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Transcriptome changes caused by Tudor-SN mutations in rice seed

ABSTRACT: One OsTudor-SN mutant, EM1084, carrying E503K point mutation and one associated WT-OsTSN complemented transgenic (pHL8042/EM1084 ) were applied in this study. EM1084 was obtained by TILLING studies (http://www.shigen.nig.ac.jp/rice/oryzabase). The E503K mutation site in EM1084 lies within the SN3 domain, while the EM1084 complemented transgenic plant was complemented with the full-length WT OsTSN gene driven by native OsTSN promoter. This mutation results in affecting storage protein mRNA localization and, in turn, with a strong reduction in grain weight and storage protein accumulation. Transcriptome analysis on the dehulled 10-14 days old developing seeds from wild type, EM1084 and pHL8042/EM1084 indicates that partial loss of Tudor-SN function caused the differential expression of storage protein genes and relevant genes involved in several essential biological processes during rice development.

ORGANISM(S): Oryza sativa

PROVIDER: GSE132303 | GEO | 2019/06/07

REPOSITORIES: GEO

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Project description:Implications for neuroprotection in Parkinson's disease Parkinson’s disease and its characteristic symptoms are thought to arise from the progressive degeneration of specific midbrain dopamine (DA) neurons. In humans, DA neurons of the substantia nigra (SN) and their projections to the striatum show selective vulnerability, while neighboring DA neurons of the ventral tegmental area (VTA) are relatively spared from degeneration. This pattern of cell loss is mimicked in humans, primates, and certain rodents by the neurotoxin MPTP. In this study, we aimed to test the hypothesis that there are factors in the VTA that are potentially neuroprotective against MPTP and that these factors change over time. We have found a differential transcriptional response within the cells of the SN and VTA to sustained exposure to a low dose of MPTP. Specifically, the VTA has increased expression of 148 genes as an early response to MPTP and 113 genes as a late response to MPTP toxicity. This response encompasses many areas of cellular function, including protein regulation (Phf6) and ion/metal regulation (PANK2, Car4). Notably, these responses were largely absent from the cells of the SN. Our data show a clear dynamic response in maintaining the homeostasis and viability of the neurons in the VTA that is lacking in the SN after neurotoxin challenge. We used microarrays to analyze the differential response of the substantia nigra (SN) and ventral tegmental area (VTA) to a chronic low dose of the neurotoxin MPTP. Transgenic hTH-GFP mice were treated with MPTP (4mg/kg) for either 2 or 10 days. Control mice were given an equal volume of saline for 10 days. Dopamine neurons from the substantia nigra and ventral tegmental areas of control and MPTP treated animals were laser captured. The RNA was isolated and processed for microarray hybridization. Each group had three biological replicates, for a total of 18 samples. Three each in the following: Control SN, Control VTA, 2 day MPTP SN, 2 day MPTP VTA, 10 day MPTP SN, 10 day MPTP VTA. Samples were log2 transformed and RMA normalized using Agilent Genespring 10.0 GX.

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Transcriptome changes caused by Tudor-SN mutations in rice seed

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