Peter Redder

Peter Redder

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05 61 33 59 61



Early career research (briefly):

During my Master and PhD, I was interested in the genomics of thermophilic Archaea, and examined the genomic instability of certain Sulfolobus species, which, among other things, resulted in the discovery of a class of non-autonomous mobile elements and the evolution of CRISPR elements in Sulfolobus (Redder et al. 2001; Redder and Garrett, 2006; Lillestøl et al. 2006; Lillestøl et al. 2009). During my post-doc at Institut Pasteur, I isolated several new thermophilic archaeal viruses from the environment, by using microbiological isolation of their hosts and electron microscopy analyses. I was then able to obtain DNA for sequencing of these viruses, thus enabling further studies on the genomic level, and leading to new insights into their evolution (Redder et al. 2009; Happonen et al. 2010).

Research in the Linder lab (University of Geneva):

Having worked with archaea for several years, I decided to switch the direction of my research and joined the laboratory of Prof. Patrick Linder, at the University of Geneva, Switzerland, where the main focus is the two DEAD-box RNA helicases found in Staphylococcus aureus, CshA and CshB. S. aureus has fascinating abilities to resist treatments, and I was attracted by its intriguing systems of regulation via small RNAs, as well as other RNA-centered open questions about S. aureus and its virulence.

We discovered that CshA affects the stability of RNA, presumably due to CshA's proposed association with the newly characterised Gram-positive RNA degradosome. In particular, we examined the consequences of incorrect turnover of the agrBDCA mRNA, which is responsible for regulation of quorum-sensing and virulence (Oun, Redder et al. 2013). In parallel to the work on CshA, I developed a new system for generating allelic replacements in S. aureus that was specifically designed to allow the isolation of mutants that have severe loss-of-fitness (Redder and Linder, 2012a).

I  branched off from the main focus of the Linder laboratory (i.e. RNA helicases) and developed my own project which studies the RNases of S. aureus. The set of RNases in S. aureus and other Gram-positive bacteria are very different from the well-studied systems of E. coli. Therefore, in order to understand why some RNAs have long and some short half-lives, and which RNases are involved in this regulation, I used the allelic replacement system described above to delete the key RNases in S. aureus. These RNase mutants were then used to map thousands of cleavage/processing sites, and where possible, assign them to specific RNases. via a novel transcriptome-wide method (EMOTE) for mapping the 5'-ends of processed RNA that I developed specifically for this purpose (Linder, Lemeille and Redder, 2014; Redder, 2015; Khemici, Prados, Linder and Redder, 2015).

The first manuscript based on these studies describes how the two 5' exoribonucleases RNases J1 and J2 collaborate, to not only be major factors in bulk mRNA decay, but also to be responsible for the maturation of important molecules such as 16S rRNA (Linder, Lemeille and Redder, 2014).

In a second study, of the membrane-anchored endonuclease RNase Y, we have discovered the preferred cleavage motif, a first for any Gram-positive bacterial decay-endoribonuclease, we show a link between RNase Y and RNA half-lives for about a hundred transcripts, and we additionally include experiments that examine how the intra-cellular localisation regulates RNA cleavage (Khemici, Prados, Linder and Redder, 2015).

Another fertile off-shoot from the transcriptome-wide mapping of RNA processing sites, is the study of toxin-antitoxin systems, specifically RNase toxins, where we have identified the specificity of the HigB toxin in Caulobacter crescentus – in a collaboration with the group of Prof. Patrick Viollier (Kirkpatrick et al. 2016).

Research in Toulouse:

In 2016 I was recruited as professor and research team-leader at CBI, Paul Sabatier University, Toulouse. Where my team studies the flux of RNA in Staphylococcus aureus, in terms of spacial position, epi-transcriptomic modifications, secondary structures, and degradation. Please see the team home-page for more information:


  • Guimarães VA, Le Scornet A, Khemici V, Hausmann S, Armitano J, Prados J, Jousselin A, Manzano C, Linder P, Redder P. .
    RNase J1 and J2 Are Host-Encoded Factors for Plasmid Replication.
    Front Microbiol. 2021 May 4;12:586886.
    2021 May doi: 10.3389/fmicb.2021.586886. PMID: 34017314; PMCID: PMC8129170.
  • Boufafa M, Kadri S, Redder P, Bensouilah M. .
    Occurrence and distribution of fecal indicators and pathogenic bacteria in seawater and Perna perna mussel in the Gulf of Annaba (Southern Mediterranean).
    Environ Sci Pollut Res Int. 2021 Sep;28(33):46035-46052.
    2021 Sep doi: 10.1007/s11356-021-13978-4.
  • Sierra R, Prados J, Panasenko OO, Andrey DO, Fleuchot B, Redder P, Kelley WL, Viollier PH, Renzoni A.
    Insights into the global effect on Staphylococcus aureus growth arrest by induction of the endoribonuclease MazF toxin
    Nucleic Acids Res.
    2020 Sep doi: 10.1093/nar/gkaa617. PMID: 32735661; PMCID: PMC7470975.
  • Redder, P.
    Molecular and genetic interactions of the RNA degradation machineries in Firmicute bacteria
    Wiley Interdiscip Rev RNA
    2018 Mar
  • Le Scornet A, Redder P.
    Post-transcriptional control of virulence gene expression in Staphylococcus aureus
    Biochim Biophys Acta
    2019 Jul

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Université Paul Sabatier
118 Route de Narbonne

31062 TOULOUSE Cedex

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