Efficiency of Phytoseiulus longipes Evans as a control agent of Tetranychus evansi Baker & Pritchard (Acari: Phytoseiidae: Tetranychidae) on screenhouse tomatoes

The spider mite Tetranychus evansi Baker & Pritchard can cause severe damage to tomato crops. The predatory mite Phytoseiulus longipes Evans was recently reported in association with T. evansi in Uruguaiana, Rio Grande do Sul State, Brazil. The objective of the present study was to evaluate the effects of P. longipes on the population of T. evansi on tomatoes under screenhouse condition. The study consisted on four experiments, in each of which 80 potted plantlets were distributed in two plots of 40 plantlets each. Two weeks later, each plantlet of both plots was infested with eight adult females of T. evansi; one week after, four adult females of P. longipes were released onto each plant of one plot. The population levels of T. evansi and the damage caused by these mites were significantly lower (P < 0.05; linear mixed-effect model) in the plots where P. longipes had been released. The results indicate the potential of this predator as a candidate for classical biological control of T. evansi by inoculative releases on tomato plants.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Federal Ministry for Economic Cooperation and Developmen

Detection of Chromosomal Breakpoints in Patients with Developmental Delay and Speech Disorders

<div><p>Delineating candidate genes at the chromosomal breakpoint regions in the apparently balanced chromosome rearrangements (ABCR) has been shown to be more effective with the emergence of next-generation sequencing (NGS) technologies. We employed a large-insert (7–11 kb) paired-end tag sequencing technology (DNA-PET) to systematically analyze genome of four patients harbouring cytogenetically defined ABCR with neurodevelopmental symptoms, including developmental delay (DD) and speech disorders. We characterized structural variants (SVs) specific to each individual, including those matching the chromosomal breakpoints. Refinement of these regions by Sanger sequencing resulted in the identification of five disrupted genes in three individuals: guanine nucleotide binding protein, q polypeptide <i>(GNAQ),</i> RNA-binding protein, fox-1 homolog <i>(RBFOX3),</i> unc-5 homolog D (<i>C.elegans) (UNC5D</i>), transmembrane protein 47 (<i>TMEM47</i>), and X-linked inhibitor of apoptosis (<i>XIAP</i>). Among them, <i>XIAP</i> is the causative gene for the immunodeficiency phenotype seen in the patient. The remaining genes displayed specific expression in the fetal brain and have known biologically relevant functions in brain development, suggesting putative candidate genes for neurodevelopmental phenotypes. This study demonstrates the application of NGS technologies in mapping individual gene disruptions in ABCR as a resource for deciphering candidate genes in human neurodevelopmental disorders (NDDs).</p></div

List of SVs obtained after filtration of four patients.

a<p>Discordantly mapped PETs (dPETs) which connect the same two genomic regions are clustered together.</p>b<p>dPET clusters which has passed quality filters to remove sequencing artefacts provided the list of predicted SVs.</p>c<p>Approximately 95% of SVs overlapped with SVs found in normal population (see Methods).</p

Screening of CNVs in cases/controls from published and public datasets.

<p>The total number of cases in Cooper et al <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0090852#pone.0090852-Cooper1" target="_blank">[28]</a> is 15,767 cases, and for DECIPHER is ∼17,000 cases <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0090852#pone.0090852-Swaminathan1" target="_blank">[29]</a>. The total number of controls in Cooper et al. is 8329 controls and for 1000 Genome SV Release set is 185 controls <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0090852#pone.0090852-Mills1" target="_blank">[22]</a>.</p

Sensitive detection of chromatin-altering polymorphisms reveals autoimmune disease mechanisms.

