Xenopus laevis
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ABSTRACT:
PROVIDER: PRJNA147733 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Multicilin drives centriole biogenesis via E2f proteins
| PRJNA255038 | ENA
Project description:Multiciliated cells (MCCs) form when progenitors massively expand centriole number, yielding the hundreds of basal bodies required to extend multiple motile cilia. This organelle biogenesis is promoted transcriptionally by Multicilin acting in a complex with the E2F transcription factors, which activates the expression of genes known to be involved required to form centrioles during the cell cycle, but also requires a cell cycle state required for the centrosome cycle. Multicilin also activates the expression of Emi2 (fbxo43) an inhibitor of the APC/C ubiquitin ligase. In Emi2 mutants, basal body formation during MCCl differentiation is blocked. RNAseq analysis is used to show that gene expression associated with MCC differentiation is upregulated normally in Emi2 mutants, but surprisingly is not downregulated when MCC differentiation is complete. Emi2 is required to promote the centrosomal cycle during MCC differentiation, but then also acts to turn off gene expression associated with centriole biogenesis in differentiated cells.
2024-03-20 | GSE195635 | GEO
Project description:Coordinated genomic control of ciliogenesis and cell movement by Rfx2
| PRJNA218018 | ENA
Project description:Excess centrosomes cause defects in mitosis, cell-signaling, and cell migration, and therefore their assembly is tightly regulated. The divergent Polo kinase, PLK4, controls centriole duplication at the heart of centrosome assembly, and elevated PLK4 levels promote centrosome amplification (CA), a founding event of tumorigenesis. Here, we investigate the transcriptional consequences of elevated PLK4 and find Unkempt (UNK), a gene encoding an RNA binding protein with roles in mRNA translational regulation, to be one of only two upregulated mRNAs. UNK protein localizes to centrosomes and CEP131-positive centriolar satellites and promotes CEP131 localization to and around centrosomes. UNK's RNA binding activity is required for PLK4-induced centriole overduplication. Consistent with the loss in PLK4-induced centriole overduplication, UNK depletion disrupts PLK4 and centriole assembly protein localization. Finally, translation is enriched at centrosomes and centriolar satellites with UNK and CEP131 promoting this localized translation. In summary, UNK and CEP131 promote PLK4 localization and local translation at centrosomes during centriole overduplication.
2025-05-17 | GSE297133 | GEO
Project description:Mitosis segregates into each daughter cell two centrioles, the older of which is uniquely capable of generating a cilium. How this older centriole, called the mother centriole, initiates ciliogenesis remains poorly understood. We have identified an evolutionarily conserved complex comprised of CEP90, OFD1, MNR and FOPNL. Human mutations in CEP90, MNR and OFD1 cause ciliopathies. Super-resolution microscopy revealed that this complex forms a ring at the distal centriole. Centrioles of cells lacking MNR or CEP90 failed to assemble distal appendages and cannot generate cilia. In addition to the centrioles, complex members localized to centriolar satellites, proteinaceous granules surrounding the centrioles. Disruption of satellites did not affect distal appendage assembly, indicating that the centriolar pool is required for ciliogenesis. Consistent with an essential role in ciliogenesis, mice lacking MNR or CEP90 did not assemble cilia, did not survive beyond embryonic day 9.5, and did not transduce Hedgehog signals. In addition to ciliogenesis, MNR, but not CEP90, restrained centriolar length. MNR recruited both OFD1, required for centriolar length control, and CEP90, which recruits CEP83 to root distal appendages. Thus, an evolutionarily conserved ciliopathy-associated complex functions at the distal centriole to control centriole length and assemble distal appendages.
2021-06-15 | PXD022372 | Pride
Project description:Primary cilium serves as a cellular M-bM-^@M-^\antennaM-bM-^@M-^] to sense environmental signals. Ciliogenesis requires the removal of CP110 to convert the mother centriole into the basal body. Actin dynamics is also critical for cilia formation. How these distinct processes are properly regulated remains unknown. Here we show that miR-129-3p, a microRNA conserved in the vertebrates, controlled cilia assembly by down-regulating both CP110 and four proteins critical for actin dynamics, Arp2, Toca1, abLIM1, and abLIM3. Consistently, blocking miR-129-3p repressed cilia formation in cultured mammalian cells, whereas its overexpression potently induced ciliogenesis in proliferating cells and extraordinary cilia elongation. Moreover, inhibition of miR-129-3p in zebrafish embryos suppressed cilia assembly in the KupfferM-bM-^@M-^Ys vesicle and pronephric duct, leading to developmental abnormalities including curved body, pericardial oedema, and randomised left-right patterning. Our results thus unravel a novel mechanism that orchestrates both the centriole-to-basal body transition and subsequent cilia assembly via microRNA-mediated posttranscriptional regulations. We want to find the targets of miR-129-3p by overexpressing miR-129-3p oligo or control oligo in hTERT-RPE1 cells. Through microarray analysis we could check the downregulated genes and these genes might be the targets of miR-129-3p. RPE1 cells were transfected with control (Ctrl) or miR-129-3p (M129) oligo for 72h, and harvested for RNA extraction and hybridization on Affymetrix microarrays. Two samples: RPE1-Ctrl, RPE1-M129
2012-05-31 | E-GEOD-34846 | biostudies-arrayexpress
Project description:The complex of LARP6 and DNAAF6 controls the expression of alpha-tubulin protein during differentiation of multi-ciliated cells.
| PRJDB14674 | ENA
Project description:Primary cilium serves as a cellular “antenna” to sense environmental signals. Ciliogenesis requires the removal of CP110 to convert the mother centriole into the basal body. Actin dynamics is also critical for cilia formation. How these distinct processes are properly regulated remains unknown. Here we show that miR-129-3p, a microRNA conserved in the vertebrates, controlled cilia assembly by down-regulating both CP110 and four proteins critical for actin dynamics, Arp2, Toca1, abLIM1, and abLIM3. Consistently, blocking miR-129-3p repressed cilia formation in cultured mammalian cells, whereas its overexpression potently induced ciliogenesis in proliferating cells and extraordinary cilia elongation. Moreover, inhibition of miR-129-3p in zebrafish embryos suppressed cilia assembly in the Kupffer’s vesicle and pronephric duct, leading to developmental abnormalities including curved body, pericardial oedema, and randomised left-right patterning. Our results thus unravel a novel mechanism that orchestrates both the centriole-to-basal body transition and subsequent cilia assembly via microRNA-mediated posttranscriptional regulations. We want to find the targets of miR-129-3p by overexpressing miR-129-3p oligo or control oligo in hTERT-RPE1 cells. Through microarray analysis we could check the downregulated genes and these genes might be the targets of miR-129-3p.
2012-06-01 | GSE34846 | GEO
Project description:Genome-wide analysis reveals conserved transcriptional responses downstream of resting potential change in Xenopus embryos, axolotl regeneration, and human mesenchymal cell differentiation [frog data]
| PRJNA292919 | ENA
Project description:Genome-wide binding pattern of β-catenin during Xenopus gastrulation
| PRJNA310141 | ENA