Ontology highlight
ABSTRACT:
PROVIDER: PRJNA691424 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13415800_1.fastq.gz | Fastqsanger.gz | |||
| SRR13415800_2.fastq.gz | Fastqsanger.gz | |||
| SRR13415801_1.fastq.gz | Fastqsanger.gz | |||
| SRR13415801_2.fastq.gz | Fastqsanger.gz | |||
| SRR13415802_1.fastq.gz | Fastqsanger.gz |
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Project description:Innovative strategies for increasing the yield of rice, the staple food for more than half of the global population, are needed to keep pace with the expected worldwide population increase, and sustainably forefront the challenges posed by climate change. Traditionally, in Southern-East Asian countries, rice farming benefits from the use of Azolla spp., either as green manure or as co-cultivated plants, for the supply of nitrogen. Azolla spp. are ferns that, in virtue of their symbiosis with the nitrogen-fixing cyanobacterium Trichormus azollae, fix atmospheric nitrogen and release it to the environment upon decomposition of their biomass. However, if and to what extent actively growing Azolla plants impact on the development of co-cultivated rice plantlets remains to be understood. To address this point here we employed an experimental model to follow the growth and development of roots and aerial organs of rice seedlings when co-cultivated with Azolla filiculoides. We show that actively growing A. filiculoides plants alter the architecture of the roots, the transcriptome of the roots, and the hormonal profiles of both roots and leaves.
2024-10-10 | GSE278294 | GEO
Project description:In this work we evaluated the impact of nutritional unbalances, as lipids/nitrogen unbalances, on wine yeast survival during alcoholic fermentation. We showed that lipids limitations (actually ergosterol limitation) lead to a rapid loss of viability during the stationary phase of fermentation but that cell death rate is strongly modulated by the amount of nitrogen sources. Yeast survival is reduced when an excess of nitrogen is available in lipid-limited fermentations. Such rapid dying yeast cells fermenting with high nitrogen level and lipids-limited amounts displayed a low storage of carbohydrate trehalose and glycogen compared to nitrogen limited cells. Consistently, examination of the cells stress response using an HSP12 promoter-driven GFP expression showed that lipids limitation triggered a weaker stress response than nitrogen limitation. We examined the involvement of nitrogen signalling pathway in the triggering of cell death using a sch9-deleted strain. We showed that deletion of SCH9 restored a high yeast viability indicating that the signaling pathway acting through Sch9p is involved in the enhanced cell death triggered by nitrogen excess. In addition we showed that various nitrogen sources provoked cell death but that histidine and proline did not trigger a similar effect. As a whole our data indicate that lipids limitation does not elicit a transcriptional program leading to a stress response which protects yeast cells and that nitrogen excess triggers cell death through a modulation of this stress response, but not by HSP12. These results point a potential negative role of nitrogen in fermentation which has until now never been described and taken into account in the management of alcoholic fermentations.
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Project description:In order to identify microRNAs involved in response to nitrogen excess stress we performed deep sequencing of sRNA libraries constructed form RNA isolated from roots and shoots of two week old barley plants that have been grown under nitrogen excess stress and control conditions.
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Project description:We show that NtrC couples the Ntr stress response and stringent response in N starved E. coli, which appears to be a conserved adaptive strategy employed by many bacteria to manage conditions of nutritional adversity. N starved Escherichia coli initiate the nitrogen regulation (Ntr) stress response as an adaptive mechanism to scavenge for alternative N sources. The Ntr stress response requires the global transcriptional regulator nitrogen regulatory protein C (NtrC). We discovered that the transcription of relA, the key gene responsible for the synthesis of the major effector nucleotide alamorne of the bacterial stringent response, guanosine pentaphosphate (ppGpp), is positively regulated by NtrC in N starved E. coli. we addressed Ntr stress response-ppGpp alarmone links and mapped the genome-wide binding targets of NtrC in E. coli during N starvation using chromatin immunoprecipitation (ChIP) followed by high-throughput sequencing (ChIP-seq) to gain insight into the NtrC-dependent gene networks. To identify candidate genome regions that are preferentially associated with NtrC, we introduced an in-frame fusion encoding three repeats of the FLAG epitope to the 3-prime end of glnG in E. coli strain NCM3722, a prototrophic E. coli K-12 strain.
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Project description:Nitrogen (N) is an abundant and essential macronutrient for plants growth and development processes, especially for the huge banana trees with high biomass. In this paper, we studied the response of banana resists to low N stress ueing Illumina RNA-Seq technology, and analyzed the DEGs associated with the absorption, transport, and ulitilize of nitrogen.
2020-07-11 | GSE134166 | GEO
Project description:In this work we evaluated the impact of nutritional unbalances, as lipids/nitrogen unbalances, on wine yeast survival during alcoholic fermentation. We showed that lipids limitations (actually ergosterol limitation) lead to a rapid loss of viability during the stationary phase of fermentation but that cell death rate is strongly modulated by the amount of nitrogen sources. Yeast survival is reduced when an excess of nitrogen is available in lipid-limited fermentations. Such rapid dying yeast cells fermenting with high nitrogen level and lipids-limited amounts displayed a low storage of carbohydrate trehalose and glycogen compared to nitrogen limited cells. Consistently, examination of the cells stress response using an HSP12 promoter-driven GFP expression showed that lipids limitation triggered a weaker stress response than nitrogen limitation. We examined the involvement of nitrogen signalling pathway in the triggering of cell death using a sch9-deleted strain. We showed that deletion of SCH9 restored a high yeast viability indicating that the signaling pathway acting through Sch9p is involved in the enhanced cell death triggered by nitrogen excess. In addition we showed that various nitrogen sources provoked cell death but that histidine and proline did not trigger a similar effect. As a whole our data indicate that lipids limitation does not elicit a transcriptional program leading to a stress response which protects yeast cells and that nitrogen excess triggers cell death through a modulation of this stress response, but not by HSP12. These results point a potential negative role of nitrogen in fermentation which has until now never been described and taken into account in the management of alcoholic fermentations. 2 conditions with 2 biological replicates compared: 59A and 59A-Sch9
2013-03-31 | E-GEOD-42027 | biostudies-arrayexpress
Project description:Legumes can utilize atmospheric nitrogen via symbiotic nitrogen fixation, but this process is inhibited by high soil inorganic nitrogen. So far, how high nitrogen inhibits N2 fixation in mature nodules is still poorly understood. Here we construct a co-expression network in soybean nodule and find that a dynamic and reversible transcriptional network underlies the high N inhibition of N2 fixation. Intriguingly, several NAC transcription factors (TFs), designated as Soybean Nitrogen Associated NAPs (SNAPs), are amongst the most connected hub TFs. The nodules of snap1/2/3/4 quadruple mutants show less sensitivity to the high N inhibition of nitrogenase activity and acceleration of senescence. Integrative analysis shows that these SNAP TFs largely influence the high N transcriptional response through direct regulation of a subnetwork of senescence-associated genes and transcriptional regulators. We propose that the SNAP-mediated transcriptional network may trigger nodule senescence in response to high N.
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