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SRX26512701: GSM8596561: 6.6._CS_t=0; Nostoc sp. PCC 7120 = FACHB-418; RNA-Seq
1 DNBSEQ (DNBSEQ-G400) run: 42.8M spots, 8.6G bases, 6Gb downloads

External Id: GSM8596561_r1
Submitted by: Photomicrobes, Life Sciences, Turku University
Study: The role of the ??LysR-type transcription factor PacR in regulating nitrogen metabolism in Anabaena sp. PCC7120
show Abstracthide Abstract
Deletion of the global transcription factor PacR in Anabaena triggers heterocyst formation even in NO3- containing medium, likely due to impaired NO3- uptake and disrupted NH4+ assimilation in the GOGAT cycle. This phenotype may be exacerbated by reduced PSI-yield and reduced expression of ferredoxin, which may lead to less reducing equivalents for nitrogen uptake and fixation. These results highlight PacR's role as a global regulator of carbon metabolism and photosynthesis while also establishing its involvement in regulating nitrogen metabolism. Overall design: To investigate the effect of PacR-deletion in Anabaena sp. PCC7120, we used a ?pacR strain and a control strain which expressed PacR. We took samples directly before changing the nitrogen source from NH4+ to NO3- as well as 1h after and 12h after the shift. RNA was extracted from 3 biological replicates per timepoint and strain. We then performed differential expression anaysis between the strains and between the timepoints for each strain.
Sample: 6.6._CS_t=0
SAMN44467244 • SRS23025261 • All experiments • All runs
Library:
Name: GSM8596561
Instrument: DNBSEQ-G400
Strategy: RNA-Seq
Source: TRANSCRIPTOMIC
Selection: cDNA
Layout: PAIRED
Construction protocol: Total RNA was isolated using the hot-phenol method. DNAse treatment was performed with the Invitrogen kit. RNA concentration was measured with DS-11+ spectrophotometer (DeNovix) and 3ug of RNA from each sample was sent to BGI (China) for RNA-sequencing. Library construction was performed as a service by BGI
Runs: 1 run, 42.8M spots, 8.6G bases, 6Gb
Run# of Spots# of BasesSizePublished
SRR3113075642,840,8228.6G6Gb2024-11-05

ID:
35832702

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