Expression data from OsUBA-overexpressed, RNA interferenced, and wild-type rice seedlings
Ontology highlight
ABSTRACT:
ORGANISM(S): Oryza sativa
PROVIDER: GSE126878 | GEO | 2022/02/21
REPOSITORIES: GEO
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2020-02-19 | GSE124209 | GEO
Project description:Background and study aims
Colorectal cancer (CRC) is one of the most commoncancers among humans worldwide. Recent studies demonstrated that the composition of the bacterial community in the human gut, as well as inflammation occurring in the gut, are some of the factors that modify the risk of an individual to develop CRC. The human gut is home to more than 1000 bacterial species, including health-promoting species and disease-causing species.
The consumption of rice bran, a by-product of rice milling, was previously shown to positively modify bacterial composition in the gut among healthy adults. The protective effect of a long-term rice bran consumption against CRC among individuals known to have higher risk of CRC, such as older individuals who are regular smokers and having a family history of CRC, needs to be established.
This study aims to investigate whether the implementation of a 24-week dietary programme involving rice bran consumption among adults at high risk of CRC is feasible, and whether it has any effect in inducing a health-promoting modification of the bacterial community, as well as a reduction of inflammation, in the gut of these individuals.
Who can participate?
Chinese adults of either gender, who are aged 50 or above and are categorised to be in the high risk CRC group by the Asian-Pacific Colorectal Screening tool, in which classification is based on age, smoking status and family history of CRC.
What does the study involve?
After the recruited subjects were screened for eligibility of study participation and written informed consent had been obtained from them, they were randomly assigned into either Group A or Group B. Participants in Group A were given packets of rice bran and were asked to consume 30 grams of the rice bran at 24-hour intervals for 24 weeks. Participants in Group B were given packets of rice powder that has similar appearance and colour as the rice bran, and were asked to consume 30 grams of the rice powder, also at 24-hour intervals for 24 weeks. All participants were asked to provide a stool sample and blood sample at various time points during the study, namely just before rice bran consumption, as well as 6 weeks, 12 weeks and 24 weeks after the start of rice bran consumption. Laboratory tests were conducted on these samples. All participants were also instructed to complete a log book, detailing the date and time of rice bran or rice powder intake each day, and the amount consumed. The participants also completed a faecal diary where they documented the frequency of egestion, and the shape and amount of stool egested each day, as well as the occurrence of any abdominal discomfort or pain.
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Project description:Hepatocellular carcinoma (HCC) emerges from chronic inflammation to which activation of hepatic stellate cells (HSCs) contributes by shaping a pro-tumorigenic microenvironment. Key to this process is p62, whose inactivation leads to enhanced hepatocarcinogenesis. Here, we show that while p62 positively regulates STING ubiquitination by TRIM32 by displacing NBR1, which results in the activation of the interferon (IFN) cascade, NBR1 prevents TRIM32 interaction with and the activation of STING, leading to impaired IFN synthesis. NBR1 also antagonizes STING function by promoting its trafficking from the Golgi to the endosome-lysosomal degradative cascade independent of autophagy. Importantly, NBR1 deletion completely reverts the tumor-promoting function of p62-deficient HSCs. The upregulation of the STING-IFN pathway by NBR1 deficiency enhances the anti-tumor response mediated by CD8+ T cells. These results identify NBR1 as a synthetic vulnerability of p62-deficiency in HSCs. NBR1 loss, by promoting the STING/IFN pathway, boosts anti-tumor CD8+ T cell responses to restrain HCC.
2024-10-22 | GSE254277 | GEO
Project description:Hepatocellular carcinoma (HCC) emerges from chronic inflammation to which activation of hepatic stellate cells (HSCs) contributes by shaping a pro-tumorigenic microenvironment. Key to this process is p62, whose inactivation leads to enhanced hepatocarcinogenesis. Here, we show that while p62 positively regulates STING ubiquitination by TRIM32 by displacing NBR1, which results in the activation of the interferon (IFN) cascade, NBR1 prevents TRIM32 interaction with and the activation of STING, leading to impaired IFN synthesis. NBR1 also antagonizes STING function by promoting its trafficking from the Golgi to the endosome-lysosomal degradative cascade independent of autophagy. Importantly, NBR1 deletion completely reverts the tumor-promoting function of p62-deficient HSCs. The upregulation of the STING-IFN pathway by NBR1 deficiency enhances the anti-tumor response mediated by CD8+ T cells. These results identify NBR1 as a synthetic vulnerability of p62-deficiency in HSCs. NBR1 loss, by promoting the STING/IFN pathway, boosts anti-tumor CD8+ T cell responses to restrain HCC.
