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Genes with high penetrance for syndromic and non-syndromic autism typically function within the nucleus and regulate gene expression / Emily L. CASANOVA in Molecular Autism, 7 (2016)
[article]
Titre : Genes with high penetrance for syndromic and non-syndromic autism typically function within the nucleus and regulate gene expression Type de document : Texte imprimé et/ou numérique Auteurs : Emily L. CASANOVA, Auteur ; J. L. SHARP, Auteur ; H. CHAKRABORTY, Auteur ; N. S. SUMI, Auteur ; Manuel F. CASANOVA, Auteur Article en page(s) : 18p. Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/epidemiology/genetics/psychology Autistic Disorder/epidemiology/genetics/psychology Body Patterning/genetics Cell Nucleus/metabolism Chromatin Assembly and Disassembly/genetics Comorbidity Databases, Genetic Epigenomics Epilepsy/epidemiology/genetics/psychology Gene Expression Regulation Gene Ontology Genetic Association Studies Humans Intellectual Disability/epidemiology/genetics Nerve Tissue Proteins/genetics/physiology Neurogenesis/genetics Nuclear Proteins/genetics/physiology Penetrance Protein Interaction Maps/genetics Risk Syndrome Body patterning Chromatin assembly and disassembly Epilepsy Mental retardation Regulation of gene expression Index. décimale : PER Périodiques Résumé : BACKGROUND: Intellectual disability (ID), autism, and epilepsy share frequent yet variable comorbidities with one another. In order to better understand potential genetic divergence underlying this variable risk, we studied genes responsible for monogenic IDs, grouped according to their autism and epilepsy comorbidities. METHODS: Utilizing 465 different forms of ID with known molecular origins, we accessed available genetic databases in conjunction with gene ontology (GO) to determine whether the genetics underlying ID diverge according to its comorbidities with autism and epilepsy and if genes highly penetrant for autism or epilepsy share distinctive features that set them apart from genes that confer comparatively variable or no apparent risk. RESULTS: The genetics of ID with autism are relatively enriched in terms associated with nervous system-specific processes and structural morphogenesis. In contrast, we find that ID with highly comorbid epilepsy (HCE) is modestly associated with lipid metabolic processes while ID without autism or epilepsy comorbidity (ID only) is enriched at the Golgi membrane. Highly comorbid autism (HCA) genes, on the other hand, are strongly enriched within the nucleus, are typically involved in regulation of gene expression, and, along with IDs with more variable autism, share strong ties with a core protein-protein interaction (PPI) network integral to basic patterning of the CNS. CONCLUSIONS: According to GO terminology, autism-related gene products are integral to neural development. While it is difficult to draw firm conclusions regarding IDs unassociated with autism, it is clear that the majority of HCA genes are tightly linked with general dysregulation of gene expression, suggesting that disturbances to the chronology of neural maturation and patterning may be key in conferring susceptibility to autism spectrum conditions. En ligne : http://dx.doi.org/10.1186/s13229-016-0082-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328
in Molecular Autism > 7 (2016) . - 18p.[article] Genes with high penetrance for syndromic and non-syndromic autism typically function within the nucleus and regulate gene expression [Texte imprimé et/ou numérique] / Emily L. CASANOVA, Auteur ; J. L. SHARP, Auteur ; H. CHAKRABORTY, Auteur ; N. S. SUMI, Auteur ; Manuel F. CASANOVA, Auteur . - 18p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 18p.