Most disease associations detected by genome-wide association studies (GWAS) lie outside coding genes, but very few have been mapped to causal regulatory variants. Here, we present a method for detecting regulatory quantitative trait loci (QTLs) that does not require genotyping or whole-genome sequencing. The method combines deep, long-read chromatin immunoprecipitation-sequencing (ChIP-seq) with a statistical test that simultaneously scores peak height correlation and allelic imbalance: the genotype-independent signal correlation and imbalance (G-SCI) test. We performed histone acetylation ChIP-seq on 57 human lymphoblastoid cell lines and used the resulting reads to call 500,066 single-nucleotide polymorphisms de novo within regulatory elements. The G-SCI test annotated 8,764 of these as histone acetylation QTLs (haQTLs)—an order of magnitude larger than the set of candidates detected by expression QTL analysis. Lymphoblastoid haQTLs were highly predictive of autoimmune disease mechanisms. Thus, our method facilitates large-scale regulatory variant detection in any moderately sized cohort for which functional profiling data can be generated, thereby simplifying identification of causal variants within GWAS loci

Patient CD10 with translocation t(6;8).

<p>A) The pedigree of patient CD10 is indicated. The familial translocation is inherited from asymptomatic carrier mother and shared with his affected sister (CD11). B) Sanger sequencing analysis refined the chromosomal breakpoint regions and revealed a loss of 11 bp on chromosome 6 and 8 bp on chromosome 8, with a microhomology of 3 bp between the paired breakpoints. C) <i>UNC5D</i> mRNA expression in human tissue panel showed high expression in the fetal brain, adult brain and cerebellum compared to other tissues. D) The translocation breakpoint is located at intron 1 of <i>UNC5D</i> indicated by the black arrow, encompasses 15 CNVs cases described in the DECIPHER.</p

Patient CD8 with a complex chromosomal inversion.

<p>A) Karyogram of normal chromosome X compared to der(X) in patient CD8. B) FISH validation of 10 SVs shown in Table S5 (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0090852#pone.0090852.s001" target="_blank">Supporting Information S1</a>) with the respective FISH probes: Hybridization of RP1-296G17-Biot (SV15) and RP1-315-Dig (SV16) were localized on the centromere of the patient’s metaphase. Probes for SV17 and SV21 on Xp21 (RP11-330K13-Biot) and Xq25 (W12-499N23-Dig), respectively resulted in a split signal between Xp21 and the centromeric region in the patient’s chromosome. Further FISH analysis was performed by using probe RP11-762M23-Biot on Xq11.1 (SV22) that was found to localize on the upper chromosomal arm. Probe RP11-655E22 on Xp11.2 was localized on the lower arm of derivative chromosome X. C) Reconstructed derivative chromosome X for patient CD8. Normal human chromosome X according to ISCN 2009 with the arrow orientation from <i>a</i> to <i>d</i> and the proposed mechanism of sequential double inversion in patient CD8. Based on our FISH analysis, an inversion occurred first between Xp21 and Xq25, changing the orientation of p and q arm with a shift of the centromere position towards the lower q-arm shown by inverted red arrow <i>b</i> and <i>c</i>. This was followed by the second inversion that occurred between Xq11.1 and Xq25, altering the orientation of the q-arm (inverted green arrow <i>c</i>). D) Expression of <i>TMEM47</i> in human tissue panel assessed by qRT-PCR. E) Expression analysis of four disrupted genes in patient CD8 assessed by qRT-PCR.</p

Validated breakpoints and disrupted candidate genes from DNA-PET sequencing in four patients.

<p>Validated breakpoints and disrupted candidate genes from DNA-PET sequencing in four patients.</p

Patient CD5 with translocation t(9;17).

<p>A) The pedigree of patient CD5 is indicated. The translocation is transmitted to his two sons (CD21 and CD22). B) Translocation between chromosome 9 and 17 were validated by Sanger sequencing in three translocation carriers. The reference sequence is indicated, showing the fusion of two genes at the genomic level: the first five exons of <i>GNAQ</i> fused to exon 3–14 of <i>RBFOX3</i> and the first two exons of <i>RBFOX3</i> fused to exon 6–7 of <i>GNAQ.</i> C) mRNA expression of <i>GNAQ</i> and <i>RBFOX3</i> showed high expression in fetal brain, adult brain and cerebellum in human tissue panel.</p