The covertisation of norms in contact situations : The influence of the nonnative speaker on native speaker behaviour

Recombination events. a) Detailed information of 2087 recombination events detected in TcTS gene family. b) Summary of number and percentage of newly annotated TcTS and previously annotated TcTS participating in recombination events as recombinant product, major donor or minor donor. (XLSX 549 kb

Additional file 4: Figure S3. of Recombination-driven generation of the largest pathogen repository of antigen variants in the protozoan Trypanosoma cruzi

“Correction” of translation for TcTS sequences containing in-frame stop codons. (a) Translating the DNA sequences for many TcTS genes results in one or more in-frame stop codons and out-of-frame translations (yellow bar w/ asterisks). The red bar depicts a “real” TcTS protein with no frame shifts. The pink shaded regions depict sequence homology between the two sequences when the reading frame is correct for the top protein. (b) When the reading frames were adjusted to maintain a TcTS-like protein sequence by removing one or more amino acids to maintain homology, the “corrected” sequence for the top protein shows high homology to other TcTS proteins throughout the coding sequence (entire region is pink). Note that we place an “X” in the protein sequence at the location of the frame-shifts. (c) The corrected sequence can then be utilized for protein analyses. In the example, we show motifs identified throughout the sequence, thus providing a sequence architecture. We also show the identification of a peptide that is unique to this sequence (e.g. TcCLB.509539.10) that was identified via proteomic analysis. (TIF 722 kb

Additional file 13: Figure S8. of Recombination-driven generation of the largest pathogen repository of antigen variants in the protozoan Trypanosoma cruzi

TcTS genes participating in recombination in relation to gene size. The fraction of TcTS genes in each size class that served as a minor donor, major donor or are the mosiac product of recombination. Percent active as mosaic gene was calculated by dividing the number of mosaic gene by the total number of TcTS genes for each category; Percent active as major donor was calculated by dividing the number of genes that took role (at least once) as major donor by the total number of TcTS genes for each category; Percent active as minor donor was calculated by dividing the number of genes that took role (at least once) as minor donor by the total number of TcTS genes for each category. (TIF 565 kb

Gametocytemia and COI for <i>P</i>. <i>falciparum</i> field isolates.

Gametocytemia and COI for P. falciparum field isolates.</p

Additional information on <i>P</i>. <i>falciparum</i> isolates.

MSP1-genotyping results for P. falciparum isolates (p1-p6) used in infections with An. gambiae (An. gam), An. coluzzii (An. col), and/or VK5-collected An. coluzzii (VK5-An. col) (See also Methods). (XLSX)</p

Full-factor GLMM Output for VK5 <i>An</i>. <i>coluzzii</i>.

Effect of egg development (eggs vs no eggs), oocyst number, and their interactions on oocyst size. In this model, egg development and oocyst number were considered as fixed effects whereas parasite isolate, mosquito generation, and mosquito ID were set as random effects. Significant effects are in bold. (XLSX)</p

Full-factor GLMM Output for <i>An</i>. <i>coluzzii</i>.

Effect of treatment (dsGFP vs dsEcR), oocyst number, egg number, and their interactions on oocyst size. In this model, treatment, oocyst number and egg number were considered as fixed effects whereas parasite isolate and mosquito ID were set as random effects. Significant effects are in bold. (XLSX)</p

Egg development for individual infections.

(A-B) The effects of EcR-silencing on egg development across individual infections for (A) An. coluzzii (unpaired t-test and Mann-Whitney) and (B) An. gambiae (unpaired t-test and Mann-Whitney) compared to controls (Cntrl). N = sample size. p# = parasite isolate. (TIF)</p

<i>An</i>. <i>coluzzii</i> and <i>An</i>. <i>gambiae</i> females were infected with <i>P</i>. <i>falciparum</i> field isolates following <i>EcR</i>-silencing.

(A-B)An. coluzzii and An. gambiae females were injected with either dsGFP (Cntrl) or dsEcR and then infected with P. falciparum field isolates originating from six different gametocyte carriers (designated patient, p#). (A) Two batches of An. coluzzii females were infected with parasites from p1, p2, and p3. (B) Three batches of An. gambiae females were infected with parasites from p1, p3, p4, p5, and p6. (C) In An. coluzzii, dsEcR-injections did not reduce cumulative egg development to the level of statistical significance (Mann-Whitney). (D) In An. gambiae, EcR-silencing did result in a significant reduction in cumulative egg numbers compared to controls (unpaired t-test). (E-F) In both species, (E) An. coluzzii and (F) An. gambiae, dsEcR-injections had no effect on cumulative oocyst prevalence (Fisher’s Exact) or intensity (unpaired t-test and Mann-Whitney). P next to pie charts = prevalence. N = sample size. p# = parasite isolate.</p

Full-factor GLMM Output for <i>An</i>. <i>gambiae</i>.

Effect of treatment (dsGFP vs dsEcR), oocyst number, egg number, and their interactions on oocyst size. In this model, treatment, oocyst number and egg number were considered as fixed effects whereas parasite isolate and mosquito ID were set as random effects. Significant effects are in bold. (XLSX)</p