Mots-clés : Autism Spectrum Disorder/epidemiology/genetics/psychology Autistic Disorder/epidemiology/genetics/psychology Body Patterning/genetics Cell Nucleus/metabolism Chromatin Assembly and Disassembly/genetics Comorbidity Databases, Genetic Epigenomics Epilepsy/epidemiology/genetics/psychology Gene Expression Regulation Gene Ontology Genetic Association Studies Humans Intellectual Disability/epidemiology/genetics Nerve Tissue Proteins/genetics/physiology Neurogenesis/genetics Nuclear Proteins/genetics/physiology Penetrance Protein Interaction Maps/genetics Risk Syndrome Body patterning Chromatin assembly and disassembly Epilepsy Mental retardation Regulation of gene expression Index. décimale : PER Périodiques Résumé : BACKGROUND: Intellectual disability (ID), autism, and epilepsy share frequent yet variable comorbidities with one another. In order to better understand potential genetic divergence underlying this variable risk, we studied genes responsible for monogenic IDs, grouped according to their autism and epilepsy comorbidities. METHODS: Utilizing 465 different forms of ID with known molecular origins, we accessed available genetic databases in conjunction with gene ontology (GO) to determine whether the genetics underlying ID diverge according to its comorbidities with autism and epilepsy and if genes highly penetrant for autism or epilepsy share distinctive features that set them apart from genes that confer comparatively variable or no apparent risk. RESULTS: The genetics of ID with autism are relatively enriched in terms associated with nervous system-specific processes and structural morphogenesis. In contrast, we find that ID with highly comorbid epilepsy (HCE) is modestly associated with lipid metabolic processes while ID without autism or epilepsy comorbidity (ID only) is enriched at the Golgi membrane. Highly comorbid autism (HCA) genes, on the other hand, are strongly enriched within the nucleus, are typically involved in regulation of gene expression, and, along with IDs with more variable autism, share strong ties with a core protein-protein interaction (PPI) network integral to basic patterning of the CNS. CONCLUSIONS: According to GO terminology, autism-related gene products are integral to neural development. While it is difficult to draw firm conclusions regarding IDs unassociated with autism, it is clear that the majority of HCA genes are tightly linked with general dysregulation of gene expression, suggesting that disturbances to the chronology of neural maturation and patterning may be key in conferring susceptibility to autism spectrum conditions. En ligne : http://dx.doi.org/10.1186/s13229-016-0082-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328 CRISPR/Cas9-mediated heterozygous knockout of the autism gene CHD8 and characterization of its transcriptional networks in cerebral organoids derived from iPS cells / P. WANG in Molecular Autism, 8 (2017)
[article]
Titre : CRISPR/Cas9-mediated heterozygous knockout of the autism gene CHD8 and characterization of its transcriptional networks in cerebral organoids derived from iPS cells Type de document : Texte imprimé et/ou numérique Auteurs : P. WANG, Auteur ; R. MOKHTARI, Auteur ; E. PEDROSA, Auteur ; M. KIRSCHENBAUM, Auteur ; C. BAYRAK, Auteur ; D. ZHENG, Auteur ; H. M. LACHMAN, Auteur Article en page(s) : 11p. Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/genetics Bipolar Disorder/genetics CRISPR-Cas Systems Cell Differentiation Cells, Cultured DNA-Binding Proteins/*genetics Gene Expression Profiling/*methods Gene Expression Regulation Gene Knockout Techniques *Gene Regulatory Networks Humans Induced Pluripotent Stem Cells/*cytology Mental Disorders/*genetics Mutation Organoids/*cytology Schizophrenia/genetics Sequence Analysis, RNA/*methods Telencephalon/*cytology Transcription Factors/*genetics *Autism *Beta-catenin *Bipolar disorder *Cancer *Dlx6-as1 *Distal-less homeobox *Gabaergic *Hmga2 *Schizophrenia *Tcf4 *Wnt *Znf132 Index. décimale : PER Périodiques Résumé : BACKGROUND: CHD8 (chromodomain helicase DNA-binding protein 8), which codes for a member of the CHD family of ATP-dependent chromatin-remodeling factors, is one of the most commonly mutated genes in autism spectrum disorders (ASD) identified in exome-sequencing studies. Loss of function mutations in the gene have also been found in schizophrenia (SZ) and intellectual disabilities and influence cancer cell proliferation. We previously reported an RNA-seq analysis carried out on neural progenitor cells (NPCs) and monolayer neurons derived from induced pluripotent stem (iPS) cells that were heterozygous for CHD8 knockout (KO) alleles generated using CRISPR-Cas9 gene editing. A