Pierre Pontarotti

Dr. Pierre Pontarotti

CNRS
orcid

Research Focus & Metrics

Academic Career Length

45Years (1982-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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21 July 2013 in Nature
Verified
Journal Article
Open access
JFJean-François Flot
Jean-François Flot
BHBoris Hespeels
Boris Hespeels
XLXiang Li
Xiang Li
BNBenjamin Noel
Benjamin Noel
Irina ArkhipovaIrina Arkhipova
Irina Arkhipova
KDKarine Van Doninck
Karine Van Doninck
Loss of sexual reproduction is considered an evolutionary dead end for metazoans, but bdelloid rotifers challenge this view as they appear to have persisted asexually for millions of years. Neither male sex organs nor meiosis have ever been observed in these microscopic animals: oocytes are formed through mitotic divisions, with no reduction of chromosome number and no indication of chromosome pairing. However, current evidence does not exclude that they may engage in sex on rare, cryptic occasions. Here we report the genome of a bdelloid rotifer, Adineta vaga (Davis, 1873), and show that its structure is incompatible with conventional meiosis. At gene scale, the genome of A. vaga is tetraploid and comprises both anciently duplicated segments and less divergent allelic regions. However, in contrast to sexual species, the allelic regions are rearranged and sometimes even found on the same chromosome. Such structure does not allow meiotic pairing; instead, we find abundant evidence of gene conversion, which may limit the accumulation of deleterious mutations in the absence of meiosis. Gene families involved in resistance to oxidation, carbohydrate metabolism and defence against transposons are significantly expanded, which may explain why transposable elements cover only 3% of the assembled sequence. Furthermore, 8% of the genes are likely to be of non-metazoan origin and were probably acquired horizontally. This apparent convergence between bdelloids and prokaryotes sheds new light on the evolutionary significance of sex.

18 May 2016 in BMC Genomics
Verified
Journal Article
Open access
PDF file
JPJeremy Pasquier
Jeremy Pasquier
CCCédric Cabau
Cédric Cabau
TNThaovi Nguyen
Thaovi Nguyen
EJElodie Jouanno
Elodie Jouanno
DSDany Severac
Dany Severac
JBJulien Bobe
Julien Bobe
With more than 30,000 species, ray-finned fish represent approximately half of vertebrates. The evolution of ray-finned fish was impacted by several whole genome duplication (WGD) events including a teleost-specific WGD event (TGD) that occurred at the root of the teleost lineage about 350 million years ago (Mya) and more recent WGD events in salmonids, carps, suckers and others. In plants and animals, WGD events are associated with adaptive radiations and evolutionary innovations. WGD-spurred innovation may be especially relevant in the case of teleost fish, which colonized a wide diversity of habitats on earth, including many extreme environments. Fish biodiversity, the use of fish models for human medicine and ecological studies, and the importance of fish in human nutrition, fuel an important need for the characterization of gene expression repertoires and corresponding evolutionary histories of ray-finned fish genes. To this aim, we performed transcriptome analyses and developed the PhyloFish database to provide (i) de novo assembled gene repertoires in 23 different ray-finned fish species including two holosteans (i.e. a group that diverged from teleosts before TGD) and 21 teleosts (including six salmonids), and (ii) gene expression levels in ten different tissues and organs (and embryos for many) in the same species. This resource was generated using a common deep RNA sequencing protocol to obtain the most exhaustive gene repertoire possible in each species that allows between-species comparisons to study the evolution of gene expression in different lineages. The PhyloFish database described here can be accessed and searched using RNAbrowse, a simple and efficient solution to give access to RNA-seq de novo assembled transcripts.

10 April 2009 in Biology Direct
Verified
Journal Article
Open access
PDF file
Vicky MerhejVicky Merhej
Vicky Merhej
MRManuela Royer-Carenzi
Manuela Royer-Carenzi
Pierre PontarottiPierre Pontarotti
Pierre Pontarotti
Didier RaoultDidier Raoult
Didier Raoult
Background: Genome size and gene content in bacteria are associated with their lifestyles. Obligate intracellular bacteria (i.e., mutualists and parasites) have small genomes that derived from larger free-living bacterial ancestors; however, the different steps of bacterial specialization from free-living to intracellular lifestyle have not been studied comprehensively. The growing number of available sequenced genomes makes it possible to perform a statistical comparative analysis of 317 genomes from bacteria with different lifestyles. Results: Compared to free-living bacteria, host-dependent bacteria exhibit fewer rRNA genes, more split rRNA operons and fewer transcriptional regulators, linked to slower growth rates. We found a function-dependent and non-random loss of the same 100 orthologous genes in all obligate intracellular bacteria. Thus, we showed that obligate intracellular bacteria from different phyla are converging according to their lifestyle. Their specialization is an irreversible phenomenon characterized by translation modification and massive gene loss, including the loss of transcriptional regulators. Although both mutualists and parasites converge by genome reduction, these obligate intracellular bacteria have lost distinct sets of genes in the context of their specific host associations: mutualists have significantly more genes that enable nutrient provisioning whereas parasites have genes that encode Types II, IV, and VI secretion pathways. Conclusion: Our findings suggest that gene loss, rather than acquisition of virulence factors, has been a driving force in the adaptation of parasites to eukaryotic cells. This comparative genomic analysis helps to explore the strategies by which obligate intracellular genomes specialize to particular host-associations and contributes to advance our knowledge about the mechanisms of bacterial evolution. Reviewers: This article was reviewed by Eugene V. Koonin, Nicolas Galtier, and Jeremy Selengut.

22 April 2002 in Nature Genetics
Verified
Journal Article
Closed access
LALaurent Abi-Rached
Laurent Abi-Rached
AGAndré Gilles
André Gilles
TSTakashi Shiina
Takashi Shiina
Pierre PontarottiPierre Pontarotti
Pierre Pontarotti
HIHidetoshi Inoko
Hidetoshi Inoko

1 June 2016 in Cell
Verified
Journal Article
Closed access
SHShengfeng Huang
Shengfeng Huang
XTXin Tao
Xin Tao
SYShaochun Yuan
Shaochun Yuan
YZYuhang Zhang
Yuhang Zhang
PLPeiyi Li
Peiyi Li
AXAnlong Xu
Anlong Xu

1 September 1993 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
DPD Pham-Dinh
D Pham-Dinh
MMM G Mattei
M G Mattei
JNJ L Nussbaum
J L Nussbaum
GRG Roussel
G Roussel
Pierre PontarottiPierre Pontarotti
Pierre Pontarotti
ADA Dautigny
A Dautigny
Myelin/oligodendrocyte glycoprotein (MOG) is found on the surface of myelinating oligodendrocytes and external lamellae of myelin sheaths in the central nervous system, and it is a target antigen in experimental autoimmune encephalomyelitis and multiple sclerosis. We have isolated bovine, mouse, and rat MOG cDNA clones and shown that the developmental pattern of MOG expression in the rat central nervous system coincides with the late stages of myelination. The amino-terminal, extracellular domain of MOG has characteristics of an immunoglobulin variable domain and is 46% and 41% identical with the amino terminus of bovine butyrophilin (expressed in the lactating mammary gland) and B-G antigens of the chicken major histocompatibility complex (MHC), respectively; these proteins thus form a subset of the immunoglobulin superfamily. The homology between MOG and B-G extends beyond their structure and genetic mapping to their ability to induce strong antibody responses and has implications for the role of MOG in pathological, autoimmune conditions. We colocalized the MOG and BT genes to the human MHC on chromosome 6p21.3-p22. The mouse MOG gene was mapped to the homologous band C of chromosome 17, within the M region of the mouse MHC.