Project description:We analyzed the nucleotide-binding leucine-rich repeat receptors (NLRs) of 26 recently sequenced diverse founder lines from the maize nested association mapping (NAM) population and compared them to the R gene complement present in a wild relative of maize, Zea luxurians.
Project description:These RNA-seq samples represent ten different tissue types within a diverse Nested Association Mapping (NAM) maize population that has been sequenced by the NAM Consortium Group. These samples correspond to project IDs PRJEB31061.
Project description:An ultra-high density accurate linkage map for a set of maize RILs was constructed using a GBS strategy. This map will facilitate identification of genes and exploration of QTL for complex architecture in maize. It will also be helpful for further research into the mechanisms that control complex architecture while also providing a basis for marker-assisted selection
Project description:Maize is highly sensitive to short term flooding and submergence. We aimed to discover genetic variation for submergence tolerance in maize and elucidate the genetic basis of submergence tolerance through transcriptional profiling of contrasting genotypes. A diverse set of maize nested association mapping (NAM) founder lines were screened, and two highly tolerant (Mo18W and M162W) and sensitive (B97 and B73) genotypes were identified. Transcriptome analysis was performed on these inbreds to provide genome level insights into the molecular responses to submergence.
Project description:Background and aims: Guillain-Barré syndrome (GBS) is a rare disorder, with a global incidence ranging from 1 to 2 individuals per 100,000 people/year. Infections and vaccines have been implicated as causes triggering GBS. The aim of the study was to identify host genes involved in the pathogenesis of GBS when Zika (ZIKV) and Chikungunya viruses (CHIKV) were introduced in Brazil. Methods: A case-control study of GBS was performed when ZIKV and CHIKV were introduced into a naïve population. GBS was studied during both acute and postacute phases. RNA sequencing was conducted using whole blood. Results: GBS typically manifested a week after rash and fever; acute inflammatory demyelinating polyradiculoneuropathy was more frequent. None of the GBS cases had a poor outcome. Serological assays for ZIKV and CHIKV revealed high titers of immunoglobulin G for both viruses in 9 out of 11 subjects. Metatranscriptomic analyses unveiled an increased abundance of reads attributed to Pseudomonas tolaasii and Toxoplasma gondii in the acute phase. Analysis of differentially expressed host genes during the acute phase revealed altered expression of genes associated with axogenesis, synapse assembly, and presynapse organization. Moreover, genes upregulated during acute GBS were primarily related to inflammation and the inflammasome pathways, including AIM2, NLR family genes and LRR-protein genes, and IL-10. Interpretation: These findings suggest that inflammasome activation via AIM2 could play a role in tissue damage during GBS. Further investigation into the general activation of innate inflammatory responses is warranted to elucidate their potential contribution to the pathology of GBS.
Project description:Maize is highly sensitive to short term flooding and submergence. We aimed to discover genetic variation for submergence tolerance in maize and elucidate the genetic basis of submergence tolerance through transcriptional profiling of contrasting genotypes. A diverse set of maize nested association mapping (NAM) founder lines were screened, and two highly tolerant (Mo18W and M162W) and sensitive (B97 and B73) genotypes were identified. Transcriptome analysis was performed on these inbreds to provide genome level insights into the molecular responses to submergence. RNA deep sequencing of shoot tissue from four inbreds (B73, B97, Mo18W and M162W) in three conditions 24h control (non-submerged), 24h submerged and 72h submerged.