2024-10-22 | GSE254276 | GEO
Project description:In nature, plants are constantly exposed to many transient, but recurring, stresses. Thus, to complete their life cycles they require a dynamic balance between capacities to recover following cessation of stress and maintenance of stress memory. Recently, we uncovered a new functional role of autophagy in regulating recovery from heat stress (HS) and resetting cellular memory of HS in Arabidopsis thaliana. Here, we demonstrate that NBR1 (Next-to-BRCA1) plays a crucial role as an adaptor receptor for selective autophagy during recovery from HS. Immunoblot analysis and confocal microscopy revealed that levels of NBR1 protein, NBR1-labeled puncta and NBR1 activities were all higher during the HS recovery phase than before and after this phase. Co-immunoprecipitation analysis of proteins interacting with NBR1 and comparative proteomic analysis of a nbr1 knockout mutant and wild-type plants identified 58 proteins as potential novel targets of NBR1. Cellular, biochemical and functional genetic studies confirmed that NBR1 targets Heat Shock Protein 90 (HSP90) and ROF1, a member of the FKBP family, and mediates their degradation by autophagy, which represses the expression of HSPs regulated by HsfA2 transcription factor and the response to HS. Accordingly, loss-of-function mutation of NBR1 resulted in a stronger HS memory phenotype. Together our results provide new insights into the mechanistic principles by which autophagy regulates plant response to recurrent HS.
2022-02-15 | PXD015027 | Pride
Project description:Dongxiang wild rice (Oryza rufipogon Griff.) is the progenitor of cultivated rice (Oryza sativa L.) and is well known for its superior level of tolerance against cold, drought and diseases. To date, however, little is known about the salt-tolerant character of Dongxiang wild rice. To elucidate the molecular genetic mechanisms of salt-stress tolerance in Dongxiang wild rice, the Illumina HiSeq 2000 platform was used to analyze the transcriptome profiles of the leaves and roots at the seedling stage under salt stress compared with those under normal conditions. The analysis results for the sequencing data showed that 6,867 transcripts were differentially expressed in the leaves (2,216 up-regulated and 4,651 down-regulated) and 4,988 transcripts in the roots (3,105 up-regulated and 1,883 down-regulated). Among these differentially expressed genes, the detection of many transcription factor genes demonstrated that multiple regulatory pathways were involved in salt stress tolerance. In addition, the differentially expressed genes were compared with the previous RNA-Seq analysis of salt-stress responses in cultivated rice Nipponbare, indicating the possible specific molecular mechanisms of salt-stress responses for Dongxiang wild rice. A large number of the salt-inducible genes identified in this study were co-localized onto fine-mapped salt-tolerance-related quantitative trait loci, providing candidates for gene cloning and elucidation of molecular mechanisms responsible for salt-stress tolerance in rice.
2016-01-13 | GSE73181 | GEO
Project description:This study investigated the effect of autophagy on flowering time in rice. Results provide important information of the response of flowering time to autophagy, such as specific flowerig time genes, up- or down-regulated specific flowering time functions.
