ArticlebioRxiv : the preprint server for biology2025
LiaS-dependent activation of the MadR regulon enables cross-talk between
Kara S Hood, Samie A Rizvi, Guillermo A Hoppe-Elsholz, Ana P Streling, Diana Panesso, Shivendra Pratap, Yousif Shamoo, Cesar A Arias, William R Miller
Abstract readPreprint
In one paragraphArticle in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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0citing papers in PubMed
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1 · What the graph read from itWhat it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registryThe trial behind it
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3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
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4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
9 authors.
Kara S HoodCenter for Infectious Diseases, Houston Methodist Research Institute, Houston, Texas, USA.
Samie A RizviCenter for Infectious Diseases, Houston Methodist Research Institute, Houston, Texas, USA.
Guillermo A Hoppe-ElsholzCenter for Infectious Diseases, Houston Methodist Research Institute, Houston, Texas, USA.
Ana P StrelingCenter for Infectious Diseases, Houston Methodist Research Institute, Houston, Texas, USA.ORCID 0000-0002-1662-0947 Diana PanessoCenter for Infectious Diseases, Houston Methodist Research Institute, Houston, Texas, USA.
Shivendra PratapDepartment of Biosciences, Rice University, Houston, Texas, USA.
Cesar A AriasCenter for Infectious Diseases, Houston Methodist Research Institute, Houston, Texas, USA.ORCID 0000-0001-9054-9774 William R MillerCenter for Infectious Diseases, Houston Methodist Research Institute, Houston, Texas, USA.ORCID 0000-0002-1518-2973 Funding
Project 3: Functional Microbiome and Host Signatures in Transition from Commensal to pathogenP01AI152999 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI HAAG, ANTHONY · 2020 to 2025
$12.0MVENOUS: A translational study of enterococcal bacteremiaR01AI148342 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ARIAS, CESAR AUGUSTO · 2020 to 2024
$3.9MThe LiaFSR system and antimicrobial peptide resistance in enterococciR01AI134637 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI Cesar Augusto Arias · 2018 to 2026
$3.7MClinical Impact of the Cefazolin Inoculum EffectR01AI173138 · NIAID · METHODIST HOSPITAL RESEARCH INSTITUTE · PI Cesar Augusto Arias · 2023 to 2026
$2.6MPOR Program on Genomic Prediction of Antimicrobial Resistance in VREK24AI121296 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ARIAS, CESAR AUGUSTO · 2016 to 2025
$1.5MTexas Medical Center Training Program in Antimicrobial ResistanceT32AI141349 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI GARSIN, DANIELLE A · 2019 to 2023
$1.3MEmergence of TonB-dependent receptor mediated cefiderocol resistance among multidrug-resistant (MDR) Pseudomonas aeruginosa clinical isolates.R21AI175821 · NIAID · METHODIST HOSPITAL RESEARCH INSTITUTE · PI MILLER, WILLIAM R · 2023 to 2024
$467kMechanisms of Resistance and Clinical Outcomes of non-Carbapenemase Producing Carbapenem-Resistant Klebsiella pneumoniae InfectionsR21AI190338 · NIAID · METHODIST HOSPITAL RESEARCH INSTITUTE · PI William R Miller · 2025 to 2026
$448kNIAID NIH HHS K24 AI121296NIAID NIH HHS P01 AI152999NIAID NIH HHS R01 AI134637NIAID NIH HHS R01 AI148342NIAID NIH HHS R01 AI173138NIAID NIH HHS R21 AI175821NIAID NIH HHS R21 AI190338NIAID NIH HHS T32 AI141349
6 · The paper itselfAbstract
Enterococci are gastrointestinal commensals that must defend their cell envelope against antimicrobial peptides derived from the host and other members of the microbiota. The signaling systems LiaFSR and MadRS are pivotal for survival in the presence of antimicrobial peptides and antimicrobial peptide-like antibiotics such as daptomycin. Both systems possess a signaling histidine kinase (LiaS, MadS) and cognate response regulator (LiaR, MadR) that activate transcription of distinct sets of effector genes. Using isogenic deletion strains, we noted differences in daptomycin minimum inhibitory concentration (MIC) between the laboratory strain
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PMID40667240
PMCPMC12262736
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