Dr. Florence Janody
Medical Clinic III for Oncology, Hematology and Rheumatology, University Hospital Bonn, Sigmund-Freud-Straße 25, 53127 Bonn, Germany
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Academic Career Length
30Years (1997-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications1 June 2011 in Development
Journal Article
BFBeatriz García Fernández
Beatriz García FernándezPGPedro Gaspar
Pedro Gaspar
CBCatarina Brás-Pereira
Catarina Brás-PereiraBJBarbara Jezowska
Barbara Jezowska
SRSofia Raquel Rebelo
Sofia Raquel Rebelo
Florence JanodyThe conserved Hippo tumor suppressor pathway is a key kinase cascade that controls tissue growth by regulating the nuclear import and activity of the transcription co-activator Yorkie. Here, we report that the actin-Capping Protein αβ heterodimer, which regulates actin polymerization, also functions to suppress inappropriate tissue growth by inhibiting Yorkie activity. Loss of Capping Protein activity results in abnormal accumulation of apical F-actin, reduced Hippo pathway activity and the ectopic expression of several Yorkie target genes that promote cell survival and proliferation. Reduction of two other actin-regulatory proteins, Cofilin and the cyclase-associated protein Capulet, cause abnormal F-actin accumulation, but only the loss of Capulet, like that of Capping Protein, induces ectopic Yorkie activity. Interestingly, F-actin also accumulates abnormally when Hippo pathway activity is reduced or abolished, independently of Yorkie activity, whereas overexpression of the Hippo pathway component expanded can partially reverse the abnormal accumulation of F-actin in cells depleted for Capping Protein. Taken together, these findings indicate a novel interplay between Hippo pathway activity and actin filament dynamics that is essential for normal growth control.
16 May 2017 in Nature Communications
Journal Article
STSandra Tavares
Sandra TavaresAVAndré Filipe Vieira
André Filipe VieiraATAnna Taubenberger
Anna TaubenbergerMAMargarida Araújo
Margarida AraújoNMNuno Pimpao Martins
Nuno Pimpao MartinsFlorence Janody +9
Studies of the role of actin in tumour progression have highlighted its key contribution in cell softening associated with cell invasion. Here, using a human breast cell line with conditional Src induction, we demonstrate that cells undergo a stiffening state prior to acquiring malignant features. This state is characterized by the transient accumulation of stress fibres and upregulation of Ena/VASP-like (EVL). EVL, in turn, organizes stress fibres leading to transient cell stiffening, ERK-dependent cell proliferation, as well as enhancement of Src activation and progression towards a fully transformed state. Accordingly, EVL accumulates predominantly in premalignant breast lesions and is required for Src-induced epithelial overgrowth in Drosophila. While cell softening allows for cancer cell invasion, our work reveals that stress fibre-mediated cell stiffening could drive tumour growth during premalignant stages. A careful consideration of the mechanical properties of tumour cells could therefore offer new avenues of exploration when designing cancer-targeting therapies.
6 May 2008 in Proceedings of the National Academy of Sciences
Journal Article
ICInés Carrera
Inés CarreraFlorence JanodyNLNina Leeds
Nina Leeds
FDFabien Duveau
Fabien Duveau
JTJessica E. Treisman
Jessica E. TreismanWnt target gene transcription is mediated by nuclear translocation of stabilized β-catenin, which binds to TCF and recruits Pygopus, a cofactor with an unknown mechanism of action. The mediator complex is essential for the transcription of RNA polymerase II-dependent genes; it associates with an accessory subcomplex consisting of the Med12, Med13, Cdk8, and Cyclin C subunits. We show here that the Med12 and Med13 subunits of the Drosophila mediator complex, encoded by kohtalo and skuld , are essential for the transcription of Wingless target genes. kohtalo and skuld act downstream of β-catenin stabilization both in vivo and in cell culture. They are required for transcriptional activation by the N-terminal domain of Pygopus, and their physical interaction with Pygopus depends on this domain. We propose that Pygopus promotes Wnt target gene transcription by recruiting the mediator complex through interactions with Med12 and Med13.