significant number of ASD and SZ candidate genes were among those that were differentially expressed in a comparison of heterozygous KO lines (CHD8(+/-)) vs isogenic controls (CHD8(+/-)), including the SZ and bipolar disorder (BD) candidate gene TCF4, which was markedly upregulated in CHD8(+/-) neuronal cells. METHODS: In the current study, RNA-seq was carried out on CHD8(+/-) and isogenic control (CHD8(+/+)) cerebral organoids, which are 3-dimensional structures derived from iPS cells that model the developing human telencephalon. RESULTS: TCF4 expression was, again, significantly upregulated. Pathway analysis carried out on differentially expressed genes (DEGs) revealed an enrichment of genes involved in neurogenesis, neuronal differentiation, forebrain development, Wnt/beta-catenin signaling, and axonal guidance, similar to our previous study on NPCs and monolayer neurons. There was also significant overlap in our CHD8(+/-) DEGs with those found in a transcriptome analysis carried out by another group using cerebral organoids derived from a family with idiopathic ASD. Remarkably, the top DEG in our respective studies was the non-coding RNA DLX6-AS1, which was markedly upregulated in both studies; DLX6-AS1 regulates the expression of members of the DLX (distal-less homeobox) gene family. DLX1 was also upregulated in both studies. DLX genes code for transcription factors that play a key role in GABAergic interneuron differentiation. Significant overlap was also found in a transcriptome study carried out by another group using iPS cell-derived neurons from patients with BD, a condition characterized by dysregulated WNT/beta-catenin signaling in a subgroup of affected individuals. CONCLUSIONS: Overall, the findings show that distinct ASD, SZ, and BD candidate genes converge on common molecular targets-an important consideration for developing novel therapeutics in genetically heterogeneous complex traits. En ligne : http://dx.doi.org/10.1186/s13229-017-0124-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331
in Molecular Autism > 8 (2017) . - 11p.[article] CRISPR/Cas9-mediated heterozygous knockout of the autism gene CHD8 and characterization of its transcriptional networks in cerebral organoids derived from iPS cells [Texte imprimé et/ou numérique] / P. WANG, Auteur ; R. MOKHTARI, Auteur ; E. PEDROSA, Auteur ; M. KIRSCHENBAUM, Auteur ; C. BAYRAK, Auteur ; D. ZHENG, Auteur ; H. M. LACHMAN, Auteur . - 11p.
Langues : Anglais (eng)
in Molecular Autism > 8 (2017) . - 11p.
Mots-clés : Autism Spectrum Disorder/genetics Bipolar Disorder/genetics CRISPR-Cas Systems Cell Differentiation Cells, Cultured DNA-Binding Proteins/*genetics Gene Expression Profiling/*methods Gene Expression Regulation Gene Knockout Techniques *Gene Regulatory Networks Humans Induced Pluripotent Stem Cells/*cytology Mental Disorders/*genetics Mutation Organoids/*cytology Schizophrenia/genetics Sequence Analysis, RNA/*methods Telencephalon/*cytology Transcription Factors/*genetics *Autism *Beta-catenin *Bipolar disorder *Cancer *Dlx6-as1 *Distal-less homeobox *Gabaergic *Hmga2 *Schizophrenia *Tcf4 *Wnt *Znf132 Index. décimale : PER Périodiques Résumé : BACKGROUND: CHD8 (chromodomain helicase DNA-binding protein 8), which codes for a member of the CHD family of ATP-dependent chromatin-remodeling factors, is one of the most commonly mutated genes in autism spectrum disorders (ASD) identified in exome-sequencing studies. Loss of function mutations in the gene have also been found in schizophrenia (SZ) and intellectual disabilities and influence cancer cell proliferation. We previously reported an RNA-seq analysis carried out on neural progenitor cells (NPCs) and monolayer neurons derived from induced pluripotent stem (iPS) cells that were heterozygous for CHD8 knockout (KO) alleles generated using CRISPR-Cas9 gene editing. A significant number of ASD and SZ candidate genes were among those that were differentially expressed in a comparison of heterozygous KO lines (CHD8(+/-)) vs isogenic controls (CHD8(+/-)), including the SZ and bipolar disorder (BD) candidate gene TCF4, which was markedly upregulated in CHD8(+/-) neuronal cells. METHODS: In the current study, RNA-seq was carried out on CHD8(+/-) and isogenic control (CHD8(+/+)) cerebral organoids, which are 3-dimensional structures derived from iPS cells that model the developing human telencephalon. RESULTS: TCF4 expression was, again, significantly upregulated. Pathway analysis carried out on differentially expressed genes (DEGs) revealed an enrichment of genes involved in neurogenesis, neuronal differentiation, forebrain development, Wnt/beta-catenin signaling, and axonal guidance, similar to our previous study on