RT Journal Article
T1 The apoptogenic toxin AIP56 Is secreted by the Type II secretion system of photobacterium damselae subsp piscicida
A1 Vale, Ana do
A1 Pereira, Cassilda
A1 Rodríguez Osorio, Carlos
A1 Santos, Nuro M.S. dos
K1 Exotoxin
K1 Secretion
K1 T2SS
K1 Polar localisation
AB AIP56 (apoptosis-inducing protein of 56 kDa) is a key virulence factor of Photobacteriumdamselae subsp. piscicida (Phdp), the causative agent of a septicaemia affecting warm water marine fishspecies. Phdp-associated pathology is triggered by AIP56, a short trip AB toxin with a metalloproteaseA domain that cleaves the p65 subunit of NF-κB, an evolutionarily conserved transcription factorthat regulates the expression of inflammatory and anti-apoptotic genes and plays a central rolein host responses to infection. During infection by Phdp, AIP56 is systemically disseminated andinduces apoptosis of macrophages and neutrophils, compromising the host phagocytic defenceand contributing to the genesis of pathology. Although it is well established that the secretion ofAIP56 is crucial for Phdp pathogenicity, the protein secretion systems operating in Phdp and themechanism responsible for the extracellular release of the toxin remain unknown. Here, we reportthat Phdp encodes a type II secretion system (T2SS) and show that mutation of the EpsL componentof this system impairs AIP56 secretion. This work demonstrates that Phdp has a functional T2SS thatmediates secretion of its key virulence factor AIP56
PB MDPI
YR 2017
FD 2017
LK http://hdl.handle.net/10347/22784
UL http://hdl.handle.net/10347/22784
LA eng
NO Do Vale, A.; Pereira, C.; R. Osorio, C.; M. S. dos Santos, N. The Apoptogenic Toxin AIP56 Is Secreted by the Type II Secretion System of Photobacterium damselae subsp. piscicida. Toxins 2017, 9, 368
NO This work is a result of the project Norte-01-0145-FEDER-000012-Structured programon bioengineered therapies for infectious diseases and tissue regeneration, supported by Norte PortugalRegional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, throughthe European Regional Development Fund (FEDER). Ana do Vale was supported by the FCT fellowshipSFRH/BPD/95777/2013. Work in CRO laboratory is supported by grant AGL2016-79738-R (AEI/FEDER, EU)from the State Agency for Research (AEI) of Spain, and co-funded by the FEDER Programme from the European Union
DS Minerva
RD 24 abr 2026