Survey of RNA viruses present in East African maize with symptoms of maize lethal necrosis.
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ABSTRACT:
PROVIDER: PRJEB27713 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2695960_1.fastq.gz | Fastqsanger.gz | |||
| ERR2695960_2.fastq.gz | Fastqsanger.gz | |||
| ERR2695970_1.fastq.gz | Fastqsanger.gz | |||
| ERR2695970_2.fastq.gz | Fastqsanger.gz | |||
| ERR2695980_1.fastq.gz | Fastqsanger.gz |
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Project description:Next-generation sequencing survey of maize plants exhibiting symptoms of maize lethal necrosis, collected from Kenyan and Ethiopian farmers in August 2014. Up to three samples per site were sequenced, and sites were separated by at least 10km. Data contains maize transcriptome and a variety of RNA viruses.
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Project description:Maize lethal necrosis (MLN) is emergent in East Africa, first reported in 2011 in Kenya, and is devastating to maize production in the region. MLN is caused by coinfection of maize with the emergent maize chlorotic mottle virus (MCMV) and any of several maize-infecting potyviruses endemic in East Africa and worldwide. Here, we examined the distribution of MCMV and sugarcane mosaic virus (SCMV), the major viruses contributing to MLN in Rwanda. These and other viruses in maize across Rwanda were further characterized by deep sequencing. When identified, MCMV had high titres and minimal sequence variability, whereas SCMV showed moderate titres and high sequence variability. Deep sequencing also identified maize streak virus and other maize-associated viruses, including a previously described polerovirus, maize yellow mosaic virus, and barley yellow dwarf virus, diverse maize-associated totiviruses, maize-associated pteridovirus, Zea mays chrysovirus 1, and a maize-associated betaflexivirus. Detection of each virus was confirmed in maize samples by reverse transcription polymerase chain reaction.
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Project description:BackgroundMaize lethal necrosis is caused by a synergistic co-infection of Maize chlorotic mottle virus (MCMV) and a specific member of the Potyviridae, such as Sugarcane mosaic virus (SCMV), Wheat streak mosaic virus (WSMV) or Johnson grass mosaic virus (JGMV). Typical maize lethal necrosis symptoms include severe yellowing and leaf drying from the edges. In Kenya, we detected plants showing typical and atypical symptoms. Both groups of plants often tested negative for SCMV by ELISA.MethodsWe used next-generation sequencing to identify viruses associated to maize lethal necrosis in Kenya through a metagenomics analysis. Symptomatic and asymptomatic leaf samples were collected from maize and sorghum representing sixteen counties.ResultsComplete and partial genomes were assembled for MCMV, SCMV, Maize streak virus (MSV) and Maize yellow dwarf virus-RMV (MYDV-RMV). These four viruses (MCMV, SCMV, MSV and MYDV-RMV) were found together in 30 of 68 samples. A geographic analysis showed that these viruses are widely distributed in Kenya. Phylogenetic analyses of nucleotide sequences showed that MCMV, MYDV-RMV and MSV are similar to isolates from East Africa and other parts of the world. Single nucleotide polymorphism, nucleotide and polyprotein sequence alignments identified three genetically distinct groups of SCMV in Kenya. Variation mapped to sequences at the border of NIb and the coat protein. Partial genome sequences were obtained for other four potyviruses and one polerovirus.ConclusionOur results uncover the complexity of the maize lethal necrosis epidemic in Kenya. MCMV, SCMV, MSV and MYDV-RMV are widely distributed and infect both maize and sorghum. SCMV population in Kenya is diverse and consists of numerous strains that are genetically different to isolates from other parts of the world. Several potyviruses, and possibly poleroviruses, are also involved.
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Project description:Key messageGenome-wide association analysis in tropical and subtropical maize germplasm revealed that MLND resistance is influenced by multiple genomic regions with small to medium effects. The maize lethal necrosis disease (MLND) caused by synergistic interaction of Maize chlorotic mottle virus and Sugarcane mosaic virus, and has emerged as a serious threat to maize production in eastern Africa since 2011. Our objective was to gain insights into the genetic architecture underlying the resistance to MLND by genome-wide association study (GWAS) and genomic selection. We used two association mapping (AM) panels comprising a total of 615 diverse tropical/subtropical maize inbred lines. All the lines were evaluated against MLND under artificial inoculation. Both the panels were genotyped using genotyping-by-sequencing. Phenotypic variation for MLND resistance was significant and heritability was moderately high in both the panels. Few promising lines with high resistance to MLND were identified to be used as potential donors. GWAS revealed 24 SNPs that were significantly associated (P < 3 × 10(-5)) with MLND resistance. These SNPs are located within or adjacent to 20 putative candidate genes that are associated with plant disease resistance. Ridge regression best linear unbiased prediction with five-fold cross-validation revealed higher prediction accuracy for IMAS-AM panel (0.56) over DTMA-AM (0.36) panel. The prediction accuracy for both within and across panels is promising; inclusion of MLND resistance associated SNPs into the prediction model further improved the accuracy. Overall, the study revealed that resistance to MLND is controlled by multiple loci with small to medium effects and the SNPs identified by GWAS can be used as potential candidates in MLND resistance breeding program.