NPCs and monolayer neurons. There was also significant overlap in our CHD8(+/-) DEGs with those found in a transcriptome analysis carried out by another group using cerebral organoids derived from a family with idiopathic ASD. Remarkably, the top DEG in our respective studies was the non-coding RNA DLX6-AS1, which was markedly upregulated in both studies; DLX6-AS1 regulates the expression of members of the DLX (distal-less homeobox) gene family. DLX1 was also upregulated in both studies. DLX genes code for transcription factors that play a key role in GABAergic interneuron differentiation. Significant overlap was also found in a transcriptome study carried out by another group using iPS cell-derived neurons from patients with BD, a condition characterized by dysregulated WNT/beta-catenin signaling in a subgroup of affected individuals. CONCLUSIONS: Overall, the findings show that distinct ASD, SZ, and BD candidate genes converge on common molecular targets-an important consideration for developing novel therapeutics in genetically heterogeneous complex traits. En ligne : http://dx.doi.org/10.1186/s13229-017-0124-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331 Transcriptome analysis of microglia in a mouse model of Rett syndrome: differential expression of genes associated with microglia/macrophage activation and cellular stress / D. ZHAO in Molecular Autism, 8 (2017)
[article]
Titre : Transcriptome analysis of microglia in a mouse model of Rett syndrome: differential expression of genes associated with microglia/macrophage activation and cellular stress Type de document : Texte imprimé et/ou numérique Auteurs : D. ZHAO, Auteur ; R. MOKHTARI, Auteur ; E. PEDROSA, Auteur ; R. BIRNBAUM, Auteur ; D. ZHENG, Auteur ; H. M. LACHMAN, Auteur Article en page(s) : 17p. Langues : Anglais (eng) Mots-clés : Animals Disease Models, Animal Female Gene Expression Profiling/*methods Gene Expression Regulation Heat-Shock Proteins/genetics Humans Macrophage Activation Macrophages/*cytology Methyl-CpG-Binding Protein 2/*deficiency Mice Microglia/*metabolism Mutation Oxidative Stress Rett Syndrome/*genetics Sequence Analysis, RNA/*methods *Autism *Heat shock *Innate immune system *M1 activation *M2 activation *Microglia *Rett syndrome *Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome (RTT) is a severe, neurodevelopmental disorder primarily affecting girls, characterized by progressive loss of cognitive, social, and motor skills after a relatively brief period of typical development. It is usually due to de novo loss of function mutations in the X-linked gene, MeCP2, which codes for the gene expression and chromatin regulator, methyl-CpG binding protein 2. Although the behavioral phenotype appears to be primarily due to neuronal Mecp2 deficiency in mice, other cell types, including astrocytes and oligodendrocytes, also appear to contribute to some aspects of the RTT phenotype. In addition, microglia may also play a role. However, the effect of Mecp2 deficiency in microglia on RTT pathogenesis is controversial. METHODS: In the current study, we applied whole transcriptome analysis using RNA-seq to gain insight into molecular pathways in microglia that might be dysregulated during the transition, in female mice heterozygous for an Mecp2-null allele (Mecp2(+/-); Het), from the pre-phenotypic (5 weeks) to the phenotypic phases (24 weeks). RESULTS: We found a significant overlap in differentially expressed genes (DEGs) with genes involved in regulating the extracellular matrix, and those that are activated or inhibited when macrophages and microglia are stimulated towards the M1 and M2 activation states. However, the M1- and M2-associated genes were different in the 5- and 24-week samples. In addition, a substantial decrease in the expression of nine members of the heat shock protein (HSP) family was found in the 5-week samples, but not at 24 weeks. CONCLUSIONS: These findings suggest that microglia from pre-phenotypic and phenotypic female mice are activated in a manner different from controls and that pre-phenotypic female mice may have alterations in their capacity to response to heat stress and other stressors that function through the HSP pathway. En ligne : http://dx.doi.org/10.1186/s13229-017-0134-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331
in Molecular Autism > 8 (2017) . - 17p.[article] Transcriptome analysis of microglia in a mouse model of Rett syndrome: differential expression of genes associated with microglia/macrophage activation and cellular stress [Texte imprimé et/ou numérique] / D. ZHAO, Auteur ; R. MOKHTARI, Auteur ; E. PEDROSA, Auteur ; R. BIRNBAUM, Auteur ; D. ZHENG, Auteur ; H. M. LACHMAN, Auteur . - 17p.
