Arabidopsis CRL interacts with OEP80 to facilitate its complex formation
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ABSTRACT:
PROVIDER: PRJNA796945 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: we conducted a froward genetic screen to isolate suppressors of the chloroplast-deficient crl mutant, and isolated a mutation affecting the OEP80 protein. Methods: We used EMS mutagenesis to find supressors of the crl mutant. Suppressors were phenotyped at the cellular and molecular (transcriptome) level, and OEP80 complex formation was investigated in the WT and crl mutant background. Results: a mutation in OEP80 fully restores the phenotype of the crl mutant, at the whole plant level, as well as at the cellular or transcriptome level
2025-01-13 | GSE193615 | GEO
Project description:au13-04_cdtbis; cdt1_bis crl mutants and CDT1-RNAi lines have very similar macroscopic phenotypes as well as identical defects in plastid division and biogenesis. Our goal wwas to determine how much of these similarities originated from similar alterations of gene expression. Plantlets of crl mutant and CDT1-RNAi lines were grown in vitro on MS1/2 medium for 14 days. CDT1-RNAi lines were compared to the corresponding wild-type (Ws), whereas crl mutants were compared to their wild-type siblings and are in the Col0 ecotype.
2013-09-01 | GSE48465 | GEO
Project description:The Hace1 E3 ligase is a tumor suppressor in stressed cells. Through unknown mechanisms, Hace1 indirectly targets the cyclin D1 proto-oncogene for proteasomal degradation during nutrient depletion. We now show that Hace1 targets HIF1alpha for VHL-dependent degradation during hypoxia. To better understand these diverse actions we performed mass spectrometry to identify Hace1-interacting proteins. We show that Hace1 interacts with cullin-associated NEDD8-dissociated protein 1 (CAND1) under nutrient depletion and hypoxia. CAND1 binds cullins and prevents their entry into cullin ring E3 ligase (CRL) complexes, thus blocking CRL activity. Hace1 binding releases CUL1/2 from CAND1, facilitating assembly of CRL complexes to degrade cyclin D1 and HIF1alpha, respectively. These findings suggest a broad role for Hace1 in regulating tumor suppressive CRL E3 ligases. In this study, we used gene expression profiling to characterize how Hace1 overexpression affect the transcriptional response to hypoxic stress
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Project description:In this study, we used quantitative proteomics mass spectrometry with 16-plex TMT labeling to compare individual protein levels of DMSO and 1 μM CSN5i-3-treated K562 cells for 2, 8, and 24 hours. CSN5i-3 is a selective and potent inhibitor of Cop9 Signalosome (CSN), which regulates the activity of Cullin-RING E3 ubiquitin ligases (CRLs). CSN5i-3 treatment resulted in reduced CSN activity, and consequently increased cullin neddylation and constitutively active CRL. Gene Ontology analysis of the changed proteins between DMSO- and CSN5i-3-treated samples showed the enrichment of CSN subunits, cell cycle and chromosome-related components, and phosphatase complex, which include multiple CSN subunits (e.g., CSN7B and CSN5), components of CRLs, especially CRL SRs (e.g., SKP2, ELOA and DCAF1/VPRBP), and known substrates of CRLs (e.g., MAGEA6, GLUL, and RHOB). Indeed, eight out of the top 20 most decreased proteins were CRL adaptor and substrate receptors, two out of the top 20 were E2 proteins (CDC34/UBE2R1 and UBE2R2), and two were CSN subunits. Eight out of the top 20 most increased proteins were reported CRL substrates.
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Project description:The Hace1 E3 ligase is a tumor suppressor in stressed cells. Through unknown mechanisms, Hace1 indirectly targets the cyclin D1 proto-oncogene for proteasomal degradation during nutrient depletion. We now show that Hace1 targets HIF1alpha for VHL-dependent degradation during hypoxia. To better understand these diverse actions we performed mass spectrometry to identify Hace1-interacting proteins. We show that Hace1 interacts with cullin-associated NEDD8-dissociated protein 1 (CAND1) under nutrient depletion and hypoxia. CAND1 binds cullins and prevents their entry into cullin ring E3 ligase (CRL) complexes, thus blocking CRL activity. Hace1 binding releases CUL1/2 from CAND1, facilitating assembly of CRL complexes to degrade cyclin D1 and HIF1alpha, respectively. These findings suggest a broad role for Hace1 in regulating tumor suppressive CRL E3 ligases. In this study, we used gene expression profiling to characterize how Hace1 overexpression affect the transcriptional response to hypoxic stress Using Affymetrix exon-level microarrays, we compared the expression profile of HEK293 cells overexpressing either Hace1 or MSCV vector alone, under hypoxia or normoxia
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