<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>genomiqueENS IBENS</submitter><organism>Mus musculus</organism><software>Eoulsan</software><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-15335</full_dataset_link><description>Numerous mood and behavior disorders have developmental origin resulting from genetic and environmental interactions. Maternal blood serotonin (5-HT) depletion alters embryonic brain development, but its long-term impact on progeny has never been investigated. Here we demonstrate that maternal blood hyposerotonemia (60% deficit) induced hyperlocomotion, self-care deficit and increased anxiety in adult WT male offspring. Concomitantly, norepinephrine (NE) level and dopamine (DA) turnover were significantly reduced in the mesencephalon and brainstem, whereas monoaminergic cell density was not affected. In the frontal cortex, maternal hyposerotonemia caused a significant reduction in DA, NE and 5-HT levels, accompanied by transcriptomic changes, notably in monoaminergic system signaling, synaptic function and plasticity, methylation processes and myelination. Myelination was also defective as revealed by a reduced thickness of the corpus callosum. Maternal hyposerotonemia is thus sufficient to affect the phenotype of adult WT progeny. Maternal peripheral 5-HT deficit during pregnancy could thus be considered as a risk factor for neurodevelopmental disorders in the offspring.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Nucleic Acid Extraction - Brain tissue was homogenized in 1mL TRIzolTM and total RNA was isolated using RNeasy micro kit RNA extraction according to the manufacturer’s instructions (Macherey-Nagel, France). RNA was eluted in RNase/DNase free water. The quality and concentration of the RNA extracts were assessed by spectrophotometry using the NanodropTM apparatus (Thermofisher Scientific, MA, USA)</sample_protocol><sample_protocol>Sequencing - Libraries were multiplexed by 12 on a P2 flow cells. A 118 bp read sequencing was performed on a NextSeq 2000 device (Illumina). A mean of 41 ± 5 million passing Illumina quality filter reads was obtained for each of the 12 samples.</sample_protocol><sample_protocol>Sample Collection - Animal procedures were approved by the local Ethics Committee No. 121 and were conducted in compliance with the ARRIVE guidelines. Animals were sedated and received a terminal injection of pentobarbital (150 mg/kg, i.p.). Mouse brains were removed, and the frontal cortex (from bregma levels 3.20 to 0.38) was dissected, weighed, rapidly frozen, and stored at −80 °C.</sample_protocol><sample_protocol>Library Construction - Messenger (polyA+) RNAs were purified from 1000 ng of total RNA using oligo(dT). Libraries were performed using the strand specific RNA-Seq library preparation Stranded mRNA Prep, Ligation kit (Illumina)</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><data_protocol>Sequence Alignment - The analyses were performed using the Eoulsan pipeline, including read filtering, mapping, alignment filtering, read quantification, normalisation and differential analysis: Before mapping, poly N read tails were trimmed, reads ≤40 bases were removed, and reads with quality mean ≤30 were discarded. Reads were then aligned against the human genome from Ensembl version 105 using STAR (version 2.7.8a). Alignments from reads matching more than once on the reference genome were removed using Java version of samtools. To compute gene expression, Mus musculus GTF genome annotation version 105 from Ensembl database was used. All overlapping regions between alignments and referenced exons were counted and aggregated by genes using HTSeq-count 0.5.3.</data_protocol><data_protocol>Data Transformation - The sample counts were normalized using DESeq2 1.8.1 in Eoulsan pipeline.</data_protocol><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>NextSeq 2000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><species>Mus musculus</species><pubmed_authors>Guilan Vodjdani</pubmed_authors><pubmed_authors>Tania Vitalis</pubmed_authors><pubmed_authors>Françoise Saurini</pubmed_authors><pubmed_authors>genomiqueENS IBENS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impact of maternal blood hyposerotonemia on adult wild-type progeny</name><description>Numerous mood and behavior disorders have developmental origin resulting from genetic and environmental interactions. Maternal blood serotonin (5-HT) depletion alters embryonic brain development, but its long-term impact on progeny has never been investigated. Here we demonstrate that maternal blood hyposerotonemia (60% deficit) induced hyperlocomotion, self-care deficit and increased anxiety in adult WT male offspring. Concomitantly, norepinephrine (NE) level and dopamine (DA) turnover were significantly reduced in the mesencephalon and brainstem, whereas monoaminergic cell density was not affected. In the frontal cortex, maternal hyposerotonemia caused a significant reduction in DA, NE and 5-HT levels, accompanied by transcriptomic changes, notably in monoaminergic system signaling, synaptic function and plasticity, methylation processes and myelination. Myelination was also defective as revealed by a reduced thickness of the corpus callosum. Maternal hyposerotonemia is thus sufficient to affect the phenotype of adult WT progeny. Maternal peripheral 5-HT deficit during pregnancy could thus be considered as a risk factor for neurodevelopmental disorders in the offspring.</description><dates><release>2026-06-12T00:00:00Z</release><modification>2026-06-12T09:14:06.776Z</modification><creation>2025-07-09T13:54:33.169Z</creation></dates><accession>E-MTAB-15335</accession><cross_references><ENA>ERP175138</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0004917</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003816</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>