2022-05-06 | GSE175519 | GEO
Project description:BackgroundHigh Salinity is a major environmental stress influencing growth and development of rice. Comparative proteomic analysis of hybrid rice shoot proteins from Shanyou 10 seedlings, a salt-tolerant hybrid variety, and Liangyoupeijiu seedlings, a salt-sensitive hybrid variety, was performed to identify new components involved in salt-stress signaling.ResultsPhenotypic analysis of one protein that was upregulated during salt-induced stress, cyclophilin 2 (OsCYP2), indicated that OsCYP2 transgenic rice seedlings had better tolerance to salt stress than did wild-type seedlings. Interestingly, wild-type seedlings exhibited a marked reduction in maximal photochemical efficiency under salt stress, whereas no such change was observed for OsCYP2-transgenic seedlings. OsCYP2-transgenic seedlings had lower levels of lipid peroxidation products and higher activities of antioxidant enzymes than wild-type seedlings. Spatiotemporal expression analysis of OsCYP2 showed that it could be induced by salt stress in both Shanyou 10 and Liangyoupeijiu seedlings, but Shanyou 10 seedlings showed higher OsCYP2 expression levels. Moreover, circadian rhythm expression of OsCYP2 in Shanyou 10 seedlings occurred earlier than in Liangyoupeijiu seedlings. Treatment with PEG, heat, or ABA induced OsCYP2 expression in Shanyou 10 seedlings but inhibited its expression in Liangyoupeijiu seedlings. Cold stress inhibited OsCYP2 expression in Shanyou 10 and Liangyoupeijiu seedlings. In addition, OsCYP2 was strongly expressed in shoots but rarely in roots in two rice hybrid varieties.ConclusionsTogether, these data suggest that OsCYP2 may act as a key regulator that controls ROS level by modulating activities of antioxidant enzymes at translation level. OsCYP2 expression is not only induced by salt stress, but also regulated by circadian rhythm. Moreover, OsCYP2 is also likely to act as a key component that is involved in signal pathways of other types of stresses-PEG, heat, cold, or ABA.
| S-EPMC3050798 | biostudies-literature
Project description:Autophagy involvement in plant response to nitrogen, carbon and sulfur starvation was already reported, however the mechanisms responsible for its regulation and selectivity in such conditions were not yet investigated. We observed increased amounts of NBR1 transcript in plants exposed to sulfur deficit as compared to the control plants grown in nutrient sufficient conditions. This observation prompted us to investigate the role of this selective autophagy cargo receptor in plant response to sulfur deficit. Transcriptome analysis of the wild type and NBR overexpressing plants revealed differences in gene expression changes in response to sulfur deficit. Moreover, NBR1 overexpressors have significantly shorter roots than WT, when grown in nutrient deficient conditions in the presence of TOR kinase inhibitors, namely in the conditions leading to autophagy induction. Besides, NBR1 overexpression promoted stomata closure while NBR1 depletion stomata opening. Surprisingly, all lines had more closed stomata when grown in sulfur deficient than sulfur optimal conditions, what indicates that this effect is independent from NBR1. Similarly, ABA-dependent stomatal closure was independent from NBR1 and growth conditions. Cysteine also promoted stomatal closure in NBR1-independent way in plants grown in the optimal medium but in contrast, reduced the number of open stomata in plants from sulfur deficient medium. Interaction network analysis of the proteins co-purifying with NBR1 revealed links with proteins involved in degradation systems, and endosomal trafficking and a surprizing connection with nuclear transport. In addition, several proteins co-purifying with NBR1 were found only in sulfur deficient conditions. One of them, ribosomal protein S6 (RPS6) was further confirmed as a direct NBR1 interactor. Localization of the RPS6 interaction sites in NBR1 indicated that ubiquitin binding domain of NBR1 is not required for this interaction what means that it is rather not the classical “ubiquitinated target - autophagy receptor” interaction.
2020-05-26 | PXD016026 | Pride
Project description:Cargo receptors are well established elements of the selective autophagy in all eukaryotes. The NBR1-like family of such receptors is evolutionarily conserved, however plants have only one member of the family, which is a functional and structural hybrid of its two animal counterparts, p62 (SQSTM1) and NBR1. Examination of plants overexpressing NBR1 indicates that they are oversensitive to TOR inhibitors and have more autophagosomes than the parental lines. The observed changes in shoots suggested induction of ABA signalling pathway, what was further corroborated by the germination tests and the assay of ABA level. The transcriptome changes in roots, such as lower level of snoRNA and some tRNAs, suggested inhibition of ribosome biogenesis, what is supported by identification of RPS6, an important component of TOR-dependent translational control, as a novel partner of NBR1. Grant number: 2014/15/B/NZ3/04854 Grant funding source: National Science Centre (Poland) Grantee Name: Agnieszka Sirko Grant title: Upstream regulators and cellular targets of the selective autophagy cargo receptor AtNBR1 in different phases of sulfur deficiency in plants.
2020-04-20 | GSE122705 | GEO