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Type VI secretion delivers bacteriolytic effectors to target cells

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      Abstract

      Peptidoglycan is the major structural constituent of the bacterial cell wall, forming a meshwork outside the cytoplasmic membrane that maintains cell shape and prevents lysis. In Gram-negative bacteria, peptidoglycan is located in the periplasm, where it is protected from exogenous lytic enyzmes by the outer membrane. Here we show that the type VI secretion system (T6SS) of Pseudomonas aeruginosa breaches this barrier to deliver two effector proteins, Tse1 and Tse3, to the periplasm of recipient cells. In this compartment, the effectors hydrolyze peptidoglycan, thereby providing a fitness advantage for P. aeruginosa cells in competition with other bacteria. To protect itself from lysis by Tse1 and Tse3, P. aeruginosa utilizes specific periplasmically-localized immunity proteins. The requirement for these immunity proteins depends on intercellular self-intoxication through an active T6SS, indicating a mechanism for export whereby effectors do not access donor cell periplasm in transit.

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      A human gut microbial gene catalogue established by metagenomic sequencing.

      To understand the impact of gut microbes on human health and well-being it is crucial to assess their genetic potential. Here we describe the Illumina-based metagenomic sequencing, assembly and characterization of 3.3 million non-redundant microbial genes, derived from 576.7 gigabases of sequence, from faecal samples of 124 European individuals. The gene set, approximately 150 times larger than the human gene complement, contains an overwhelming majority of the prevalent (more frequent) microbial genes of the cohort and probably includes a large proportion of the prevalent human intestinal microbial genes. The genes are largely shared among individuals of the cohort. Over 99% of the genes are bacterial, indicating that the entire cohort harbours between 1,000 and 1,150 prevalent bacterial species and each individual at least 160 such species, which are also largely shared. We define and describe the minimal gut metagenome and the minimal gut bacterial genome in terms of functions present in all individuals and most bacteria, respectively.
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        The Pfam protein families database

        Pfam is a widely used database of protein families and domains. This article describes a set of major updates that we have implemented in the latest release (version 24.0). The most important change is that we now use HMMER3, the latest version of the popular profile hidden Markov model package. This software is ∼100 times faster than HMMER2 and is more sensitive due to the routine use of the forward algorithm. The move to HMMER3 has necessitated numerous changes to Pfam that are described in detail. Pfam release 24.0 contains 11 912 families, of which a large number have been significantly updated during the past two years. Pfam is available via servers in the UK (http://pfam.sanger.ac.uk/), the USA (http://pfam.janelia.org/) and Sweden (http://pfam.sbc.su.se/).
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          Bacterial biofilms: from the natural environment to infectious diseases.

          Biofilms--matrix-enclosed microbial accretions that adhere to biological or non-biological surfaces--represent a significant and incompletely understood mode of growth for bacteria. Biofilm formation appears early in the fossil record (approximately 3.25 billion years ago) and is common throughout a diverse range of organisms in both the Archaea and Bacteria lineages, including the 'living fossils' in the most deeply dividing branches of the phylogenetic tree. It is evident that biofilm formation is an ancient and integral component of the prokaryotic life cycle, and is a key factor for survival in diverse environments. Recent advances show that biofilms are structurally complex, dynamic systems with attributes of both primordial multicellular organisms and multifaceted ecosystems. Biofilm formation represents a protected mode of growth that allows cells to survive in hostile environments and also disperse to colonize new niches. The implications of these survival and propagative mechanisms in the context of both the natural environment and infectious diseases are discussed in this review.
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            Author and article information

            Affiliations
            [1 ]Department of Microbiology, University of Washington, Seattle, WA 98195, USA
            [2 ]Centre for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, NE2 4HH, United Kingdom
            [3 ]Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195, USA
            Author notes
            [* ]To whom correspondence should be addressed: J.D.M. - mougous@ 123456u.washington.edu

            Author Contributions

            A.B.R., R.D.H., N.K.B, M.L.R., W.V., and J.DM. conceived and designed experiments. A.B.R., R.D.H., N.K.B. and J.D.M conducted experiments. A.B.R., R.D.H., W.V., and J.D.M. wrote the paper.

            Author Information

            The authors declare no competing financial interests. Correspondence and requests for materials should be addressed to J.D.M. ( mougous@ 123456u.washington.edu ).

            Journal
            0410462
            6011
            Nature
            Nature
            Nature
            0028-0836
            1476-4687
            21 July 2011
            20 July 2011
            21 January 2012
            : 475
            : 7356
            : 343-347
            3146020 21776080 10.1038/nature10244 nihpa313070

            Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

            Funding
            Funded by: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID
            Award ID: R01 AI080609-03 || AI
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