2012年9月6日 訊 /生物谷BIOON/ --近日,，一項刊登在國際雜志Molecular Microbiology上的研究表明，當細菌在某處聚集的時候,，它們會做出一種集體決策來生在某種附屬物上或者聚集起來慢慢游走,。這種行為首次是在海綿中發(fā)現(xiàn)的，這或許可以幫助我們理解如何破壞有害致病菌的生物被膜,，比如牙齒斑或者人工心臟中內(nèi)在醫(yī)療設(shè)備上的生物被膜,。
細菌彼此之間有很多種交流方式，科學家們?nèi)缃癜l(fā)現(xiàn)了一種新型的信號系統(tǒng),，這種系統(tǒng)可以促使細菌產(chǎn)生諸如鞭毛一樣的細菌附屬物,，使細菌可以自由泳動，并且抑制細菌生物被膜的形成,。研究者Hill表示,，我們發(fā)現(xiàn)的關(guān)于細菌交流的任何細節(jié)都可以幫助我們理解細菌對于人類是如何進行致病的以及細菌如何在牙齒或者醫(yī)療器械內(nèi)部形成菌膜。理解這個過程將幫助我們有效控制致病菌的生物被膜產(chǎn)生,。
細菌可以通過很多途徑聚集起來然后形成生物被膜,，而且細菌知道如何進行溝通以確定做出機體的決策，從而指導其發(fā)生某種行為,，這種行為系統(tǒng)成為群體感應系統(tǒng)（quorum sensing）,。特殊的海綿包括了復雜和不同的細菌群落，在某些情況下甚至占到了海綿生物量的30%-40%,。群體感應系統(tǒng)可以控制細菌細胞一系列的過程,，包括引發(fā)細菌舉起寄來在牙齒上形成菌斑等。
依賴于海綿的細菌,，當其細菌數(shù)量達到一定程度時,，其就可以利用群體感應系統(tǒng)來激活其運動能力，這樣就限制了其在固體表面形成生物被膜了,。研究者Clay Fuqua說道,，細菌的這種行為對于幫助其維持健康、共生的菌群系統(tǒng)非常關(guān)鍵,。當然,，相同的分子機制或許在別的微生物群落中也會出現(xiàn)，比如人類腸道微生物或者微生物共生植物中等,。（生物谷Bioon.com）
編譯自：Study: Bacteria on marine sponges can develop capacity to move and inhibit biofilm formation
doi:10.1111/j.1365-2958.2012.08149.x
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A complex LuxR–LuxI type quorum sensing network in a roseobacterial marine sponge symbiont activates flagellar motility and inhibits biofilm formation
Jindong Zan1,†, Elisha M. Cicirelli2,†,‡, Naglaa M. Mohamed1, Hiruy Sibhatu3,§, Stephanie Kroll2,¶, Ohkee Choi2,‖, Charis L. Uhlson3, Christina L. Wysoczinski3, Robert C. Murphy3, Mair E. A. Churchill3, Russell T. Hill1, Clay Fuqua2,*
Bacteria isolated from marine sponges, including the Silicibacter–Ruegeria (SR) subgroup of the Roseobacter clade, produce N-acylhomoserine lactone (AHL) quorum sensing signal molecules. This study is the first detailed analysis of AHL quorum sensing in sponge-associated bacteria, specifically Ruegeria sp. KLH11, from the sponge Mycale laxissima. Two pairs of luxR and luxI homologues and one solo luxI homologue were identified and designated ssaRI, ssbRI and sscI (sponge-associated symbiont locus A, B and C, luxR or luxI homologue). SsaI produced predominantly long-chain 3-oxo-AHLs and both SsbI and SscI specified 3-OH-AHLs. Addition of exogenous AHLs to KLH11 increased the expression of ssaI but not ssaR, ssbI or ssbR, and genetic analyses revealed a complex interconnected arrangement between SsaRI and SsbRI systems. Interestingly, flagellar motility was abolished in the ssaI and ssaR mutants, with the flagellar biosynthesis genes under strict SsaRI control, and active motility only at high culture density. Conversely, ssaI and ssaR mutants formed more robust biofilms than wild-type KLH11. AHLs and the ssaI transcript were detected in M. laxissima extracts, suggesting that AHL signalling contributes to the decision between motility and sessility and that it may also facilitate acclimation to different environments that include the sponge host.
