Ontology highlight
ABSTRACT:
PROVIDER: PRJNA565780 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10126360_1.fastq.gz | Fastqsanger.gz | |||
| SRR10126360_2.fastq.gz | Fastqsanger.gz | |||
| SRR10126361_1.fastq.gz | Fastqsanger.gz | |||
| SRR10126361_2.fastq.gz | Fastqsanger.gz | |||
| SRR10126362_1.fastq.gz | Fastqsanger.gz |
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Project description:The biotrophic fungus Ustilago maydis causes smut disease on maize (Zea mays L.), which is characterized by immense plant tumours. To establish disease and reprogram organ primordia to tumours, U. maydis deploys effector proteins in an organ-specific manner. However, the cellular contribution to leaf tumours remains unknown. We investigated leaf tumour formation on the tissue- and cell type-specific level. Cytology and metabolite analysis were deployed to understand the cellular basis for tumourigenesis. Laser-capture microdissection was performed to gain a cell-type specific transcriptome of U. maydis during tumour formation. In-vivo visualization of plant DNA synthesis identified bundle sheath cells as the origin of hyperplasic tumour cells, while mesophyll cells become hypertrophic tumour cells. Cell type specific transcriptome profiling of U. maydis revealed tailored expression of fungal effector genes. Moreover, U. maydis See1 was identified the first cell type specific fungal effector, being required for induction of cell cycle reactivation in bundle sheath cells. Identification of distinct cellular mechanisms in two different leave cell types, and See1 as an effector for induction of proliferation of bundle-sheath cells, are major steps in understanding U. maydis-induced tumor formation. Moreover, the cell-type specific U. maydis transcriptome data is a valuable resource to the scientific community.
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Project description:Transcriptome of 3 developmental stages of Colletotrichum graminicola during infection of Zea mays leaf sheaths
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Project description:As maize (Zea mays) plants undergo vegetative phase change from juvenile to adult, they both exhibit heteroblasty, an abrupt change in patterns of leaf morphogenesis, and gain the ability to produce flowers. Both processes are under the control of microRNA 156, whose levels decline at the end of the juvenile phase. Gain of ability to flower is conferred by expression of miR156 targets that encode Squamosa Promoter-Binding (SBP) transcription factors, which when derepressed in the adult phase induce the expression of MADS-box transcription factors that promote maturation and flowering. What gene expression differences underlie heteroblasty, as well as what regulates miR156 levels, remain open questions. Here, we compare gene expression in primordia that will develop into juvenile or adult leaves to identify genes that define these two developmental states and may influence vegetative phase change. In comparisons among successive leaves at the same developmental stage of plastochron 6, three-fourths of approximately 1,100 differentially expressed genes were more highly expressed in primordia of juvenile leaves. This juvenile set was enriched in photosynthetic genes, particularly those associated with cyclic electron flow at photosystem I, and in genes involved in oxidative stress and retrograde redox signaling. Pathogen- and herbivory-responsive pathways including jasmonic acid and salicylic acid were also up-regulated in juvenile primordia and indeed, exogenous application of jasmonic acid both delayed the appearance of adult traits and the decline of miR156 levels in maize seedlings. The successful amelioration of stress signals thus plays an important role in inducing vegetative phase change in maize. 12 untreated samples (8mm primordia of leaves 1-12) and 1 treated sample (leaf 5 primordium, 15mM JA treatment). 2 or more technical replicates per sample
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Project description:Aerenchyma is continuous gas space between shoot and roots that contributes to the internal aeration in plants. In response to excess water stress and the plant hormone ethylene, maize (Zea mays) forms aerenchyma in root cortical cells by programmed cell death (PCD). The aim of this study was to understand the molecular mechanism of ethylene-induced aerenchyma formation by identifying genes that are up- or down-regulated by ethylene treatment in the maize root cortical cells isolated by laser microdissection.
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Project description:Development of multicellular organisms proceeds via the correct interpretation of positional information to establish boundaries that separate developmental fields with distinct identities. The maize leaf is an ideal system to study plant morphogenesis as it is subdivided into a proximal sheath and a distal blade, each with distinct developmental patterning. Specialised ligule and auricle structures form at the blade-sheath boundary. The auricles act as a hinge, allowing the leaf blade to project at an angle from the stem, while the ligule comprises an epidermally-derived fringe. Recessive liguleless1 mutants lack ligules and auricles, and have upright leaves. We utilized laser-microdissection RNAseq to identify genes that are differentially expressed along discrete cell/tissue-specific domains along the proximal-distal axis of wild-type leaf primordia undergoing ligule initiation, and compared transcript accumulation in wild type and liguleless1 mutant leaf primordia. We identified transcripts that are specifically upregulated at the blade-sheath boundary. A surprising number of these ligule genes are also implicated to function during leaf initiation or lateral branching, and intersect multiple hormonal signalling pathways. We propose that genetic modules utilised in leaf and/or branch initiation are redeployed to regulate ligule outgrowth from leaf primordia. In this study, we analysed the transcriptome associated with ligule formation using laser microdissection RNA-sequencing (LM-RNAseq). We quantified transcript accumulation in the PLB and adjacent pre-blade and pre-sheath regions of wild-type leaf primordia in order to identify candidate genes involved in proximal-distal patterning at the blade-sheath boundary. We also compared transcript accumulation in lg1-R mutants and wild-type siblings to identity genes acting downstream of LG1.
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