1 January 1999 in Nucleic Acids Research
Journal Article
CSCatherine Sanchez
Catherine Sanchez
CLCorinne Lachaize
Corinne Lachaize
Florence JanodyBBBernard Bellon
Bernard Bellon
LRLaurence Röder
Laurence RöderBJBernard Jacq
Bernard Jacq +2
Flynets (http://gifts.univ-mrs.fr/FlyNets/FlyNets_home_page.html) is a WWW database describing molecular interactions (protein-DNA, protein-RNA and protein-protein) in the fly Drosophila melanogaster. It is composed of two parts, as follows. (i) FlyNets-base is a specialized database which focuses on molecular interactions involved in Drosophila development. The information content of FlyNets-base is distributed among several specific lines arranged according to a GenBank-like format and grouped into five thematic zones to improve human readability. The FlyNets database achieves a high level of integration with other databases such as FlyBase, EMBL, GenBank and SWISS-PROT through numerous hyperlinks. (ii) FlyNetslist is a very simple and more general databank, the long-term goal of which is to report on any published molecular interaction occuring in the fly, giving direct web access to corresponding abstracts in Medline and in FlyBase. In the context of genome projects, databases describing molecular interactions and genetic networks will provide a link at the functional level between the genome, the proteome and the transcriptome worlds of different organisms. Interaction databases therefore aim at describing the contents, structure, function and behaviour of what we herein define as the interactome world.
15 August 2003 in Development
Journal Article
Florence JanodyZMZara Martirosyan
Zara Martirosyan
ABAude Benlali
Aude Benlali
JTJessica E. Treisman
Jessica E. TreismanThe organizing centers for Drosophila imaginal disc development are created at straight boundaries between compartments; these are maintained by differences in cell affinity controlled by selector genes and intercellular signals. skuld and kohtalo encode homologs of TRAP240 and TRAP230, the two largest subunits of the Drosophila mediator complex;mutations in either gene cause identical phenotypes. We show here that both genes are required to establish normal cell affinity differences at the anterior-posterior and dorsal-ventral compartment boundaries of the wing disc. Mutant cells cross from the anterior to the posterior compartment, and can distort the dorsal-ventral boundary in either the dorsal or ventral direction. The Skuld and Kohtalo proteins physically interact in vivo and have synergistic effects when overexpressed, consistent with a skuld kohtalo double-mutant phenotype that is indistinguishable from either single mutant. We suggest that these two subunits do not participate in all of the activities of the mediator complex, but form a submodule that is required to regulate specific target genes, including those that control cell affinity.
1 March 2015 in Current Biology
Journal Article
PGPedro Gaspar
Pedro Gaspar
MHMaxine V. Holder
Maxine V. HolderBABirgit L. Aerne
Birgit L. Aerne
Florence JanodyNTNicolas Tapon
Nicolas TaponAbout Me
Florence Janody earned her Ph.D. in Cell Biology, Structural Biology and Microbiology at the Developmental Biology Institute of Marseille Luminy (IBDML) in the laboratory of Dr. Nathalie Dostatni before joining the laboratory of Dr. Jessica Treisman for postdoctoral training at Skirball Institute in New York (USA) in 2000. During these trainings, her main interest has been to understand how signal transduction cascades coordinate changes in gene expression. In a mosaic genetic screen for novel genes involved in signalling activity, she identified loss of function mutation for genes encoding actin binding proteins (ABP). She established her independency in 2007 at Instituto Gulbenkian de Ciência (IGC) in Portugal. Her lab has reported that the actin cytoskeleton conveys signals from the cell membrane into intracellular signalling pathways, leading to cancer transcriptional programmes. She moved her lab in January 2018 to Instituto de Patologia e Imunologia Molecular da Universidade do Porto (Ipatimup)/ Instituto de Investigação e Inovação em Saúde (i3S) with the goal of deciphering the cytoskeletal rules governing carcinogenesis, focusing on signalling networks promoting aberrant cell plasticity properties, as these mechanisms underlie disease progression and therapeutic resistance, using the fruit fly Drosophila melanogaster; inducible human cell lines, tumour samples and computational modelling.