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Project description:Transcriptional profiling of Yellow stripe 1 (ys1) and ys3 mutants. ys1 and ys3 are recessive mutants of maize (Zea mays L.) that result in symptoms typical of Fe deficiency, i.e., interveinal chlorosis of the leaves. The objective of the present work was to identify the genes involved in the ys1 and ys3 phenotypes, so as to extend our understanding of Fe homeostasis in maize.
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Project description:qPCR gene expression profiling of Yellow stripe 1 (ys1) and ys3 mutants. ys1 and ys3 are recessive mutants of maize (Zea mays L.) that result in symptoms typical of Fe deficiency, i.e., interveinal chlorosis of the leaves. The objective of the present work was to identify the genes involved in the ys1 and ys3 phenotypes, so as to extend our understanding of Fe homeostasis in maize.
2015-03-01 | GSE44557 | GEO
Project description:Ustilago maydis is a basidiomycete fungus that causes smut disease in maize. Most prominent symptoms of the disease are plant tumors, which can be induced by U. maydis on all aerial parts of the plant. We identified two linked genes, pit1 and pit2, which are specifically expressed during plant colonization. Deletion mutants for either pit1 or pit2 are unable to induce tumor development and elicit plant defense responses. We used the Affymetrix maize genome array to analyze the transcriptional responses of maize to deletion pit1 and pit2 mutants and found plant responses to both mutants being not significantly distinguishable.
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Project description:Background. COVID-19-induced neurological disease is a growing concern. Here we provide a comprehensive clinical, molecular, and neuroimaging investigation of patients presenting neurological symptoms to investigate underlying processes. Methods. We performed a detailed systematized clinical, laboratory, and neuroimaging (CT/MRI) data analysis from 35 mild to severe Brazilian COVID-19 hospitalised patients with clinical indications for cerebrospinal fluid (CSF) exam. In patients' CSF, we measured interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α) and the Alzheimer's disease-associated biomarkers amyloid-beta (Aβ)1-40, Aβ1-42, Tau and pTau181 levels (n=31-35). In addition, CSF proteomics and the search for SARS-CoV-2 spike protein presence using shotgun and targeted multiple reaction monitoring liquid-chromatography/mass-spectrometry were performed (n=16). We further evaluated a 29-cytokine panel in patients’ blood (n=16). An electronic questionnaire was conducted one-year post-hospitalisation (n=19, 63.3%). Findings. COVID-19 patients presented heterogeneous clinical and neurological features, including encephalopathy, encephalitis, and neuromuscular syndromes, despite low pulmonary burden. Patients showed increased circulating cytokines and CSF IL-6 and TNF-α levels compared to controls. Alzheimer’s disease-related biomarkers were unaltered compared to controls. COVID-19 altered CSF proteomic pathways associated to complement and coagulation cascades, immune-inflammatory, metabolism and amyloidosis. We found no traces of spike protein in patients’ CSF. Severe patients presented more pronounced neuroimaging alterations, altered CSF levels of IL-6, Tau, and Aβ-species compared to mild patients. Peripheral inflammation markers correlated with CSF IL-6 and Tau-species levels. Finally, in a one-year post-COVID survey, survivors were not recovered entirely (12/19) and reported confusion or memory/attention deficits (13/19). Interpretation. COVID-19 induces a broad spectrum of neurological presentations associated with changes in central nervous system (CNS) inflammatory and neurodegenerative molecular and structural biomarkers that correlate with systemic inflammation and disease severity. Given that neurological symptoms persist up to one-year post-COVID, our results urge us to investigate whether systemic, and CNS molecular changes are permanent or alleviated so that COVID-19 patients with lingering symptoms are adequately treated.
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Project description:Maize lethal necrosis (MLN) occurs when maize chlorotic mottle virus (MCMV) and sugarcane mosaic virus (SCMV) co-infect maize plant. Yield loss of up to 100% can be experienced under severe infections. Identification and validation of genomic regions and their flanking markers can facilitate marker assisted breeding for resistance to MLN. To understand the status of previously identified quantitative trait loci (QTL)in diverse genetic background, F3 progenies derived from seven bi-parental populations were genotyped using 500 selected kompetitive allele specific PCR (KASP) SNPs. The F3 progenies were evaluated under artificial MLN inoculation for three seasons. Phenotypic analyses revealed significant variability (P ? 0.01) among genotypes for responses to MLN infections, with high heritability estimates (0.62 to 0.82) for MLN disease severity and AUDPC values. Linkage mapping and joint linkage association mapping revealed at least seven major QTL (qMLN3_130 and qMLN3_142, qMLN5_190 and qMLN5_202, qMLN6_85 and qMLN6_157 qMLN8_10 and qMLN9_142) spread across the 7-biparetal populations, for resistance to MLN infections and were consistent with those reported previously. The seven QTL appeared to be stable across genetic backgrounds and across environments. Therefore, these QTL could be useful for marker assisted breeding for resistance to MLN.
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