Quark-gluon vertex in general kinematics

The original publication can be found at www.springerlink.com Submitted to Cornell University’s online archive www.arXiv.org in 2007 by Jon-Ivar Skullerud. Post-print sourced from www.arxiv.org.We compute the quark–gluon vertex in quenched lattice QCD in the Landau gauge, using an off-shell mean-field O(a)-improved fermion action. The Dirac-vector part of the vertex is computed for arbitrary kinematics. We find a substantial infrared enhancement of the interaction strength regardless of the kinematics.Ayse Kizilersu, Derek B. Leinweber, Jon-Ivar Skullerud and Anthony G. William

Triplicated mouse model phenotype associations among genes overlapped by sets of <i>de novo</i> CNVs identified in individuals with ASD.

<p>Enrichments are given as the fold change over that expected by chance (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#s4" target="_blank">Materials and Methods</a>).</p

Protein-Protein Interaction (PPI) network enrichments.

<p>Enrichments are given as the fold change over that expected by chance (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#s4" target="_blank">Materials and Methods</a>).</p

Relationships of mouse model phenotypic terms enriched among genes overlapped by <i>de novo</i> CNVs identified in individuals with ASD.

<p>Relationships between phenotypic terms within the Mammalian Phenotype Ontology are indicated by a blue arrow running from the child term to the parent term. Terms are significant (BH-adjusted <i>p</i><5%) in at least one of 4 sets of <i>de novo</i> CNVs identified in individuals with autism if they are shown with a coloured border (red, dark and light blue). Those terms whose significant enrichment is observed in three independent sets, and thus triplicated, are marked with a boxed letter “T”. Panels A–E show representative clusters of <i>Behaviour/Neurological</i> phenotypic category, while Panel F shows the enriched phenotypes from the <i>Nervous System</i> phenotypic category and Panel G shows representative enrichments from the <i>Hearing/Vestibular/Ear</i> phenotypic category. The number adjacent to the phenotypic terms indicates the rank of that phenotypic term among those phenotypes significantly enriched among a set of 22 disease genes previously implicated in ASD (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#s2" target="_blank">Results</a>).</p

Distinct duplications and deletions of genes whose proteins interact within the <i>ASD-associated</i> network perturb pathways in the same direction.

<p>Genes duplicated within ASD <i>dn</i> CNVs are indicated with green upwards arrows while those deleted are denoted by blue downwards arrows. Previously identified <i>ASD-Implicated</i> genes found to be disrupted in autism patients are denoted with red downwards arrows. The nature of the interactions/regulations between proteins/molecules are shown with different edge types (see in-figure legend). The <i>ASD-associated</i> network (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen-1003523-g002" target="_blank">Figure 2</a>) identifies several deletion/duplication pathway cascades, for example the <i>MAPK3</i> pathway (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#s3" target="_blank">Discussion</a> for additional examples). Here, deletions of the MAPK3 pathway components (i.e. <i>SYNGAP1</i>, <i>SHANK2</i>, <i>KRAS</i>, <i>MAPK3</i>, <i>PAK2</i>, and <i>CREBBP</i>) and duplications of their negative regulators (i.e. <i>FMR1</i>, <i>GDI1</i>, <i>ARHGDIA</i>, <i>CAMK2B</i>, and <i>CAMKK2</i>) found in autistic patients identify converging effects on the MAPK pathway, specifically reduced CREB-dependent transcription <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Webber1" target="_blank">[9]</a>, <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Muddashetty1" target="_blank">[62]</a>, <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Chen1" target="_blank">[63]</a>, <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Hart1" target="_blank">[64]</a>. CREB-dependent transcription has been implicated in neuroadaptation <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Levy1" target="_blank">[20]</a>. In addition, increased NO* production leads to the inhibition of <i>MAPK1/3</i> activity <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Raines1" target="_blank">[65]</a>, which fits well with the observed CNV duplications of both <i>NOS1</i> and <i>DLG4</i>, the latter gene promoting recruitment of <i>NOS1 </i><a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Nikonenko1" target="_blank">[66]</a>. Similarly, duplication of <i>PRKG1</i>, which is up-regulated by NO* and expresses a product that inhibits IP3 production, is predicted to reduced activation of the calcium-releasing IP3-receptor <i>ITPR1 </i><a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003523#pgen.1003523-Ruth1" target="_blank">[67]</a>, which is in turn found to be deleted.</p

List of significantly associated haplotypes.

<p>List of significantly associated haplotypes.</p

Differentially expressed genes by the risk alleles at 29 Mb and 33 Mb play important role in T-cell immunity.

<p>A. The risk allele at the 29 Mb at homozygous state has a clear cis-regulation effect on the expression levels of <i>TRPC6</i>, <i>KIAA1377</i>, and <i>ANGPTL5</i>, three of the most proximal genes. <i>BIRC3</i>, which is also proximal to the 29 Mb risk locus, had a significant p-value, however the FDR value was slightly above the threshold of 0.05. The risk allele at 29 Mb was also associated with a regulatory effect on genes near the 33 Mb locus and a change in the expression of <i>PIK3R6</i> significantly. B. A large network of molecules that play a major role in activation of T-lymphocyte and other immune cells (IPA category: cell-to-cell signaling and interaction, hematological system development and function). This network includes 15 molecules of which expressions are significantly altered in individuals carrying at least one copy of the shared risk allele at the 33 Mb locus. The outcomes of such expression changes are significantly linked to decrease in T-cell activation.</p

Top 10 differentially expressed genes by the risk haplotype at each locus.

<p>Top 10 differentially expressed genes by the risk haplotype at each locus.</p

Two neighboring loci on chromosome 5 are independently associated with disease risk.

<p>A. The top SNP of the first peak (29 Mb) is in high LD with nearby variants and shows no evidence of linkage to the top SNPs in the second peak (33 Mb). B. The 29 Mb peak is comprised of two haplotype blocks, and C. the risk haplotypes for the 29 Mb peak are rather common in the population. Similarly, D. the second peak also shows no linkage with the first peak in the combined analysis, whereas E. analysis of only B-cell lymphoma shows SNPs in strong LD within the second peak and in moderate LD with SNPs in the first peak. The top SNPs in the combined analysis and B-cell-lymphoma-only analysis are independent, and F. make up separate haplotypes at the second locus. G. Both risk haplotypes at the second locus are rare. Color-coding of SNPs in A, D, E, reflects their r² value relative the top SNP of that region, ranging from grey (not in LD) to red (strong LD).</p