Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Knocking out a negative regulator of photosynthesis 1 (NRP1) increases rice leaf photosynthesis and biomass production in the field

ABSTRACT: Knocking out a negative regulator of photosynthesis 1 (NRP1) increases rice leaf photosynthesis and biomass production in the field

PROVIDER: PRJNA564036 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10071300_1.fastq.gz	Fastqsanger.gz
	SRR10071300_2.fastq.gz	Fastqsanger.gz
	SRR10071301_1.fastq.gz	Fastqsanger.gz
	SRR10071301_2.fastq.gz	Fastqsanger.gz
	SRR10071302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 42

Similar Datasets

Knocking out a negative regulator of photosynthesis 1 (NRP1) increases rice leaf photosynthesis and biomass production in the field

Project description:Improving photosynthesis is a major approach to increase crop yield potential. Here we report a negative transcription factor of photosynthesis, which can be manipulated to increase rice photosynthesis and plant biomass in the field. This transcription factor named negative regulator of photosynthesis 1 (NRP1) (Os07g0471900) which was identified through a co-expression analysis using rice leaf RNA sequencing (RNA-seq) data. The NRP1 showed significantly negative correlation with the expression of many genes involved in photosynthesis. Knocking out NPR1 led to greater photosynthesis and increased biomass in the field, while overexpression of NRP1 decreased photosynthesis and biomass. Transcriptomic data analysis shows that NRP1 can negatively regulate the expression of photosynthetic genes. Protein transactivation experiments show that NRP1 is a transcription activator, implying that NRP1 may indirectly regulate photosynthesis gene expression through an unknown regulator. This study shows that combination of bioinformatics analysis with transgenic testing can be used to identify new regulators to improve photosynthetic efficiency in crops.

2019-10-15 | GSE136918 | GEO

Over-expression of a transcription factor mEmBP-1a increases rice photosynthesis, biomass and yield by regulating the expression of multiple key photosynthesis genes

Project description:Improvement in the photosynthetic efficiency is a major approach to improve crop yield potential. So far, most of the demonstrated cases of photosynthesis improvement was achieved through manipulation of one or a few photosynthesis related genes. Present study found that over-expression of one maize transcription factor, mEmBP-1 gene, led to simultaneously increased expression of nearly all genes in photosynthesis pathway, including genes encoding chlorophyll a and b-binding proteins (Lhca and Lhcb), photosystem II (PsbR3 and PsbW) and PS I reaction center subunits (PsaK and PsaN), genes encoding for chloroplast ATP synthase subunit and electron transport reaction (Fd1 and PC), and also major genes in the Calvin Benson Bassham cycle, Rubisco, GAPDH, FBA, TK and PRK. This increased photosynthesis gene expression resulted in increased leaf chlorophyll pigment, photosynthetic rate, quantum yields, biomass growth and grain yield both in the greenhouse and also in natural field conditions. Using DNA-Protein binding experiment, we found that mEmBP-1a protein can directly bind to the promoter regions of photosynthesis genes, suggesting that the direct binding of mEmBP-1a to the G-box domain of photosynthetic genes upregulates expression of these genes. Hence, this study shows that mEmBP-1a is a major regulator of photosynthesis.

2020-01-08 | GSE143259 | GEO

Proteomic experiment of lysine crotonylation modification to analysis of the role of knocking down NRP1 after IR in kidney

Project description:Neuropilin-1 (NRP1), a co-receptor for various cytokines, including TGF-β, has been identified as a potential therapeutic target for fibrosis. However, its role and mechanism in renal fibrosis remains elusive. Here, we show that NRP1 is upregulated in distal tubular (DT) cells of patients with transplant renal insufficiency and mice with renal ischemia-reperfusion (I-R) injury. Knockout of Nrp1 reduced multiple endpoints of renal injury and fibrosis. We found that Nrp1 facilitates the binding of TNF-α to its receptor in DT cells after renal injury. This signaling results in a downregulation of lysine crotonylation of the metabolic enzyme Cox4i1, decreased cellular energetics and exacerbation of renal injury. Furthermore, by single-cell RNA-sequencing we found that Nrp1-positive DT cells secrete collagen and communicate with myofibroblasts, exacerbating acute kidney injury (AKI)-induced renal fibrosis by activating Smad3. Dual genetic deletion of Nrp1 and Tgfbr1 in DT cells better improves renal injury and fibrosis than either single knockout. Together, these results reveal that targeting of NRP1 represents a promising strategy for the treatment of AKI and subsequent chronic kidney disease.

