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Hoppe, T.

Publications and source records attributed to Hoppe, T..

3 recordsLinked to original sources

A protein language model unveils the E. coli pangenome functional landscape regulating host proteostasis

Understanding how bacterial diversity at strain level resolution shapes host physiology is a central challenge in microbiome research. The vast, functionally unknown genetic diversity within a species pangenome makes it difficult to connect genes to function and their impact on host physiology. Here, we explore how the functional landscape of the Escherichia coli pangenome impacts transcriptional responses in Caenorhabditis elegans and show that traditional gene-centric methods fail to provide significant functional associations with the host. Thus, we developed a pangenome framework that leverages the protein language model ProtT5 and generates unique strain embeddings representing the functional potential of each 9,558 E. coli isolate. Stratification of the pangenome into distinct functional guilds aligned with key host processes such as cell division, metabolism and proteostasis. Further, we identify a critical interplay between the extensive network of bacterial chaperones and proteases in regulating host proteostasis. We find that the bacterial chaperone DNAK/HSP70 and protease ClpX fine-tune the host ubiquitin-proteasome system by controlling propionate and vitamin B12 availability. These findings reveal a conserved co-proteostasis mechanism as a key phenomenon modulating host-microbe interactions through metabolic communication. Our pangenome-to-phenotype approach offers a powerful strategy to decode bacterial pangenome functional diversity, directly linking microbial genomic variation to host physiological outcomes.

systems biology↗

Heterotypic Assembly Mechanism Regulates CHIP E3 Ligase Activity

The E3 ubiquitin ligases CHIP/CHN-1 and UFD-2 team up to accelerate ubiquitin chain formation. However, it remained largely unclear how the high processivity of this E3 set is achieved. Here we studied the molecular mechanism and function of the CHN-1/UFD-2 complex in Caenorhabditis elegans. Our data show that UFD-2 binding promotes the cooperation between CHN-1 and ubiquitin-conjugating E2 enzymes by stabilizing the CHN-1 U-box dimer. The HSP-1 chaperone outcompetes UFD-2 for CHN-1 binding and promotes the auto-inhibited CHN-1 state by acting on the conserved position of the U-box domain. The interaction with UFD-2 enables CHN-1 to efficiently ubiquitinate S-Adenosylhomocysteinase (AHCY-1), an enzyme crucial for lipid metabolism. Our results define the molecular mechanism underlying the synergistic cooperation of CHN-1 and UFD-2 in substrate ubiquitylation. HIGHLIGHTSO_LIE3 ligase UFD-2 stimulates ubiquitylation activity of CHIP/CHN-1 C_LIO_LIUFD-2 binding promotes dimerization of CHIP/CHN-1 U-box domains and utilization of E2 enzymes C_LIO_LIHSP70/HSP-1 by latching the U-box and TPR domains stabilizes the autoinhibitory state of CHIP/CHN-1, limiting interactions with E2s and UFD-2 C_LIO_LIAssembly with UFD-2 enables CHIP/CHN-1 to regulate lipid metabolism by ubiquitylation of S-Adenosylhomocysteinase C_LI

molecular biology↗

Olfaction regulates organismal proteostasis and longevity via microRNA-dependent signaling

Introductory Paragraph Introductory Paragraph Materials and Methods tir-1 3'UTR mutant tir-1::gfp CrispR/Cas9 repair templates References The maintenance of proteostasis is crucial for any organism to survive and reproduce in an ever-changing environment, but its efficiency declines with age1,2. Posttranscriptional regulators such as microRNAs control protein translation of target mRNAs with major consequences for development, physiology, and longevity3,4. However, the precise function of lifespan- determining microRNAs remains poorly understood. Here we show that the microRNA mir-71 controls organismal proteostasis and aging in Caenorhabditis elegans by regulating its conserved target tir-1 in AWC ol ...

cell biology↗