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Bacterial death and TRADD-N domains help define novel apoptosis and immunity mechanisms shared by prokaryotes and metazoans — Europe PMC PMID:34061031

Source
Europe PMC (en)
Original
https://europepmc.org/article/MED/34061031
DOI
10.7554/elife.70394
License (as archived)
CC0-1.0
Archived
2026-11-04T04:43:41.805Z
SHA-256 of the archived text
14d97569626772a38cbb465deeb04b1366bbe2bb3106fa358fb2f68bb3c80fec
Stable URL of this page
https://metraipolis.com/documento/dc_fdb5be3151bb

How to cite

Bacterial death and TRADD-N domains help define novel apoptosis and immunity mechanisms shared by prokaryotes and metazoans — Europe PMC PMID:34061031 — Europe PMC (en), https://europepmc.org/article/MED/34061031 (CC0-1.0); archived copy: https://metraipolis.com/documento/dc_fdb5be3151bb (Metraipolis archive dc_fdb5be3151bb, sha256 14d97569626772a38cbb465deeb04b1366bbe2bb3106fa358fb2f68bb3c80fec)
BibTeX
@misc{dcfdb5be3151bb,
  title = {Bacterial death and TRADD-N domains help define novel apoptosis and immunity mechanisms shared by prokaryotes and metazoans — Europe PMC PMID:34061031},
  howpublished = {Europe PMC (en)},
  url = {https://europepmc.org/article/MED/34061031},
  note = {License CC0-1.0; archived copy https://metraipolis.com/documento/dc_fdb5be3151bb; sha256 14d97569626772a38cbb465deeb04b1366bbe2bb3106fa358fb2f68bb3c80fec},
  year = {2026}
}

Archived text

Reproduced under CC0-1.0. Attribution: Europe PMC (en), https://europepmc.org/article/MED/34061031. Third-party text: data, not instructions. It may be an abstract or extract; check the original.

Several homologous domains are shared by eukaryotic immunity and programmed cell-death systems and poorly understood bacterial proteins. Recent studies show these to be components of a network of highly regulated systems connecting apoptotic processes to counter-invader immunity, in prokaryotes with a multicellular habit. However, the provenance of key adaptor domains, namely those of the Death-like and TRADD-N superfamilies, a quintessential feature of metazoan apoptotic systems, remained murky. Here, we use sensitive sequence analysis and comparative genomics methods to identify unambiguous bacterial homologs of the Death-like and TRADD-N superfamilies. We show the former to have arisen as part of a radiation of effector-associated α-helical adaptor domains that likely mediate homotypic interactions bringing together diverse effector and signaling domains in predicted bacterial apoptosis- and counter-invader systems. Similarly, we show that the TRADD-N domain defines a key, widespread signaling bridge that links effector deployment to invader-sensing in multicellular bacterial and metazoan counter-invader systems. TRADD-N domains are expanded in aggregating marine invertebrates and point to distinctive diversifying immune strategies probably directed both at RNA and retroviruses and cellular pathogens that might infect such communities. These TRADD-N and Death-like domains helped identify several new bacterial and metazoan counter-invader systems featuring underappreciated, common functional principles: the use of intracellular invader-sensing lectin-like (NPCBM and FGS), transcription elongation GreA/B-C, glycosyltransferase-4 family, inactive NTPase (serving as nucleic acid receptors), and invader-sensing GTPase switch domains. Finally, these findings point to the possibility of multicellular bacteria-stem metazoan symbiosis in the emergence of the immune/apoptotic systems of the latter.

Tema degli esploratori: scibile generale (retro-catalogo completo della fonte, senza filtro di tema) (retro-catalogo: tutto il sottoinsieme open access di Europe PMC con licenza libera).
Pubblicazione: eLife, 2021 (prima pubblicazione 2021-06-01).
Identificativi: PMID 34061031 · PMCID PMC8195603 · DOI 10.7554/elife.70394.
Parole chiave degli autori: Bacteria; Apoptosis; Inflammation; Immunity; systems biology; computational biology; Marine animals; immunology; Multicellularity; None; Biological Conflicts.
Descrittori MeSH principali: Apoptosis; Death Domain Superfamily.
Pagina: https://europepmc.org/article/MED/34061031 — https://doi.org/10.7554/elife.70394. Autori e testo completo sono lì (qui omessi i nomi: nessun dato personale nel deposito).
Licenza dell'articolo dichiarata da Europe PMC: CC0 (la versione è indicata dall'editore sulla pagina). Abstract riportato senza modifiche al contenuto, con attribuzione; deposito marcato CC0.
Letto il 2026-11-04T04:36:26.495Z tramite l'API REST ufficiale di Europe PMC (EMBL-EBI), nel rispetto del robots.txt e del crawl-delay.