Functional and physical interaction between ASH2 and Sin3A mediated by HCF

<p><b>Copyright information:</b></p><p>Taken from "Functional dissection of the and transcriptomes provides insights into the transcriptional basis of wing phenotypes and reveals conserved protein interactions"</p><p>Genome Biology 2007;8(4):R67-R67.</p><p>Published online 28 Apr 2007</p><p>PMCID:PMC1896016.</p><p></p> ASH2 and Sin3A mutants share a large number of commonly misregulated genes. Each full circle encompasses the total number of genes that are downregulated (left) or upregulated (right) in -deficient cells (according to Pile . [43]) and have valid logratios in one or both of the alleles. The number of genes that are downregulated (green), upregulated (red) or do not display altered expression (yellow) over 1.5 times in one or both of the alleles is shown in brackets. An asterisk indicates statistically significant overlap: = 1.06 × 10(left), = 5.88 × 10(right). Diagram showing Sin3A-HA, HCF-Flag and ASH2-V5 fusion proteins. The number of amino acids and the predicted molecular weight without counting tags are indicated above each construct. HCF interacts with ASH2 and Sin3A in S2 cells. Anti-Flag immunoprecipitations were performed using cells expressing HCF-Flag and ASH2-V5, or ASH2-V5 alone as a negative control, and immunoblotted with anti-V5 (left). Anti-HA immunoprecipitations were performed with S2 cells transfected with Sin3-HA and HCF-Flag, or HCF-Flag alone as a negative control, and immunoblotted with anti-Flag (right). Input lane shows 4% of the total extract volume used for co-immunoprecipitations. HCF interacts with ASH2 and Sin3A in embryos. Co-immunoprecipitation experiments were performed in transgenic embryos overexpressing ASH2-HA (left) or HCF-Flag (right) with gal4. embryos were used as a negative control. Input lane shows 10% of the total extract volume used for co-immunoprecipitations

Workflow of the study.

<p>Workflow of the study.</p

Pathogenicity assessment of the variants identified by WES.

<p>Pathogenicity assessment of the variants identified by WES.</p

Apoptosis pathway.

<p>Red boxes indicate proteins identified in our 454 results and grey boxes the absent ones. Connectors finishing in a circle indicate inhibition. Green connectors highlight the survival pathways and grey ones indicate apoptosis. AIF: Apoptosis-inducing factor 1 mitochondrial; AKT/PKB: RAC-alpha serine/threonine-protein kinase = Protein kinase B; APAF-1: Apoptotic protease-activating factor 1; APIP: APAF1-interacting protein; APP: Amyloid beta A4 protein; Bax: Apoptosis regulator BAX; Bcl-2: Apoptosis regulator Bcl-2; Bcl-W: Bcl-2-like protein 2; Bcl-XL: Bcl-2-like protein 1; BI-1: Bax inhibitor 1; Casp: Caspase; Cit C: Cytochrome C; FAIM: Fas apoptotic inhibitory molecule 2; Fas: Apoptosis-mediating surface antigen FAS (CD95); Fas decoy: Decoy receptor for Fas ligand; Fas-L: Fas antigen ligand; GHITM: Growth hormone-inducible transmembrane protein = Transmembrane BAX inhibitor motif-containing protein 5; HSP: Heat shock protein; IAP: Inhibitor of apoptosis; IkB: Inhibitor of NF-kB; IL-1: Interleukin 1; IL-1 R: Interleukin 1 receptor; IRAK4: Interleukin-1 receptor-associated kinase 4; MyD88: Myeloid differentiation primary response protein MyD87; NF-kB: Nuclear factor kappa B; p53: Tumor suppressor p53; PI3K: Phosphatidylinositol 3- kinase; PIDD: p53-induced protein with a death domain; PKC: Protein kinase C; PTEN: Phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN; RAIDD: Caspase and RIP adapter with death domain; TNF R1: Tumor necrosis factor receptor 1; TNF-a: Tumor necrosis factor alpha; TRADD: TNF receptor type 1-associated DEATH domain protein; TRAF2: TNF receptor-associated factor 2; TRAIL: TNF-related apoptosis-inducing ligand; TRAIL decoy: Decoy TRAIL receptor without death domain; TRAIL-R: TRAIL receptor.</p

Venn diagram showing the comparison of <i>R. philippinarum</i> sequences with <i>B. azoricus</i> (B), <i>L.elliptica</i> (L), <i>M.galloprovincialis</i> (M) and <i>C.gigas</i> (C) known sequences.

<p>Numbers refer to the n° sequences belonging to each group.</p

Flow chart summarizing work tasks and the data processing pipeline.

<p>Flow chart summarizing work tasks and the data processing pipeline.</p

Classification of annotated sequences by BLASTx and GeneOntology Terms at level 2.

<p><b>A:</b> The top 35 hit sequences by BLASTx. Numbers refer to the n° of occurrences <b>B:</b> Cellular component. <b>C:</b> Molecular function. <b>D:</b> Biological process. Numbers in B, C and D refer to the percentage of occurrences.</p

Comparison between Milan <i>et al.</i> and the current <i>R.philippinarum</i> transcriptome.

<p>Comparison between Milan <i>et al.</i> and the current <i>R.philippinarum</i> transcriptome.</p

Putative bivalve pathogen sequences.

<p>Putative bivalve pathogen sequences.</p

Transcriptome assembly statistics.

<p><b>A:</b> Distribution of contig composition by EST. <b>B:</b> Distribution of contig length. <b>C:</b> Distribution of cluster composition by contigs.</p