Whole genome bisulfite sequencing data of Russian wheat aphid biotypes SA1 and SAM
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA489432 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10669532_1.fastq.gz | Fastqsanger.gz | |||
| SRR10669532_2.fastq.gz | Fastqsanger.gz | |||
| SRR10669533_1.fastq.gz | Fastqsanger.gz | |||
| SRR10669533_2.fastq.gz | Fastqsanger.gz | |||
| SRR10669534_1.fastq.gz | Fastqsanger.gz |
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Project description:The aim for this study was to compare the differences in the methylome of 2 Russian wheat aphid biotypes that are genealogically linked, but at opposite ends of the virulence scale. We studied genic as well as intergenic methylation in all three available contexts in the Bismark pipeline, CpG, CHG and CHH. We were also interested to see how methylation patterns in the Russian wheat aphid compares to that of other investigated insects. Specifically the ratio of genic to intergenic methylation and to what extent contexts other than CpG are methylated. Grant number: CPR20110615000019459 Funding body: National Science Foundation ZA Grantholders name: Anna-Maria Botha-Oberholster
2020-07-15 | GSE119504 | GEO
Project description:The aim for this study was to compare the differences in the methylome of three Russian wheat aphid populations that differ in virulence and bacterial load. Differences in the methylome of US Russian wheat aphid biotype 2 (US-RWA2) that have undergone removal of their phytobiomes through isolation of newly born nymphs from their mothers compared to nymphs who stayed in close proximity to their progenitors. US-RWA1 is the least virulent biotype and US-RWA2 is the most virulent biotype. The isolated US-RWA2 population (with a reduced bacterial load) has been shown to be less virulent than the co-fed population (Luna et al., 2018). The corresponding two methylomes were then compared to the methylome of US Russian wheat aphid biotype 1 (US-RWA1 is less virulent than US-RWA2) to ascertain the contribution (or lack thereof) of the phytobiome in regards to the increased/decreased virulence of phytobiome present and absent aphids. We investigated the overall, genic, intergenic, exonic and intronic methylation - as well as genic and intergenic hemimethylation -all three available contexts ( CpG, CHG and CHH) through use of the Bismark pipeline. These findings were used to ascertain to what effect the phytobiome (bacterial load) had on methylation within the US Russian wheat aphid biotypes.
2022-06-30 | GSE185975 | GEO
Project description:Phenotypic responses to biotic stresses are often studied as the interactions between two species; however, in the phytobiome, these responses frequently result from complex interactions involving several organisms. Here, we show that variation in chlorosis caused by Russian wheat aphid (Diuraphis noxia) feeding is determined, in part, by aphid-associated bacteria. Proteomic analysis of fluids injected into a sterile medium by the aphid during feeding indicate that 99% of the proteins are of bacterial origin. Of these, the greatest proportion are produced by bacteria in the order Enterobacteriales. Bacteria from five genera in four families that have the capacity to produce these proteins were isolated directly from aphids as well as from wheat leaves only after D. noxia feeding. By themselves or in combination, these bacteria were not virulent to wheat, even at high inoculum levels. Metagenomic analysis showed that the same five D. noxia-associated genera dominated the non-Buchnera component of the aphid microbiome, and that representation of these genera was reduced in aphids from colonies established after isolation of newborn nymphs from their mothers prior to feeding (‘isolated’ aphids). Isolation or treatment with antibiotics reduced bacterial numbers, and these aphids caused less feeding damage on wheat than non-isolated or non-antibiotic treated aphids. Our data show that bacterial proteins are a significant component of Russian wheat aphid saliva, that the bacteria producing these proteins are associated with aphids and plants fed upon by aphids, and that these aphid-associated bacteria facilitate aphid virulence to wheat.
2020-11-09 | PXD010663 | Pride
Project description:RNA was extracted from all instar (insect developmental) stages for both D. noxia biotypes SA1 and SAM with the purpose to capture as many expressed transcripts as possible. South African D. noxia biotype SA1 is known to be the least virulent aphid, while its offspring, the South African D. noxia biotype SAM is the most virulent. The overall purpose of the experiment was to establish a baseline availability of transcripts to the aphids as well as help improve on current genome assemblies. Three biological replicates of 100 aphids each was collected from both biotypes SA1 and SAM that were respectively reared on preference host cultivars. Whole aphids were flash frozen in liquid nitrogen, ground to a powder with micro pistils and RNA was extracted making use of a Qiagen RNeasy kit. Library preparation for sequencing was performed using an Illumina TruSeq Stranded mRNA LT Sample Prep Kit following the TruSeq Stranded mRNA Sample Preparation Guide, Part # 15031047 Rev. E protocol. The replicate samples from the SAM biotype yielded between 120 – 140 million 100bp PE reads and the replicate samples from the SA1 biotype yielded between 113 – 137 million 100bp PE reads (with a Q20 phred score above 98% for all replicates) after sequencing on the NovaSeq6000 system. De novoassembly was performed making use of the Trinity package.
2020-12-31 | GSE143502 | GEO
Project description:Whole genome bisulfite sequencing data of Russian wheat aphid biotypes US-RWA1 (co-fed), US-RWA2 (co-fed) and US-RWA2 (isolated)
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Project description:RNA was extracted from a pooled sample of salivary glands that were excised from adult Diuraphis noxia aphids of two biotypes SA1 and SAM2.0. South African D. noxia biotype SA1 is known to be the least virulent aphid, while its offspring, the South African D. noxia biotype SAM2.0 is a newly developed biotype that is capable of feeding on several resistant cultivars. The overall purpose of the experiment was to establish a baseline availability of transcripts contained in the salivary glands of D. noxia aphids as well as help improve on current genome assemblies. In total, 200 glands were excised from both biotypes feeding on various wheat hosts (Tugela, Tugela Dn1, Gamtoss R, SST387). Aphid glands were excised in PBS buffer and stored in RNA-later until RNA extraction with a Qiagen Rneasy kit could commence. Library preparation for sequencing was performed using an Illumina TruSeq Stranded mRNA LT Sample Prep Kit following the TruSeq Stranded mRNA Sample Preparation Guide, Part # 15031047 Rev. E protocol. The single library was then sequenced on a NovaSeq6000 system. De novoassembly was performed making use of the Trinity package.
2023-12-31 | GSE200382 | GEO
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS.
2012-03-15 | GSE32234 | GEO
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Two-condition experiment, SA1 KO vs. WT cells. 3 Biological replicates.
2012-03-15 | E-GEOD-32234 | biostudies-arrayexpress
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS.
2012-03-15 | GSE32319 | GEO