Identifying crossover locations in Arabidopsis thaliana wild type and asy1 Col-0 × Ws-4 F2 populations using genotyping-by-sequencing
Ontology highlight
ABSTRACT:
INSTRUMENT(S): NextSeq 500
ORGANISM(S): Arabidopsis thaliana
SUBMITTER: Christophe Lambing
PROVIDER: E-MTAB-8715 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Genomic DNA from 191 asy1/+ Col x Ler F2 individuals was extracted using CTAB and used to generate sequencing libraries as described (Lawrence et al, 2019 Current Biology). Sequencing data was analysed to identify crossovers using the TIGER pipeline as previously described (Rowan et al, 2015 G3 (Bethesda); Yelina et al, 2015 Genes & Dev; Lawrence et al, 2019 Current Biology).
2020-05-18 | E-MTAB-8725 | biostudies-arrayexpress
Project description:In recent years, several small molecule cytotoxic drugs have been identified as potential inhibitors of ribosome biogenesis (Drygin et al., 2011; Peltonen et al., 2014a; Peltonen et al., 2014b). CX-5461 is one such drug that has also demonstrated anticancer potential for a wide range of malignancies (Bywater et al., 2012; Cornelison et al., 2017; Devlin et al., 2015; Drygin et al., 2011; Hald et al., 2019; Hein et al., 2017; Ismael et al., 2019; Lawrence et al., 2018; Lee et al., 2017; Negi and Brown, 2015; Taylor et al., 2019; Xu et al., 2017; Yan et al., 2017) (Haddach et al., 2012), and is presently under phase I trials for the treatment of both hematological cancers and solid tumours (Group, 2016; Khot et al., 2019). CX-5461 was initially characterized as an inhibitor of RNA Polymerase I (RPI/PolR1/PolI) that is responsible for the synthesis of the major ribosomal RNAs and the initial step in ribosome biogenesis (Drygin et al., 2011). Since RPI and its corresponding core transcription factors are dedicated to this task alone, they present ideal molecular targets by which to modulate ribosome biogenesis. However, the specificity of CX-5461 has been questioned and it has been suggested that this drug may also act by stabilizing DNA G-quadruplexes or by “poisoning” topoisomerase II (Topo II). Thus, the primary target of this drug and its mode of action are still in doubt. Here we used Deconvolution-ChIP-Seq in NIH3T3 and HEK293T cells treated for different times with CX-5461. The data show that the primary target of CX5461 is the initiation of ribosomal RNA gene (rDNA) transcription. CX-5461 blocks transcription initiation in vitro and in vivo by arresting RNA polymerase I (RPI/Pol1) within the preinitiation complex. In contrast to previous suggestions, CX-5461 does not effect recruitment of the TBP-TAF complex SL1 to the rDNA promoter, the recruitment of the initiation competent RPI-Rrn3 complex or ongoing transcription elongation, arguing against a role for G-quadruplex stabilization or topoisomerase II poisoning. Inhibition of transcription by CX-5461 is not reversible, the RPI-Rrn3 complex remains arrested in the preinitiation complex even after drug removal. This leads to nucleolar stress, extensive DNA damage and cell senescence. Our data show that the cytotoxicity of CX-5461 is the downstream result of the highly specific inhibition of rDNA transcription. The observation that this inhibition is irreversible will be important for the future design of chemotherapeutic strategies and the avoidance of drug resistance.
2021-04-07 | E-MTAB-9242 | biostudies-arrayexpress
Project description:RNA-sequencing data from human iPSC PGP1 cells (n=4) differentiated into mesoderm (day-2) (n=4) or cardiomyocytes (days 25-30) (n=4) through modulation of Wnt/β-catenin signaling as previously described (Cohn et al., 2019; Hinson et al., 2017; Hinson et al., 2015; Lian et al., 2012).
2020-11-10 | GSE158578 | GEO
Project description:While DNA methylation is an important gene regulatory mechanism in mammals (Razin and Riggs 1980; Moore, Le, and Fan 2013), its function in arthropods remains poorly understood. Studies in eusocial insects have argued for its role in caste development by regulating gene expression and splicing (Elango et al. 2009; Lyko et al. 2010; Bonasio et al. 2012; Flores et al. 2012; Foret et al. 2012; Li-Byarlay et al. 2013; Marshall, Lonsdale, and Mallon 2019; Shi et al. 2013)(Alvarado et al. 2015; Kucharski et al. 2008). However, such findings are not always consistent across studies, and have therefore remained controversial (Arsenault, Hunt, and Rehan 2018; Cardoso-Junior et al. 2021; Harris et al. 2019; Herb et al. 2012; Libbrecht et al. 2016; Oldroyd and Yagound 2021b; Patalano et al. 2015). Here we use CRISPR/Cas9 to mutate the maintenance DNA methyltransferase DNMT1 in the clonal raider ant, Ooceraea biroi. Mutants have greatly reduced DNA methylation but no obvious developmental phenotypes, demonstrating that, unlike mammals (Brown and Robertson 2007; En Li, Bestor, and Jaenisch 1992; Jackson-Grusby et al. 2001; Panning and Jaenisch 1996), ants can undergo normal development without DNMT1 or DNA methylation. Additionally, we find no evidence of DNA methylation regulating caste development. However, mutants are sterile, while in wildtypes, DNMT1 is localized to the ovaries and maternally provisioned into nascent oocytes. This supports the idea that DNMT1 plays a crucial but unknown role in the insect germline (Amukamara et al. 2020; Arsala et al. 2021; Bewick et al. 2019; Schulz et al. 2018; Ventós-Alfonso et al. 2020; Washington et al. 2020).
