Seminar “Old dogs teaching us old tricks: Alkaline phosphatase modulation of Lipid A signaling in the squid/Vibrio symbiosis” by Bethany Rader

Date

2017年2月2日 (木) 10:30 11:30

Location

C700, Lab 3

Description

Speaker:
Bethany Rader
Assistant Professor
Department of Microbiology
Southern Illinois University
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Date: Thursay, February 2, 2017
Time: 10:30-11:30am
Venue: C700, Lab 3
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Title: "Old dogs teaching us old tricks: Alkaline phosphatase modulation of Lipid A signaling in the squid/Vibrio symbiosis"

Abstract:
Lipopolysaccharide (LPS), a potent antigen, can also act as a signal promoting beneficial host-bacterial interactions.  Hosts therefore have to utilize LPS as a signal while ameliorating its potential for causing inflammation.  Alkaline phosphatases (APs) have recently been to detoxify bacterial LPS in symbiotic organs of vertebrate animals, promoting tolerance to the microbiome while allowing LPS to signal host development and immune maturation.  However, APs may have multiple roles in such organs positing the question:  Is AP detoxification of bacterial LPS a byproduct of its location or an evolutionarily conserved mechanism for host tolerance?  To try and answer this question, we explored the role of host-derived alkaline phosphatases in symbiont signaling and tolerance in the Euprymna scolopes/Vibrio fischeri (squid/Vibrio) symbiosis.  We obtained full-length open-reading frames for two host alkaline phosphatase (AP) mRNAs (esap1 and esap2) present in the symbiotic organ, the light organ.  Levels of total EsAP activity and protein increased with symbiosis and were regulated over the day-night cycle concurrent with changes in population density of the symbiont.  Inhibition of total EsAP activity impaired normal colonization and persistence by the symbiont.  EsAP activity localized to the internal regions of the symbiotic juvenile light organ, including the lumina of the crypt spaces where the symbiont resides.  These data provide evidence that EsAPs change the signaling properties of bacterial products and thereby promote persistent colonization by the symbiont.  Because the light organ is an organ dedicated to symbiosis and APs have no other described function that would benefit the light organ (to our knowledge), we conclude that AP detoxification of bacterial LPS is an evolutionarily conserved mechanism for promotion of host tolerance to symbiotic bacteria.

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