Comptes Rendus Biologies最新文献

I joined the laboratory of Professor Francois Gros in 1987 and worked there as a postdoc with Robert Whalen until 1992. I recount the research we carried out and mention that of the other scientists also working on skeletal muscle on the 6th floor of the Molecular Biology Department of the Institut Pasteur at that time. I then present my subsequent research when I returned to Japan. I pay tribute to the influence of Professor Gros and to his support in establishing Japanese/French meetings on muscle biology and muscular dystrophy. I also invoke personal memories of Robert Whalen and Margaret Buckingham and remember the occasions when I returned to Paris to honour François Gros.

I joined François Gros' laboratory in 1975, to study mechanisms of gene expression in eukaryotes. Despite the lack of powerful tools, that would be brought later by genetic engineering, I obtained publishable results and was allowed to defend a third cycle thesis. Thereafter, I joined Margaret Buckingham's group, which was empowering within François' laboratory. I maintained regular meetings with François, a leading figure but a secretive man, who did not readily open up. It was my privilege, over the more than 45 years I have been around him, to have glimpses over what had been really significant to him. This has been a rich and very precious experience.

Gillian Butler-Browne began working on muscle at the Institut Pasteur in the laboratory of François Gros in 1978. She characterized the expression profile of different myosin isoforms during both human and rodent development. Vincent Mouly joined this laboratory for his PhD in 1982, and defined the different populations of myoblasts appearing during development in birds and then in humans. Together, they demonstrated the impact of the limit in proliferation of the precursor cells on the regenerative capacity of human skeletal muscle, and their group developed models to evaluate the regenerative potential of skeletal muscle in vitro, measuring the telomeric erosion, and identified the involvement of a stress pathway in the proliferative arrest of muscle progenitors. A platform to produce human immortalized muscle cell lines was the successful result of this research, initiated with François Gros and W. E. Wright. The in vivo regenerative potential of human muscle cells was evaluated by injection into muscles of immunodeficient mice. Their group in collaboration with the clinical team of Professor Jean Lacau St-Guily and Professor Sophie Perié completed a successful autologous myoblast transplantation clinical trial for Oculo-pharyngeal muscular dystrophy. This common scientific career was made possible thanks to the precious and always benevolent support of François Gros.

I joined the laboratory of François Gros as a young student in the mid-1980s and worked on the characterization of the $\beta$-tropomyosin gene in chicken and the regulation of alternative splicing of its transcript, under the supervision of Marc Fiszman. In particular, I was interested in how secondary structures of the RNA influence the recognition of exons specifically used in muscle cells. I will recall a few memories on how interacting with François on this project shaped my perception of the scientific process and of the relationships between models and data. Later I worked on many aspects of RNA biology, from transcription to mRNP biogenesis and non-coding RNAs.

It was at the Pasteur Institute, in François Gros' laboratory, that I had the opportunity to discover the world of research. An opportunity in more ways than one, first because of the nature of the subject, myogenesis, which lent itself particularly well to cellular and genetic approaches to development and differentiation in vertebrates. An opportunity also because the head of the laboratory, François Gros, who was responsible for the choice of this topic, had created an environment in which researchers could develop their projects with great confidence and freedom.

Congenital heart defects (CHD) affect 1 in 100 live births and result from defects in cardiac development. Growth of the early heart tube occurs by the progressive addition of second heart field (SHF) progenitor cells to the cardiac poles. The SHF gives rise to ventricular septal, right ventricular and outflow tract myocardium at the arterial pole, and atrial, including atrial septal myocardium, at the venous pole. SHF deployment creates the template for subsequent cardiac septation and has been implicated in cardiac looping and in orchestrating outflow tract development with neural crest cells. Genetic or environmental perturbation of SHF deployment thus underlies a spectrum of common forms of CHD affecting conotruncal and septal morphogenesis. Here we review the major properties of SHF cells as well as recent insights into the developmental programs that drive normal cardiac progenitor cell addition and the origins of CHD.

Tracing the phylogenetic relationships between species is one of the fundamental objectives of evolutionary biology. Since Charles Darwin's seminal work in the 19th century, considerable progress has been made towards establishing a tree of life that summarises the evolutionary history of species. Nevertheless, substantial uncertainties still remain. Specifically, the relationships at the origins of teleost fishes have been the subject of extensive debate over the last 50 years. This question has major implications for various research fields: there are almost 30,000 species in the teleost group, which includes invaluable model organisms for biomedical, evolutionary and ecological studies. Here, we present the work in which we solved this enigma. We demonstrated that eels are more closely related to bony-tongued fishes than to the rest of teleost fishes. We achieved this by taking advantage of new genomic data and leveraging innovative phylogenetic markers. Notably, in addition to traditional molecular phylogeny methods based on the evolution of gene sequences, we also considered the evolution of gene order along the DNA molecule. We discuss the challenges and opportunities that these new markers represent for the field of molecular phylogeny, and in particular the possibilities they offer for re-examining other controversial branches in the tree of life.

Antibiotic resistance is the direct deleterious consequence of two synergistic causes linked to human activity: the massive use of antibiotics in human and animal health, which leads to the selection of the most resistant bacteria, and the spread of these selected resistant bacteria, directly by cross-transmission within human and animal populations and indirectly via the environment. The "one health" concept enables an integrated approach of the various components of the issue, linking human, animal and environmental ecosystems and their dynamics.

Transferring an asexual mode of reproduction by seeds (apomixis) to cultivated plants would enable clonal reproduction of heterozygous genotypes such as F1 hybrids with hybrid vigor (heterosis), facilitating their access and multiplication by small-scale growers. Although sources of apomixis and the genetic loci controlling its constituent elements have been identified in wild species, their transfer by crossing to cultivated species has so far been unsuccessful. Here, we have introduced synthetic apomixis in hybrid rice to produce a high (95-100%) frequency of clonal seeds, via the inactivation of three meiotic genes-resulting in unreduced, non-recombined gametes-and the addition of an egg cell parthenogenesis trigger. The genotype and phenotype, including grain quality, of the F1 hybrid are reproduced identically in the clonal apomictic progenies. These results make synthetic apomixis compatible with future use in agriculture.

The medial prefrontal cortex (mPFC) is at the core of numerous psychiatric conditions, including fear and anxiety-related disorders. Whereas an abundance of evidence suggests a crucial role of the mPFC in regulating fear behaviour, the precise role of the mPFC in this process is not yet entirely clear. While studies at the single-cell level have demonstrated the involvement of this area in various aspects of fear processing, such as the encoding of threat-related cues and fear expression, an increasingly prevalent idea in the systems neuroscience field is that populations of neurons are, in fact, the essential unit of computation in many integrative brain regions such as prefrontal areas. What mPFC neuronal populations represent when we face threats? To address this question, we performed electrophysiological single-unit population recordings in the dorsal mPFC while mice faced threat-predicting cues eliciting defensive behaviours, and performed pharmacological and optogenetic inactivations of this area and the amygdala. Our data indicated that the presence of threat-predicting cues induces a stable coding dynamics of internally driven representations in the dorsal mPFC, necessary to drive learned defensive behaviours. Moreover, these neural population representations primary reflect learned associations rather than specific defensive behaviours, and the construct of such representations relies on the functional integrity of the amygdala.