2023-03-23 | GSE182212 | GEO
Project description:A previous study has shown that PML-dependent recruitment of HIRA to ISG promoters contributes to the up-regulation of gene expression as a result of cytokine release in response to HSV infection (McFarlane et al., 2019). Although carried out in non-neuronal cells, this study and others (Ulbricht et al., 2012, Kim and Ahn, 2015, Scherer et al., 2016, Chen et al., 2015) suggest that PML itself may contribute to ISG upregulation, so to determine whether PML was indeed required for ISG stimulation in SCG neurons, we carried out RNA sequence analysis in IFNα-treated neurons depleted of PML.
2021-06-21 | GSE166738 | GEO
Project description:The neural behavior of glioblastoma, including the formation of tumor microtubes and synaptic circuitry, is increasingly understood to be pivotal for disease manifestation (Osswald et al. 2015; Venkatesh et al. 2015; Weil et al. 2017; Venkataramani et al. 2019; Venkatesh et al. 2019; Alcantara Llaguno et al. 2019; Venkataramani et al. 2022). Nonetheless, the few approved treatments for glioblastoma target its oncological nature, while its neural vulnerabilities remain incompletely mapped and clinically unexploited. Here, we systematically survey the neural molecular dependencies and cellular heterogeneity across 27 glioblastoma patients and diverse model systems. In patient tumor samples taken directly after surgery, we identify a spectrum of neural stem cell morphologies indicative of poor prognosis, and discover a set of repurposable neuroactive drugs with unexpected and consistent anti-glioma efficacy. Glioblastoma cells exhibit functional dependencies on highly expressed drug targets including neurological ion channels and receptors, while interpretable molecular machine learning reveals downstream convergence on secondary drug targets (COSTAR) involving AP-1-driven tumor suppression. COSTAR enables in silico drug screening on >1 million compounds that are validated with high accuracy. Multi-omic profiling of drug-treated glioblastoma cells confirms rapid Ca2+-driven AP-1 pathway induction to represent a tumor-intrinsic vulnerability at the intersection of oncogenesis and neural activity-dependent signaling. Finally, the consistent anti-glioma activity across patients and model systems is epitomized by the antidepressant Vortioxetine, which synergizes in vivo with approved glioblastoma chemotherapies. In all, our global analysis reveals that the neural vulnerabilities of glioblastoma converge on an AP-1 mediated gene regulatory network with direct translatable potential.
2024-08-01 | PXD037015 | panorama
Project description:In recent decades, the food system has been faced with the significant problem of increasing food waste. Indeed, as reported by the Food and Agriculture Organisation of the United Nations (FAO), approximately 1.3 billion tonnes of food are lost or wasted globally each year (FAO, 2011). For this reason, the European Union has implemented multiple strategies to ensure the sustainability of the food/feed sector. Among these, the Agenda 2030, later supported by the Green Deal, plays a major role, whose goal is to ensure a competitive, clean and circular economy (Fetting, 2020; Vastolo et al., 2022). For this reason, scientific research is investigating the use of non-edible biomass produced along the food chain as co-products (any product obtained from different agro-industrial processes) for livestock (Pinotti et al., 2020; Rakita et al., 2021). As shown by Govoni et al. (2023), the introduction of co-products (11-16%) to replace energy-rich food crops (such as cereals) would conserve 15.4-27.8 Mha of land, 3-19.6 km3 of blue water and 74.2-137.8 km3 of green water, representing an important strategy to ensure environmental sustainability. To date, although many co-products have already been tested (grape marcs, beet pulp, hempseed cake), several more are attracting the interest of the scientific community (Serena and Knudsen, 2007; Muhlack et al., 2018; Lanzoni et al., 2023a). Among these are camelina (Camelina Sativa L. Crantz) and cardoon (Cynara cardunculus), due to both the low environmental footprint and the high nutritional profile (Turco et al., 2019; Singh et al., 2023). More specifically, camelina and cardoon seeds are characterised by a good protein (25.9±2.07% and 16.7% on DM, respectively) and a high lipid (38.9±1.26% and 25-30% on DM, respectively) content (Genovese et al., 2015; Turco et al., 2019; Singh et al., 2023). As reported by Singh et al. (2023) and Petropoulos et al. (2018), the high fatty acid profile of camelina and cardoon seeds, rich in polyunsaturated fatty acids (55.6% and 65.43±0.08, respectively) and low in saturated fatty acids (9.04% and 13.23±0. 07%, respectively), prompted the food and feed industry to isolate the lipid fraction for nutritional and nutraceutical purposes, creating in parallel waste products. Among them, camelina cake (CAMC), cardoon cake (CC) and cardoon meal (CM) could be used in animal feed due to their high nutritional profile, as reported by Lolli et al. (2020), Nannucci et al. (2021) and Serrapica et al. (2019). However, the characterisation of the antioxidant profile and the study of bioactive peptides are still at an early stage. Therefore, in light of the above, the aim of this work was to investigate the modulation of total phenolic content (TPC) and antioxidant activity during the in vitro digestion process with 2′-azinobis-(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS), ferric reducing antioxidant power (FRAP) and oxygen radical absorbance capacity (ORAC) assays of CAMC, CC, and CM. In parallel, peptidomics analyses of in vitro digested CAMC, CC, and CM have been carried out.