Project description:The three-dimensional architecture of the eukaryotic genome is a critical determinant in the regulation of gene expression programs. Repressive chromatin regions are localized either at the nuclear lamina or the nucleolus. While the role of the nuclear lamina in genome organization has been widely studied, the role of the nucleolus has only recently come under investigation. Here, we present a new method called nucleolus architecture mapping (NAM) for identifying nucleolus-associated genomic domains (NADs) at a single nucleolus resolution. NAM combines laser capture microdissection and DNA sequencing. We applied NAM to embryonic stem cells (ESCs) and neural progenitor cells and observed a distinct pattern of nucleolus-to-nucleolus heterogeneity for NADs. NAM not only identified characteristic features of NADs, such as high levels of H3K9me2, depletion of H3K27me3, low active histone marks, and repressed gene expression but also revealed that the genomic domains seen in cell population studies to contact both nucleoli and nuclear lamina (NAD/LAD regions) can contact the nucleolus in one cell and the NL in another cell, but rarely both nucleolus and NL in the same cell. Additionally, we found that ribosomal protein (RP) genes are frequently associated with the nucleolus, suggesting a potential direct crosstalk between the nucleolus and the regulation of RP genes, and hence ribosome biogenesis. We also performed NAM upon perturbation of the nucleolus structure by inhibiting PolI transcription with Actinomycin D. This showed a loss of mostly NADs from the nucleolus other than the chromosomes containing rRNA genes, demonstrating that nucleolar integrity is required for genomic contacts with the nucleoli. Additionally, NAM applied to hybrid ESCs demonstrates a predominantly monoallelic distribution of NADs in single cells. We identify parental-specific NADs exhibiting a non-uniform distribution across different chromosomes. Our findings underscore NAM as an invaluable tool for investigating nucleolar organization in individual cells and, potentially, genome organization in other large phase-separated organelles in the future.
Project description:In the present study, genomic binding sites of glucocorticoid receptors (GR) were identified in vivo in the rat hippocampus applying chromatin immunoprecipitation followed by next-generation sequencing. We identified 2470 significant GR-binding sites (GBS) and were able to confirm GR binding to a random selection of these GBS covering a wide range of P values. Analysis of the genomic distribution of the significant GBS revealed a high prevalence of intragenic GBS. Gene ontology clusters involved in neuronal plasticity and other essential neuronal processes were overrepresented among the genes harboring a GBS or located in the vicinity of a GBS. Male adrenalectomized rats were challenged with increasing doses of the GR agonist corticosterone (CORT) ranging from 3 to 3000 μg/kg, resulting in clear differences in the GR-binding profile to individual GBS. Two groups of GBS could be distinguished: a low-CORT group that displayed GR binding across the full range of CORT concentrations, and a second high-CORT group that displayed significant GR binding only after administering the highest concentration of CORT. All validated GBS, in both the low-CORT and high-CORT groups, displayed mineralocorticoid receptor binding, which remained relatively constant from 30 μg/kg CORT upward. Motif analysis revealed that almost all GBS contained a glucocorticoid response element resembling the consensus motif in literature. In addition, motifs corresponding with new potential GR-interacting proteins were identified, such as zinc finger and BTB domain containing 3 (Zbtb3) and CUP (CG11181 gene product from transcript CG11181-RB), which may be involved in GR-dependent transactivation and transrepression, respectively. In conclusion, our results highlight the existence of 2 populations of GBS in the rat hippocampal genome. - See more at: http://press.endocrine.org/doi/10.1210/en.2012-2187?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed#sthash.LqK088DP.dpuf
Project description:Group B Streptococcus (GBS) is a pervasive perinatal pathogen, yet factors driving GBS dissemination in utero are poorly defined. Gestational diabetes mellitus (GDM), a complication marked by dysregulated immunity and maternal microbial dysbiosis, increases risk for GBS perinatal disease. We interrogated host-pathogen dynamics in a novel murine GDM model of GBS colonization and perinatal transmission. GDM mice had greater GBS in utero dissemination and subsequently worse neonatal outcomes. Dual-RNA sequencing revealed differential GBS adaptation to the GDM reproductive tract, including a putative glycosyltransferase (yfhO), and altered host responses. GDM disruption of immunity included reduced uterine natural killer cell activation, impaired recruitment to placentae, and altered vaginal cytokines. Lastly, we observed distinct vaginal microbial taxa associated with GDM status and GBS invasive disease status. Our translational model of GBS perinatal transmission in GDM hosts recapitulates several clinical aspects and enables discovery of host and bacterial drivers of GBS perinatal disease.