Project description:Transcriptional profiling of the bacteria Paenibacillus vortex comparing control untreated cells with kanamycin treated cells after 18 hours of exposure. Goal was to determine the effect of the antibiotic kanamycin in concentration which affect the colony morphology on global bacteria gene expression. Two-condition experiment, control cells vs. kanamycin treated cells. Biological replicates: 2 control replicates, 2 treated replicates. Pooling of 5 technical replicates for each biological replicate.

2012-01-24 | E-GEOD-35271 | biostudies-arrayexpress

Transcriptome analysis reveals that sporulation is used as an iron deficiency resistance mechanism in Paenibacillus riograndensis SBR5

Project description:Transcriptome analysis of Paenibacillus riograndensis SBR5. SBR5 strain was grown in sufficient iron media and limited iron media.

2015-04-11 | E-GEOD-66816 | biostudies-arrayexpress

KCNH2-3.1 mediates aberrant complement activation to impair hippocampal-medial prefrontal pathway associated with schizophrenia

Project description:Although elevated KCNH2-3.1 potassium channel expression is associated with cognitive dysfunctions and with schizophrenia, little is known about the pathophysiology of synapses in patient neurons and how elevated levels of KCNH2-3.1 potassium channel could lead to synaptic deficits in humans. Here, we identified specific and delayed disruption of hippocampal-mPFC synaptic transmission and connection unexpectedly associated with age-dependent reduction of SERPING1, CFH and CD74 in the KCNH2-3.1 overexpression transgenic mice, and dysfunctional interactions between hippocampus and prefrontal cortex in the fMRI coupling signal during working memory encoding in healthy subjects carrying schizophrenia-associated risk alleles of KCNH2 potassium channel. These three genes are enriched in neurons or microglia, and reduced expression of these genes dysregulates the complement cascade activation underlying impaired synaptic connectivity of hippocampal-mPFC projections. Knockdown of these genes’ expression impairs synapse formation, and replenishing reduced CFH gene expression rescues KCNH2-3.1-induced impaired synaptogenesis. Our results uncover a previously unrecognized role of truncated KCNH2-3.1 potassium channel mediating reduced expression of three genes mentioned above, which enhances aberrant complement cascade activation during development. These results direct an important conceptual advance that truncated KCNH2-3.1 causes synapse loss mediated by abnormally activated complement system, rather than aberrant neuronal firing, may represent the therapeutic targets for a number of patients with schizophrenia.

2019-08-23 | GSE118989 | GEO