Special Issue "Toxin-Antitoxin System"
A special issue of Toxins (ISSN 2072-6651).
Deadline for manuscript submissions: 20 September 2013
Prof. Dr. Laurence Van Melderen
Laboratoire de Génétique et Physiologie Bactérienne, Faculté de Sciences, IBMM, Université Libre de Bruxelles (ULB), Gosselies, B-6041, Belgium
Toxin-antitoxin (TA) systems are small genetic modules encoding a stable toxic protein and its cognate unstable antitoxin, which can be either RNA or protein. Five TA types are currently recognized, among them type II systems are probably the best documented. TA systems are surprisingly abundant in eubacterial and archeal genomes. TA systems were originally discovered on plasmids in the mid 1980s. Their function when located on such mobile genetic elements is to contribute to their stability by a phenomenon denoted as addiction (or post-segregational killing). Addiction relies on the differential stability of the antitoxin and toxin components. In daughter-bacteria that did not receive a plasmid copy at cell division, antitoxins are degraded and as a consequence toxins are released from inhibition thereby leading to the killing of plasmid-free cells. Homologues of plasmidic systems as well as novel types of TA systems were subsequently found in chromosomes and for some of them extensively studied. The biological role of these systems is still under debate and conflicting hypotheses have been proposed, at least for type II systems, from persistence to stabilization of large genomic islands or competition between mobile genetic elements. TA systems might also operate at the selfish level to promote their own dissemination in bacterial genomes although in certain conditions, at the expense of host survival. In addition to the functional aspects, essential questions regarding these diverse and mysterious genetic entities remain to be answered such as their origin and evolution and maybe the most intriguing which concerns the basis of their evolutionary success.
Prof. Dr. Laurence Van Melderen
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed Open Access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs) for well prepared manuscripts submitted before 1 July 2013. The APC for manuscripts submitted from 1 July 2013 onwards are 1000 CHF per accepted paper.
- selfish genes
- programmed cell death
- biofilm formation
- stress responses
- DNA-gyrase inhibitor
- translation inhibition
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Article
Title: The toxAvapA Toxin-Antitoxin Locus Contributes to the Survival of Nontypeable Haemophilus Influenzae During Infection
Authors: Dabin Ren, Alexis A. Kordis and Dayle A. Daines
Affiliation: Department of Biological Sciences, Old Dominion University, Norfolk, VA 23529, USA; E-Mail: firstname.lastname@example.org
Abstract: One uncharacterized toxin-antitoxin (TA) module in nontypeable Haemophilus influenzae, NTHI1912-1913, is a host inhibition of growth (hig)BA homologue. We hypothesized that the products of this gene pair, designated toxAvapA, contributed to bacterial survival. Accordingly, we deleted this TA locus from strain 86-028NP, creating ΔtoxAvapA. The mutant was found to be attenuated for survival compared to the parent strain during long-term co-culture with primary human respiratory epithelial tissue in vitro and in the chinchilla model of otitis media in vivo. Biochemical and transcriptome studies confirmed that this module acted to influence metabolic regulation.
Last update: 13 May 2013