<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cai Y</submitter><funding>Basic Research Program of Jiangsu</funding><funding>Excellence Research Group Program of NSFC</funding><funding>National Key R&amp;D Program of China</funding><funding>Research Funds of Hangzhou Institute for Advanced Study, UCAS</funding><funding>Zhejiang Provincial Natural Science Foundation of China</funding><funding>National Natural Science Foundation of China</funding><funding>Major Innovation Projects in Shandong Province</funding><funding>National Key Research and Development Program of China</funding><funding>Taishan Scholars Program for Young Experts of Shandong Provinceof Shandong Province</funding><pagination>e17423</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12903998</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(9)</volume><pubmed_abstract>Eukaryotic translation initiation factor 5A (eIF5A) facilitates protein synthesis and impacts diverse biological processes, yet its role in transcriptional regulation is poorly understood. Here eIF5A highly expressed in diverse spermatogenic cell types are found. Conditional knockout of Eif5a (SKO) causes complete infertility in male mice due to round spermatid arrest. Interestingly, eIF5A deletion severely compromises chromocenter integrity in round spermatids. Proteomic profiling reveals widespread dysregulation in eIF5A-deficient round spermatids, downregulated proteins are enriched for chromatin-associated functions, likely contributing to chromocenter dysfunction. Notably, ATAC-seq (Assay for Transposase-Accessible Chromatin with high-throughput sequencing) analysis shows increased ch</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>EIF5A Couples Translational Control With Transcriptional Reprogramming Through Chromocenter Reorganization During Spermiogenesis.</pubmed_title><pmcid>PMC12903998</pmcid><funding_grant_id>LZ23C050001</funding_grant_id><funding_grant_id>82071699</funding_grant_id><funding_grant_id>2025HLAS-ZL008</funding_grant_id><funding_grant_id>32271347</funding_grant_id><funding_grant_id>32588201</funding_grant_id><funding_grant_id>2023HIAS-Y022</funding_grant_id><funding_grant_id>82471644</funding_grant_id><funding_grant_id>2024YFA1108100</funding_grant_id><funding_grant_id>BK20240427</funding_grant_id><funding_grant_id>82371619</funding_grant_id><funding_grant_id>2021ZDSYS16</funding_grant_id><funding_grant_id>tsqn202103192</funding_grant_id><funding_grant_id>82501941</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Bao Z</pubmed_authors><pubmed_authors>Qi H</pubmed_authors><pubmed_authors>Kong F</pubmed_authors><pubmed_authors>Zhang M</pubmed_authors><pubmed_authors>Liu W</pubmed_authors><pubmed_authors>Guan Y</pubmed_authors><pubmed_authors>Li T</pubmed_authors><pubmed_authors>Jiang X</pubmed_authors><pubmed_authors>Fang Q</pubmed_authors><pubmed_authors>Cai Y</pubmed_authors><pubmed_authors>Chen ZJ</pubmed_authors><pubmed_authors>Wang W</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Wang X</pubmed_authors></additional><is_claimable>false</is_claimable><name>EIF5A Couples Translational Control With Transcriptional Reprogramming Through Chromocenter Reorganization During Spermiogenesis.</name><description>Eukaryotic translation initiation factor 5A (eIF5A) facilitates protein synthesis and impacts diverse biological processes, yet its role in transcriptional regulation is poorly understood. Here eIF5A highly expressed in diverse spermatogenic cell types are found. Conditional knockout of Eif5a (SKO) causes complete infertility in male mice due to round spermatid arrest. Interestingly, eIF5A deletion severely compromises chromocenter integrity in round spermatids. Proteomic profiling reveals widespread dysregulation in eIF5A-deficient round spermatids, downregulated proteins are enriched for chromatin-associated functions, likely contributing to chromocenter dysfunction. Notably, ATAC-seq (Assay for Transposase-Accessible Chromatin with high-throughput sequencing) analysis shows increased ch</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-07-15T15:38:10.944Z</modification><creation>2026-07-06T03:11:39.966Z</creation></dates><accession>S-EPMC12903998</accession><cross_references><pubmed>41486816</pubmed><doi>10.1002/advs.202517423</doi></cross_references></HashMap>