<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE275nnn/GSE275918/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE275918</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Whole brain transcriptome analysis of heterozygous and homozygous Chd8 mutation (Asn2373LysfsX2) mice age of P0, P25 and P56 with C57BL6/J x 129/Sv background</name><description>Autism spectrum disorders (ASD) are 4–5 times more common in males, possibly due to female protective effects (FPEs), which suggests females are less susceptible to ASD unless a genetic mutation is particularly strong. If this is the case, increasing the strength of a ASD-risk mutation above the female threshold may induce ASD symptoms both in females and males. To this end, we compared male and female phenotypes in heterozygous and homozygous mice carrying a patient-derived CHD8 mutation (Asn2373LysfsX2), using a hybrid genetic background to overcome homozygous lethality. Heterozygous Chd8+/N2373K males and females displayed sexually dimorphic phenotypes stronger than those in homozygous Chd8 N2373 /N2373K males and females in behaviors, brain blood flow, neuronal activity, synaptic transmission, and transcriptomes. These results suggest that a stronger Chd8 mutation suppresses sexual dimorphism in mice, supporting the FPE hypothesis in ASD.</description><dates><publication>2026/09/17</publication></dates><accession>GSE275918</accession><cross_references><GSM>GSM8488075</GSM><GSM>GSM8488031</GSM><GSM>GSM8488030</GSM><GSM>GSM8488074</GSM><GSM>GSM8488033</GSM><GSM>GSM8488077</GSM><GSM>GSM8488032</GSM><GSM>GSM8488076</GSM><GSM>GSM8488035</GSM><GSM>GSM8488079</GSM><GSM>GSM8488078</GSM><GSM>GSM8488034</GSM><GSM>GSM8488037</GSM><GSM>GSM8488036</GSM><GSM>GSM8488039</GSM><GSM>GSM8488038</GSM><GSM>GSM8488071</GSM><GSM>GSM8488070</GSM><GSM>GSM8488073</GSM><GSM>GSM8488072</GSM><GSM>GSM8488042</GSM><GSM>GSM8488086</GSM><GSM>GSM8488041</GSM><GSM>GSM8488085</GSM><GSM>GSM8488044</GSM><GSM>GSM8488088</GSM><GSM>GSM8488087</GSM><GSM>GSM8488043</GSM><GSM>GSM8488046</GSM><GSM>GSM8488045</GSM><GSM>GSM8488089</GSM><GSM>GSM8488048</GSM><GSM>GSM8488047</GSM><GSM>GSM8488049</GSM><GSM>GSM8488080</GSM><GSM>GSM8488082</GSM><GSM>GSM8488081</GSM><GSM>GSM8488084</GSM><GSM>GSM8488040</GSM><GSM>GSM8488083</GSM><GSM>GSM8488053</GSM><GSM>GSM8488097</GSM><GSM>GSM8488096</GSM><GSM>GSM8488052</GSM><GSM>GSM8488055</GSM><GSM>GSM8488099</GSM><GSM>GSM8488098</GSM><GSM>GSM8488054</GSM><GSM>GSM8488057</GSM><GSM>GSM8488056</GSM><GSM>GSM8488059</GSM><GSM>GSM8488058</GSM><GSM>GSM8488019</GSM><GSM>GSM8488091</GSM><GSM>GSM8488090</GSM><GSM>GSM8488093</GSM><GSM>GSM8488092</GSM><GSM>GSM8488095</GSM><GSM>GSM8488051</GSM><GSM>GSM8488050</GSM><GSM>GSM8488094</GSM><GSM>GSM8488064</GSM><GSM>GSM8488020</GSM><GSM>GSM8488063</GSM><GSM>GSM8488022</GSM><GSM>GSM8488066</GSM><GSM>GSM8488021</GSM><GSM>GSM8488065</GSM><GSM>GSM8488024</GSM><GSM>GSM8488101</GSM><GSM>GSM8488068</GSM><GSM>GSM8488067</GSM><GSM>GSM8488100</GSM><GSM>GSM8488023</GSM><GSM>GSM8488026</GSM><GSM>GSM8488103</GSM><GSM>GSM8488102</GSM><GSM>GSM8488025</GSM><GSM>GSM8488069</GSM><GSM>GSM8488028</GSM><GSM>GSM8488105</GSM><GSM>GSM8488104</GSM><GSM>GSM8488027</GSM><GSM>GSM8488107</GSM><GSM>GSM8488029</GSM><GSM>GSM8488106</GSM><GSM>GSM8488108</GSM><GSM>GSM8488060</GSM><GSM>GSM8488062</GSM><GSM>GSM8488061</GSM><GPL>21103</GPL><GSE>275918</GSE><taxon>Mus musculus</taxon><PMID>[42106518]</PMID></cross_references></HashMap>