Langues : Anglais (eng)
in Molecular Autism > 8 (2017) . - 17p.
Mots-clés : Animals Disease Models, Animal Female Gene Expression Profiling/*methods Gene Expression Regulation Heat-Shock Proteins/genetics Humans Macrophage Activation Macrophages/*cytology Methyl-CpG-Binding Protein 2/*deficiency Mice Microglia/*metabolism Mutation Oxidative Stress Rett Syndrome/*genetics Sequence Analysis, RNA/*methods *Autism *Heat shock *Innate immune system *M1 activation *M2 activation *Microglia *Rett syndrome *Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome (RTT) is a severe, neurodevelopmental disorder primarily affecting girls, characterized by progressive loss of cognitive, social, and motor skills after a relatively brief period of typical development. It is usually due to de novo loss of function mutations in the X-linked gene, MeCP2, which codes for the gene expression and chromatin regulator, methyl-CpG binding protein 2. Although the behavioral phenotype appears to be primarily due to neuronal Mecp2 deficiency in mice, other cell types, including astrocytes and oligodendrocytes, also appear to contribute to some aspects of the RTT phenotype. In addition, microglia may also play a role. However, the effect of Mecp2 deficiency in microglia on RTT pathogenesis is controversial. METHODS: In the current study, we applied whole transcriptome analysis using RNA-seq to gain insight into molecular pathways in microglia that might be dysregulated during the transition, in female mice heterozygous for an Mecp2-null allele (Mecp2(+/-); Het), from the pre-phenotypic (5 weeks) to the phenotypic phases (24 weeks). RESULTS: We found a significant overlap in differentially expressed genes (DEGs) with genes involved in regulating the extracellular matrix, and those that are activated or inhibited when macrophages and microglia are stimulated towards the M1 and M2 activation states. However, the M1- and M2-associated genes were different in the 5- and 24-week samples. In addition, a substantial decrease in the expression of nine members of the heat shock protein (HSP) family was found in the 5-week samples, but not at 24 weeks. CONCLUSIONS: These findings suggest that microglia from pre-phenotypic and phenotypic female mice are activated in a manner different from controls and that pre-phenotypic female mice may have alterations in their capacity to response to heat stress and other stressors that function through the HSP pathway. En ligne : http://dx.doi.org/10.1186/s13229-017-0134-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331 Possible sexually dimorphic role of miRNA and other sncRNA in ASD brain / C. M. SCHUMANN in Molecular Autism, 8 (2017)
[article]
Titre : Possible sexually dimorphic role of miRNA and other sncRNA in ASD brain Type de document : Texte imprimé et/ou numérique Auteurs : C. M. SCHUMANN, Auteur ; F. R. SHARP, Auteur ; Bradley P. ANDER, Auteur ; B. STAMOVA, Auteur Article en page(s) : 4p. Langues : Anglais (eng) Mots-clés : Adolescent Adult Autism Spectrum Disorder/*genetics Child Child, Preschool Female Gene Expression Profiling/*methods Gene Expression Regulation Humans Male MicroRNAs/*genetics Middle Aged Oligonucleotide Array Sequence Analysis/*methods RNA, Small Untranslated/*genetics Sex Characteristics Young Adult *Auditory cortex *Autism *Myelin *Oligodendrocytes *Postmortem human brain *Sex *Sexual dimorphism *Superior Temporal Sulcus *miR-125 *miR-181 *miR-219 *miR-338 *miR-448 *microRNA *small noncoding RNA Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is sexually dimorphic in brain structure, genetics, and behaviors. In studies of brain tissue, the age of the population is clearly a factor in interpreting study outcome, yet sex is rarely considered. To begin to address this issue, we