<HashMap><database>iProX</database><scores/><additional><omics_type>Proteomics</omics_type><submitter>Xiancheng Li</submitter><species>Proteus Mirabilis</species><full_dataset_link>http://www.iprox.org/page/project.html?id=IPX0013336000</full_dataset_link><submitter_email>lxc2620@163.com</submitter_email><submitter_affiliation>The Second Affiliated Hospital of Dalian Medical University</submitter_affiliation><sample_protocol></sample_protocol><repository>iProX</repository><data_protocol></data_protocol></additional><is_claimable>false</is_claimable><name>Decoding the Regulatory Networks of Proteus mirabilis Under Succinic Acid Stress: A Multi-Omics Approach</name><description>Proteus mirabilis, a key catheter-associated urinary tract infection pathogen that forms antibiotic-resistant crystalline biofilms, was shown via multi-omics analyses to be multimodally inhibited by succinic acid. At 15 mM, succinic acid reduced the bacterium’s growth by 70% and biofilm formation by 50%. Metabolomics revealed dysregulation in tryptophan/arginine metabolism, nucleotide biosynthesis, and the tricarboxylic acid cycle; transcriptomics showed downregulated ribosomal genes, oxidative phosphorylation, and efflux pumps plus upregulated arginine transport; and proteomics demonstrated suppressed T6SS virulence factors and iron acquisition proteins. Mechanistically, succinic acid is proposed to reduce K6 acetylation of the histone-like nucleoid structuring protein, enhancing its oligomerization to repress T6SS genes and inhibit biofilm formation. By targeting metabolism, virulence, and stress adaptation, succinic acid circumvents single-target resistance, offering a strategy to combat multidrug-resistant P. mirabilis via biofilm disruption and pathogenicity suppression.The uploaded data comprise two omics datasets:Acetyl-proteomics: Folders prefixed with XB10893DPAc (treatment: H1–H3; control: T1–T3)；Proteomics: Folders prefixed with XB10893DA (treatment: H1–H3; control: T1–T3).</description><dates><publication>Mon Sep 08 00:00:00 BST 2025</publication></dates><accession>PXD068166</accession><cross_references><TAXONOMY>584</TAXONOMY></cross_references></HashMap>