<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/GSE318nnn/GSE318255/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Methylation profiling</omics_type><species>Mus musculus</species><gds_type>Methylation profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE318255</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>TET1 non-catalytic activity shapes the chromatin-landscape that directs de novo methylation establishment in the male germline [5hmCSeal]</name><description>In the germline, DNA methylation is globally erased in primordial germ cells (PGCs), enabling establishment of sex-specific methylomes in prospermatogonia or oocytes. The catalytic activity of TET1 is required for complete demethylation in PGCs, yet sperm from Tet1-/- mice display methylation defects not explained by incomplete erasure. Instead, these defects arise from abnormal de novo methylation during development, coinciding with erosion of H3K4me3, a chromatin modification that blocks DNMT3A/3L. Using a catalytically inactive Tet1HxD mouse line, we demonstrate a non-catalytic role of TET1 in promoting H3K4me3 deposition and protecting a subset of sperm hypomethylated regions from aberrant methylation in prospermatogonia.</description><dates><publication>2026/07/22</publication></dates><accession>GSE318255</accession><cross_references><GSM>GSM9491425</GSM><GSM>GSM9491426</GSM><GPL>32159</GPL><GSE>318255</GSE><taxon>Mus musculus</taxon><PMID>[42448565]</PMID></cross_references></HashMap>