2024-06-03 | PXD052293 | Pride

Quantitative proteomic analysis of the role of knocking down NRP1 after OGD/R in primary renal tubular epithelial cells

2024-06-03 | PXD052244 | Pride

Comparison of Splenic Nrp1- and Nrp1+ Treg Populations

Project description:To compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg Cells were FACS sorted based upon expression of CD4, Foxp3 and expression of Nrp1.

2012-08-30 | E-GEOD-40441 | biostudies-arrayexpress

Comparison of Splenic Nrp1- and Nrp1+ Treg Populations

Project description:To compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg

2012-08-30 | GSE40441 | GEO

Wildtype and NRP1 knockout macrophages

Project description:Obesity gives rise to metabolic complications by mechanisms that are poorly understood. While chronic inflammatory signaling in adipose tissue is typically associated with metabolic deficiencies linked to excessive weight gain, we identified a subset of NRP1-expressing myeloid cells that accumulate in adipose tissue and protect against obesity and metabolic syndrome. Ablation of NRP1 in macrophages compromised lipid uptake in these cells, which reduced substrates for fatty acid β-oxidation and shifted energy metabolism of these macrophages towards a more inflammatory glycolytic metabolism. Conditional deletion of NRP1 in LysM Cre-expressing cells lead to inadequate adipose vascularization, accelerated weight gain and reduced insulin sensitivity even independent of weight gain. Transfer of NRP1+ hematopoietic cells improved glucose homeostasis, resulting in the reversal of a prediabetic phenotype. Our findings suggest a pivotal role for adipose tissue resident NRP1+-expressing macrophages in driving healthy weight gain and maintaining glucose tolerance.

2018-02-11 | GSE110447 | GEO

Effect of knocking out SOCS3 in mouse ES cells

Project description:Series contains four arrays - two wildtype, two null. The experiment studied the effect of knocking out SOCS3 in mouse ES cells. Keywords: other

2005-02-02 | GSE2202 | GEO

Wildtype and NRP1 knockout macrophages

Project description:Wildtype and NRP1 knockout macrophages

| PRJNA433729 | ENA

Knocking out the LRRK2 gene increases sensitivity to wavelength information in rats.

Project description:Leucine-rich repeat kinase 2 (LRRK2) is a gene related to familial Parkinson's disease (PD). It has been associated with nonmotor symptoms such as disturbances in the visual system affecting colour discrimination and contrast sensitivity. This study examined how deficiency of LRRK2 impacts visual processing in adult rats. Additionally, we investigated whether these changes can be modelled in wild-type rats by administering the LRRK2 inhibitor PFE360. Visual evoked potentials (VEPs) and steady-state visual evoked potentials (SSVEPs) were recorded in the visual cortex and superior colliculus of female LRRK2-knockout and wild-type rats to study how the innate absence of LRRK2 changes visual processing. Exposing the animals to stimulation at five different wavelengths revealed an interaction between genotype and the response to stimulation at different wavelengths. Differences in VEP amplitudes and latencies were robust and barely impacted by the presence of the LRRK2 inhibitor PFE360, suggesting a developmental effect. Taken together, these results indicate that alterations in visual processing were related to developmental deficiency of LRRK2 and not acute deficiency of LRRK2, indicating a role of LRRK2 in the functional development of the visual system and synaptic transmission.

| S-EPMC10904730 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data