extend our previously published microarray analyses to examine expression of small noncoding RNAs (sncRNAs), including microRNAs (miRNAs), in ASD and in the control temporal cortex in males and females. Predicted miRNA targets were identified as well as the pathways they overpopulate. FINDINGS: After considering age, sexual dimorphism in ASD sncRNA expression persists in the temporal cortex and in the patterning that distinguishes regions. Among the sexually dimorphic miRNAs are miR-219 and miR-338, which promote oligodendrocyte differentiation, miR-125, implicated in neuronal differentiation, and miR-488, implicated in anxiety. Putative miRNA targets are significantly over-represented in immune and nervous system pathways in both sexes, consistent with previous mRNA studies. Even for common pathways, the specific target mRNAs are often sexually dimorphic. For example, both male and female target genes significantly populate the Axonal Guidance Signaling pathway, yet less than a third of the targets are common to both sexes. CONCLUSIONS: Our findings of sexual dimorphism in sncRNA levels underscore the importance of considering sex, in addition to age, when interpreting molecular findings on ASD brain. En ligne : http://dx.doi.org/10.1186/s13229-017-0117-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331
in Molecular Autism > 8 (2017) . - 4p.[article] Possible sexually dimorphic role of miRNA and other sncRNA in ASD brain [Texte imprimé et/ou numérique] / C. M. SCHUMANN, Auteur ; F. R. SHARP, Auteur ; Bradley P. ANDER, Auteur ; B. STAMOVA, Auteur . - 4p.
Langues : Anglais (eng)
in Molecular Autism > 8 (2017) . - 4p.
Mots-clés : Adolescent Adult Autism Spectrum Disorder/*genetics Child Child, Preschool Female Gene Expression Profiling/*methods Gene Expression Regulation Humans Male MicroRNAs/*genetics Middle Aged Oligonucleotide Array Sequence Analysis/*methods RNA, Small Untranslated/*genetics Sex Characteristics Young Adult *Auditory cortex *Autism *Myelin *Oligodendrocytes *Postmortem human brain *Sex *Sexual dimorphism *Superior Temporal Sulcus *miR-125 *miR-181 *miR-219 *miR-338 *miR-448 *microRNA *small noncoding RNA Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is sexually dimorphic in brain structure, genetics, and behaviors. In studies of brain tissue, the age of the population is clearly a factor in interpreting study outcome, yet sex is rarely considered. To begin to address this issue, we extend our previously published microarray analyses to examine expression of small noncoding RNAs (sncRNAs), including microRNAs (miRNAs), in ASD and in the control temporal cortex in males and females. Predicted miRNA targets were identified as well as the pathways they overpopulate. FINDINGS: After considering age, sexual dimorphism in ASD sncRNA expression persists in the temporal cortex and in the patterning that distinguishes regions. Among the sexually dimorphic miRNAs are miR-219 and miR-338, which promote oligodendrocyte differentiation, miR-125, implicated in neuronal differentiation, and miR-488, implicated in anxiety. Putative miRNA targets are significantly over-represented in immune and nervous system pathways in both sexes, consistent with previous mRNA studies. Even for common pathways, the specific target mRNAs are often sexually dimorphic. For example, both male and female target genes significantly populate the Axonal Guidance Signaling pathway, yet less than a third of the targets are common to both sexes. CONCLUSIONS: Our findings of sexual dimorphism in sncRNA levels underscore the importance of considering sex, in addition to age, when interpreting molecular findings on ASD brain. En ligne : http://dx.doi.org/10.1186/s13229-017-0117-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331