2024-07-03 | PXD049333 | Pride
Project description:Low concentrations of pharmaceutical compounds were shown to induce transcriptional responses in isolated microorganisms, which could have consequences on ecosystem dynamics. In order to test if these transcriptional responses could also be observed in complex river microbial communities, biofilm reactors were inoculated with water from two distinct rivers and supplemented with environmentally relevant doses of four pharmaceutical products (erythromycin-ER, gemfibrozil-GM, sulfamethazine-SN and sulfamethoxazole-SL). To follow the expression of functional genes, we constructed a 9,600 features anonymous DNA microarray platform onto which cDNA from the various biofilms was hybridized. The reactor design for biofilm development has been previously described (Lawrence et al., 2004; Lawrence et al., 2000). Two duplicate experiments were carried out, with reactors being inoculated with either water from the WC (nutrient rich) or the SSR (nutrient poor). Treatments consisted in the addition of various pharmaceutical compounds: 1 µg l-1 erythromycin (ER), 1 µg l-1 gemfibrozil (GM), 0.5 µg l-1 sulfamethazine (SN), 0.5 µg l-1 sulfamethoxazole (SL). Nothing was added to control reactors (CO). All treatments were replicated independently three times. A reference sample (composite sample from Wascana Creek reactors used to construct the microarray) was hybridized (Cy5) on each slide.
2010-07-06 | E-GEOD-20501 | biostudies-arrayexpress
Project description:CD47 is a transmembrane glycoprotein that is ubiquitously expressed in different organs and tissues (Barclay and Van den Berg 2014; Liu, et al. 2017). In the human immune system, CD47 interacts with some integrins, two counter-receptor signal regulator protein (SIRP) family members, and the secreted thrombospondin-1 (TSP1) (Barclay and Van den Berg 2014; Gao, et al. 2016; Kaur, et al. 2013; Oldenborg, et al. 2000). CD47 has two established roles in the immune system. The CD47-SIRPα interaction was identified as a critical innate immune checkpoint, which delivers an antiphagocytic signal to macrophages and inhibits neutrophil cytotoxicity (Martínez- Sanz, et al. 2021). Its interaction with inhibitory SIRPα is a physiological anti-phagocytic “don’t eat me” signal on circulating red blood cells that is co-opted by cancer cells (Matlung, et al. 2017). Many malignant cells overexpress CD47 (Betancur, et al. 2017; Chao, et al. 2011; Jaiswal, et al. 2009; Majeti, et al. 2009; Oronsky, et al. 2020; Petrova, et al. 2017). CD47/SIRPα-targeted therapeutics have been developed to overcome this immune checkpoint for cancer treatment (Kaur, et al. 2020; Matlung, et al. 2017). Secondly, engagement of CD47 on T cells by TSP1 regulates their differentiation and survival (Grimbert, et al. 2006; Lamy, et al. 2007) and inhibits T cell receptor signaling and antigen presentation by dendritic cells (DCs) (Kaur, et al. 2014; Li, et al. 2002; Liu, et al. 2015; Miller, et al. 2013; Soto-Pantoja, et al. 2014; Weng, et al. 2014). TSP1/CD47 signaling has similar inhibitory functions to limit NK cell activation (Kim, et al. 2008; Nath, et al. 2018; Nath, et al. 2019; Schwartz, et al. 2019) and IL1β production by macrophages (Stein, et al. 2016). CD47 is therefore a checkpoint that regulates both innate and adaptive immunity. The recent understanding of CD47 antagonism associated with increased antigen presentation by DCs (Liu, et al. 2016) and natural killer cell cytotoxicity (Nath, et al. 2019) contributes to the heightened interest in CD47 as a therapeutic target (Kaur, et al. 2020).
2022-09-21 | GSE198820 | GEO