene throughout development, e.g. in brain, eyes, branchial arches, somites and limbs. This diverse expression pattern suggests pleiotropic effects of Eya3 in mammalian organisms. In contrast to D. melanogaster, a close examination of the eye by various methods did not show any obvious ocular defects in mutant animals. A broad phenotypical characterization of homozygous mutants displayed decreased body weight and body length. Additionally, behavioral changes as a educed forward locomotor activity and altered exploratory behaviour were identified. A significant reduction of forelimb grip strength and an impairment of cardiac processes in Eya3-/- mice suggest a role for Eya3 in muscle development and heart function. Our results implicate that Eya3 plays various roles outside the eye with effects particularly on heart and muscle function in the mouse. Keywords: Eya3-deficient mice, cDNA microarrays, brain, heart, muscle analysis of 4 Eya3 mutant mice versus a pool of 5 wildtype animals; brain, heart, and muscle; 8 hybridisations for each tissue: two technical replicates for each mutant animal including one dye-swap experiments

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Proteomic analysis of Eya3 binding partners

Project description:Eyes absent homolog 3 (EYA3) is a transcriptional cofactor that is known to partner with the sine oculis homeobox (SIX) family to regulate gene expression. In this study, we characterized a novel splice isoform of EYA3, including the alternative cassette exon 7 (EYA3+ex7), that becomes more highly expressed compared to the isoform lacking exon 7 (EYA3Δex7) during muscle cell differentiation and muscle development. This developmentally-regulated splicing pattern was evolutionarily conserved in humans, mice, rats, chickens, and zebrafish. We found that EYA3 isoforms are vital to proliferation and differentiation of myoblasts in a cell culture model of myogenesis. To understand the underlying mechanism, we defined the transcriptional networks controlled by EYA3 through RNA-sequencing of EYA3 depleted cells. We then hypothesized that binding partners of EYA3+ex7 and EYA3Δex7 might contribute to the mechanism by which they regulate transcription. An affinity-purification mass spectrometry approach was used to identify binding partners of EYA3 isoforms by heterologous expression of hemagglutinin (HA) tagged isoforms in HEK293T cells. 26 binding partners (defined as those with log2(FC) > 1 and p < 0.05 compared to HA epitope tag control) were shared among the EYA3 isoforms, including five transcription factors: zinc finger and BTB domain containing 1 (ZBTB1), tumor protein p53 (TP53), SIX5, SIX2, and SIX4. We next demonstrated that ZBTB1 and SIX4 share overlapping transcriptional targets with EYA3, indicating that EYA3 partners with ZBTB1 or SIX4 to regulate gene expression. Three and thirteen unique binding partners were discovered for EYA3Δex7 and EYA3+ex7, respectively. Therefore, inclusion of Eya3 exon 7 may allow for unique interactions and contribute to functions of EYA3+ex7 that are distinct from EYA3Δex7. This dataset includes affinity purified data for Eya3 isoforms in HEK293T cells.

2023-10-13 | PXD037572 | Pride

RNA-sequencing of differentiated mouse skeletal muscle cells following the depletion of EYA3

Project description:Mouse skeletal muscle cells were subjected to treatment with siRNAs targeting EYA3 or a non-targeting siRNA (si-Ctrl). Differential gene expression analysis was performed on the resulting data.

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Bead-based kinase phosphorylation profiling identifies SRC as a therapeutic target in glioblastoma

Project description:Here we describe a bead-based method capable of profiling tyrosine kinase phosphorylations in a multiplexed, high-throughput and low-cost manner. This approach allows for the discovery of tyrosine kinase-activating events, even when the DNA sequence is wild-type. In an effort to pilot the establishment of a tyrosine kinase activation catalog, we profiled tyrosine phosphorylation levels of 62 tyrosine kinases in 130 human cancer lines, and followed-up on the frequent SRC phosphorylation in glioblastoma. Keywords: quantitative measurements of tyrosine phosphorylation levels on tyrosine kinases Total protein lysates were collected from 130 cancer cell lines. Tyrosine phosphorylation levels on 62 tyrosine kinases were measured with the bead assay.

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Project description:The membrane anchored Src tyrosine kinase is involved in numerous pathways and its deregulation is involved in human cancer. Our knowledge on Src regulation relies on crystallography, which revealed intramolecular interactions to control active Src conformations. However, Src contains a N-terminal intrinsically disordered unique domain (UD) whose function remains unclear. Using NMR, we reported that UD forms an intramolecular fuzzy complex involving a conserved region with lipid-binding capacity named Unique Lipid Binding Region (ULBR), which could modulate Src membrane anchoring. Here we show that the ULBR is essential for Src’s oncogenic capacity. ULBR inactive mutations inhibited Src transforming activity in NIH3T3 cells and in human colon cancer cells. It also reduced Src-induced tumor development in nude mice. An intact ULBR was required for MAPK signaling without affecting Src kinase activity nor sub-cellular localization. Phospho-proteomic analyses revealed that, while not impacting on the global tyrosine phospho-proteome in colon cancer cells, this region modulates phosphorylation of specific membrane-localized tyrosine kinases needed for Src oncogenic signaling, including EPHA2 and Fyn. Collectively, this study reveals an important role of this intrinsically disordered region in malignant cell transformation and suggests a novel layer of Src regulation by this unique region via membrane substrate phosphorylation.

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