<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/GSE318670/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><species>Mus musculus</species><gds_type>Non-coding RNA profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE318670</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>mRNA 3ʹ UTRs direct microRNA degradation to participate in imprinted gene networks and regulate growth dataset 1</name><description>MicroRNAs direct downregulation of target mRNAs. Sometimes, however, this regulatory paradigm inverts, and a target RNA triggers degradation of a microRNA. This target-directed microRNA degradation (TDMD) requires ZSWIM8. Zswim8-/- mice exhibit reduced growth and perinatal lethality, accompanied by stabilization of >40 microRNAs. Nonetheless, studies of TDMD function in mammals have been limited because only two TDMD-triggering RNAs have been identified in mice. Here, we computationally identify and validate five new TDMD-triggering sites in mouse models. One site in Atp6v1g1 and two in Lpar4 direct degradation of miR-335-3p, showing that in mammals, two sites in the same transcript, and multiple sites in different transcripts, can collaborate to destabilize a microRNA. Moreover, sites in Plagl1 and Lrrc58 direct degradation of miR-322 and miR-503, respectively. Mice lacking the Plagl1 and Lrrc58 sites were smaller, demonstrating that target-directed degradation of miR-322 and miR-503 promotes growth. Both miR-335-3p and Plagl1 are maternally imprinted, implying their participation in parental conflict, but their corresponding triggers or target microRNA partner are not imprinted. Thus, 3¢ UTRs can participate in parental conflict not only by regulating protein production but also directly by engaging TDMD to access an additional layer of regulation within a network of imprinted and biallelic genes.</description><dates><publication>2026/04/08</publication></dates><accession>GSE318670</accession><cross_references><GSM>GSM9500312</GSM><GSM>GSM9500301</GSM><GSM>GSM9500300</GSM><GSM>GSM9500311</GSM><GSM>GSM9500310</GSM><GSM>GSM9500299</GSM><GSM>GSM9500298</GSM><GSM>GSM9500297</GSM><GSM>GSM9500296</GSM><GSM>GSM9500295</GSM><GSM>GSM9500294</GSM><GSM>GSM9500309</GSM><GSM>GSM9500308</GSM><GSM>GSM9500307</GSM><GSM>GSM9500306</GSM><GSM>GSM9500305</GSM><GSM>GSM9500304</GSM><GSM>GSM9500303</GSM><GSM>GSM9500302</GSM><GSM>GSM9500293</GSM><GSM>GSM9500292</GSM><GPL>17021</GPL><GSE>318670</GSE><taxon>Mus musculus</taxon><PMID>[41871909]</PMID></cross_references></HashMap>