Characterization of the transcriptomic profile of Plagl1+/-pat retina
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ABSTRACT:
PROVIDER: PRJNA727582 | ENA |
REPOSITORIES: ENA
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Project description:Retinal damage triggers reactive gliosis in Müller glia across vertebrate species, but only in regenerative animals, such as teleost fish, do Müller glia initiate repair; proliferating and undergoing neurogenesis to replace lost cells. We found that Plagl1, a maternally imprinted gene, is dynamically regulated in reactive Müller glia post-insult, with transcript levels transiently increasing before stably declining. To study Plagl1 retinal function, we examined Plagl1+/-pat null mutants postnatally, revealing defects in retinal architecture, visual signal processing and a reactive gliotic phenotype. Plagl1+/-pat Müller glia proliferate ectopically and give rise to inner retinal neurons and photoreceptors. Transcriptomic and ATAC-seq profiles revealed similarities between Plagl1+/-pat retinas and neurodegenerative and injury models, including an upregulation of pro-gliogenic and pro-proliferative pathways, such as Notch, not observed in wild-type retinas Plagl1 is thus an essential component of the transcriptional regulatory networks that retain mammalian Müller glia in quiescence.
2021-05-06 | GSE173942 | GEO
Project description:Retinal damage triggers reactive gliosis in Müller glia across vertebrate species, but only in regenerative animals, such as teleost fish, do Müller glia initiate repair; proliferating and undergoing neurogenesis to replace lost cells. We found that Plagl1, a maternally imprinted gene, is dynamically regulated in reactive Müller glia post-insult, with transcript levels transiently increasing before stably declining. To study Plagl1 retinal function, we examined Plagl1+/-pat null mutants postnatally, revealing defects in retinal architecture, visual signal processing and a reactive gliotic phenotype. Plagl1+/-pat Müller glia proliferate ectopically and give rise to inner retinal neurons and photoreceptors. Transcriptomic and ATAC-seq profiles revealed similarities between Plagl1+/-pat retinas and neurodegenerative and injury models, including an upregulation of pro-gliogenic and pro-proliferative pathways, such as Notch, not observed in wild-type retinas Plagl1 is thus an essential component of the transcriptional regulatory networks that retain mammalian Müller glia in quiescence.
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Project description:Coronary artery disease (CAD) poses a worldwide health threat. Compelling evidence shows that pericardial adipose tissue (PAT), a brown-like adipose adjacent to the external surface of the pericardium, is associated with CAD. However, the specific molecular mechanisms of PAT in CAD are elusive. For characterizing human PAT and explore its association with CAD, the transcriptome characteristics were assessed in 5 CAD patients and 4 controls via RNA-sequencing.
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Project description:The Arabidopsis genome encodes 3 PAT mRNA decapping factors: PAT1(AT1g79090), PATH1 (AT3g22270) and PATH2 (AT4g14990). We generated single, double and triple knockouts (KOs) of the three PATs by CRISPR/CAS9-mediated genome editing in the summ2-8 background to avoid immune activation. The 6 weeks-old soil-grown pat triple mutants exhibited markedly stunted growth compared to the other pat single or double mutants indicating functional redundancy of PATs in regulating plant development. To identify genes which affect different developmental programs regulated by PATs, we performed RNA-seq from plants of pat1-1path1-4path2-1summ2-8 and all single and double mutant combinations.
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Project description:Throughout pregnancy, the placenta is important for the well-being of the fetus, transporting nutrients and waste between the maternal and fetal blood supply, secreting hormones, and serving as a protective barrier. To obtain a more complete understanding of placental development, we must understand how placental gene expression is regulated. We used RNA-seq data and ChIP-seq data for the enhancer associated mark, H3k27Ac, to study gene regulation in the mouse placenta at embryonic day (e) 9.5, when the placenta is developing a complex network of blood vessels which facilitate maternal-fetal exchange of material. We identified several transcription factors upregulated at e9.5 with enriched binding sites in e9.5-specific enhancers. We performed follow up studies to investigate the role of the most enriched transcription factor, PLAGL1, in placental development. The PLAGL1 binding motif was found in 233 regions which were significantly associated with genes involved in vasculature development. To further understand the role of PLAGL1, we performed an siRNA knockdown in a human placental cell line and analyzed the genes that significantly changed in expression compared to cells treated with a negative control siRNA. Genes that significantly decreased in expression along with PLAGL1 were associated with placental vasculature development terms. Using a tube assay, we found that decreased PLAGL1 expression lead to reduced tube formation. By identifying PLAGL1 as an important regulator in the placenta, our analysis improves our understanding of gene regulation in the placenta, an important step towards developing methods to diagnose and treat placental diseases.
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