CRY2 knockout in MCF7 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE14617 | GEO | 2009/01/29
SECONDARY ACCESSION(S): PRJNA112315
REPOSITORIES: GEO
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Project description:Disruption of circadian rhythms increases the risk of several types of cancer. Mammalian cryptochromes (CRY1 and CRY2) are circadian transcriptional repressors that are related to DNA repair enzymes. While CRYs lack DNA repair activity, they modulate the transcriptional response to DNA damage, and CRY2 can promote SCFFBXL3-mediated ubiquitination of c-MYC and other targets. Here, we characterize five mutations in CRY2 observed in human cancers in The Cancer Genome Atlas. We demonstrate that two orthologous mutations of mouse CRY2 (D325H and S510L) accelerate the growth of primary mouse fibroblasts expressing high levels of c-MYC. Neither mutant affects steady state levels of overexpressed c-MYC, and they have divergent impacts on circadian rhythms and on the ability of CRY2 to interact with SCFFBXL3. Unexpectedly, stable expression of either CRY2 D325H or of CRY2 S510L robustly suppresses P53 target gene expression, suggesting that this is the primary mechanism by which they influence cell growth.
2021-06-16 | GSE165647 | GEO
Project description:Transcriptional profiling of human MCF7 cells comparing mock control MCF7cells with MCF7cells transfected by siRNA against calreticulin. The latter was shown to be of having significantly decreased expression of calreticulin followed by significant decrease in migrative and invasive potentials of the MCF7 cells. Goal was to determine the effect of calreticulin knockdown on the global gene expression of MCF7 cells. Two-condition experiment, Mock control MCF7 cells vs. calreticulin siRNA knockdown MCF7 cells. Biological replicates: 3 mock control replicates, 3 transfected replicates.
2013-02-26 | E-GEOD-44371 | biostudies-arrayexpress
Project description:OBJECTIVES: Abnormal chondrocyte gene expression promotes osteoarthritis (OA) pathogenesis. RNA-sequencing revealed that circadian rhythm pathway and expression of core clock protein cryptochrome 2 (Cry2) are dysregulated in human OA cartilage. Here we determined expression patterns and function Cry1 and Cry2. METHODS: Cry mRNA and protein expression was analyzed in normal and OA human and mouse cartilage. Mice with deletion of Cry1 or Cry2 were analyzed for severity of experimental OA and to determine genes and pathways that are regulated by CRY. RESULTS: In human OA cartilage, CRY2 but not CRY1 staining and mRNA expression was significantly decreased. Cry2 was also suppressed in mice with surgical or aging-related OA. Cry2 KO but not Cry1 KO mice with experimental OA showed significantly increased severity of histopathological changes in cartilage, subchondral bone and synovium. In OA chondrocytes, the levels of Cry1 and Cry2 and the amplitude of circadian fluctuation were significantly lower. RNA-seq on knee articular cartilage of wild-type and Cry2 KO mice identified 53 differentially expressed genes, including known CRY2 target circadian genes Nr1d1, Nr1d2, Dbp and Tef. Pathway analysis indicated that circadian rhythm and extracellular matrix remodeling were dysregulated in Cry2 KO mice. CONCLUSIONS: These results show an active role of the circadian clock in general, and of CRY2 in particular, in maintaining ECM homeostasis in cartilage. This cell autonomous network of circadian rhythm genes is disrupted in OA chondrocytes. Targeting CRY2 has potential to correct abnormal gene expression patterns and reduce the severity of OA.
2019-06-19 | GSE132894 | GEO
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Project description:Skeletal muscle has remarkable capacity to regenerate upon injury due to the presence of satellite cells. The maintenance and function of satellite cells are regulated by circadian clock. Cryptocrhome 2 (CRY2) is a key component of the circadian clock and its role in skeletal muscle regeneration remains controversial. Here, we report that CRY2 is down-regulated during muscle regeneration. Using the satellite cell specific CRY2 knockout mice (CRY2scko), we show that deletion of CRY2 enhances muscle regeneration. Single myofiber analysis showed that deletion of CRY2 enhances satellite cell self-renewal. In the absence of CRY2, the ERK1/2 and JNK1/2 signaling pathways become activated, which phosphorylates the transcription factor ETS1, which in turn binds to the promoter of PAX7 to induce its transcription. CRY2 deficient myoblasts survived better in ischemic muscle. Deletion of CRY2 also alleviated myopathy in mdx mice. Therefore, CRY2 plays an essential role in regulating satellite cell function and skeletal muscle regeneration.
2024-04-07 | GSE171651 | GEO
Project description:Cryptochromes are blue-light receptors in plants and animals. Homodimers are the physiologically active form of plant cryptochromes that mediates blue light regulation of gene expression and photomorphogenesis, but how light regulates the photoreceptor activation and inactivation remains unclear. We identified an Arabidopsis protein BIC1 (Blue-light Inhibitor of Cryptochromes 1) that inhibits all photoreactions of plant cryptochrome 2 (CRY2) examined, allowing direct tests of the photoactivation and inactivation mechanisms of CRY2. We found that blue light stimulates homodimerization of CRY2, whereas BIC1 binds to CRY2 to suppress CRY2 dimerization and the interaction of CRY2 with its signaling partners. We further show that cryptochromes and phytochromes mediate light induction of BIC1 transcription, evoking the negative feedback circuitry to control homeostasis of the active cryptochromes under the broad spectra of solar radiation in nature.
2016-12-02 | GSE80350 | GEO
Project description:Light is a crucial exogenous signal sensed by cryptochrome (CRY) blue light receptors to modulate growth and the circadian clock in plants and animals. However, how CRYs interpret light quantity to regulate growth in plants remains poorly understood. Furthermore, CRY2 protein levels and activity are tightly regulated in light to fine-tune hypocotyl growth; however, details of the mechanisms that explain precise control of CRY2 levels are not fully understood. We show that in Arabidopsis, UBP12 and UBP13 deubiquitinases physically interact with CRY2 in light. UBP12/13 negatively regulates CRY2 by promoting its ubiquitination and turnover to modulate hypocotyl growth. Growth and development were explicitly affected in blue light when UBP12/13 were disrupted or overexpressed, indicating their role alongside CRY2. UBP12/13 also interacted with and stabilized COP1, which is partially required for CRY2 turnover. Our combined genetic and molecular data support a mechanistic model in which UBP12/13 interact with CRY2 and COP1, leading to the stabilization of COP1. Stabilized COP1 then promotes the ubiquitination and degradation of CRY2 under blue light. Despite decades of studies on deubiquitinases, the knowledge of how their activity is regulated is limited. Our study provides insight into how exogenous signals and ligands, along with their receptors, regulate deubiquitinase activity by protein-protein interaction. Collectively, our results provide a framework of cryptochromes and deubiquitinases to detect and interpret light signals to control plant growth at the most appropriate time.
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Project description:IP mass spectrometry of Arabidopsis CRY2 in dark and blue light
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