<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Srivastav SP</submitter><funding>NICHD NIH HHS</funding><funding>NIA NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>e49948</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6917496</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8</volume><pubmed_abstract>Without transposon-silencing Piwi-interacting RNAs (piRNAs), transposition causes an ovarian atrophy syndrome in &lt;i>Drosophila&lt;/i> called gonadal dysgenesis (GD). &lt;i>Harwich&lt;/i> (&lt;i>Har&lt;/i>) strains with &lt;i>P&lt;/i>-elements cause severe GD in F1 daughters when &lt;i>Har&lt;/i> fathers mate with mothers lacking &lt;i>P&lt;/i>-element-piRNAs (i.e. &lt;i>ISO1&lt;/i> strain). To address the mystery of why &lt;i>Har&lt;/i> induces severe GD, we bred hybrid &lt;i>Drosophila&lt;/i> with &lt;i>Har&lt;/i> genomic fragments into the &lt;i>ISO1&lt;/i> background to create &lt;i>HISR-D or HISR-N&lt;/i> lines that still cause &lt;u>D&lt;/u>ysgenesis or are &lt;u>N&lt;/u>on-dysgenic, respectively. In these lines, we discovered a highly truncated &lt;i>P&lt;/i>-element variant we named '&lt;i>Har-P&lt;/i>' as the most frequent de novo insertion. Although &lt;i>HISR-D&lt;/i> lines st</pubmed_abstract><journal>eLife</journal><pubmed_title>&lt;i>Har-P&lt;/i>, a short &lt;i>P&lt;/i>-element variant, weaponizes &lt;i>P&lt;/i>-transposase to severely impair &lt;i>Drosophila&lt;/i> development.</pubmed_title><pmcid>PMC6917496</pmcid><funding_grant_id>R21-HD088792</funding_grant_id><funding_grant_id>R01-AG052465</funding_grant_id><funding_grant_id>R21 HD088792</funding_grant_id><funding_grant_id>R01 AG052465</funding_grant_id><pubmed_authors>Rahman R</pubmed_authors><pubmed_authors>Ma Q</pubmed_authors><pubmed_authors>Pierre J</pubmed_authors><pubmed_authors>Bandyopadhyay S</pubmed_authors><pubmed_authors>Lau NC</pubmed_authors><pubmed_authors>Srivastav SP</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Har-P&lt;/i>, a short &lt;i>P&lt;/i>-element variant, weaponizes &lt;i>P&lt;/i>-transposase to severely impair &lt;i>Drosophila&lt;/i> development.</name><description>Without transposon-silencing Piwi-interacting RNAs (piRNAs), transposition causes an ovarian atrophy syndrome in &lt;i>Drosophila&lt;/i> called gonadal dysgenesis (GD). &lt;i>Harwich&lt;/i> (&lt;i>Har&lt;/i>) strains with &lt;i>P&lt;/i>-elements cause severe GD in F1 daughters when &lt;i>Har&lt;/i> fathers mate with mothers lacking &lt;i>P&lt;/i>-element-piRNAs (i.e. &lt;i>ISO1&lt;/i> strain). To address the mystery of why &lt;i>Har&lt;/i> induces severe GD, we bred hybrid &lt;i>Drosophila&lt;/i> with &lt;i>Har&lt;/i> genomic fragments into the &lt;i>ISO1&lt;/i> background to create &lt;i>HISR-D or HISR-N&lt;/i> lines that still cause &lt;u>D&lt;/u>ysgenesis or are &lt;u>N&lt;/u>on-dysgenic, respectively. In these lines, we discovered a highly truncated &lt;i>P&lt;/i>-element variant we named '&lt;i>Har-P&lt;/i>' as the most frequent de novo insertion. Although &lt;i>HISR-D&lt;/i> lines st</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Dec</publication><modification>2026-04-14T21:08:34.292Z</modification><creation>2020-05-22T00:05:07Z</creation></dates><accession>S-EPMC6917496</accession><cross_references><pubmed>31845649</pubmed><doi>10.7554/eLife.49948</doi></cross_references></HashMap>