Ruth Chiquet-Ehrismann's research focused on the influence of the extracellular matrix on cell behavior, a very new field at the time. Today it is recognized that different matrix proteins influence cell adhesion, cell growth and migration, tissue morphology and signal transduction in specific and decisive ways. Chiquet-Ehrismann contributed pioneering work on the tenascin gene family of matricellular proteins, of which some members were discovered, cloned and sequenced by her group. Different tenascins have related domain organisations and their 3-6 subunits oligomerize into star-like structures. Tenascin C interferes with the adhesion of many cells to fibronectin, which led to the concept that it is anti-adhesive. Tenascin C accumulates in the stroma of carcinomas and is a sensitive tumor marker that is involved in cancer metastasis. More recently, Ruth Chiquet-Ehrismann and her group discovered roles for tenascin C and tenascin W in stem cell and cancer metastatic niches, and elucidated how tenascin C expression is controlled by the transcription factorMKL1, that links cellular mechanosensation to fibrosis and cancer progression. Chiquet-Ehrismann and her group also discovered the teneurin gene family. These type II trans-membrane proteins are conserved throughout animals and function in germ cell development, neuronal pathfinding and CNS development. The cleaved intracellular domain functions in transcriptional regulation. During 31 years of work at the Friedrich Miescher Institute, Chiquet-Ehrismann guided a very active research group. Many excellent Ph.D. students and postdoctoral fellows emerged from this group, who continue to develop the interesting field of matrix research. Her group had a high international reputation and collaborated with many scientists around the world . She won the Huggenberger-Bischoff Prize for Cancer Research in 1990.
Key publications
Chiquet-Ehrismann, R., Kalla, P., Pearson, C. A., Beck, K., and Chiquet, M.. Tenascin interferes with fibronectin action. Cell 53, 383–390.
Spring, J., Beck, K., and Chiquet-Ehrismann, R.. Two contrary functions of tenascin: Dissection of the active sites by recombinant tenascin fragments. Cell 59, 325–334.
Hendaoui, I., Tucker, R. P., Zingg, D., Bichet, S., Schittny, J., and Chiquet-Ehrismann, R.. Tenascin-C is required for normal Wnt/b-catenin signaling in the whisker follicle stem cell niche. Matrix Biol. 40, 46–53.
Sivasankaran, B., Degen, M. et al.. Tenascin-C is a novel RBPJkappa-induced target gene for Notch signaling in gliomas. Cancer Res. 69, 458–465.
Asparuhova, M. B., Feralli, J., Chiquet, M., and Chiquet-Ehrismann, R.. The transcriptional regulator megakaryoblastic leukemia-1 mediates serum response factor-independent activation of tenascin-C transcription by mechanical stress. FASEB J. 25, 3477–34883.
Baumgartner, S., Martin, D., Hagios, C., and Chiquet-Ehrismann, R.. tenm, a Drosophila gene related to tenascin, is a new pair-rule gene. EMBO J. 13, 3728–3740.
Rubin, B. P., Tucker, R. P., Martin, D., and Chiquet-Ehrismann, R.. Teneurins, a novel family of neuronal cell surface proteins in vertebrates, homologous to the Drosophila pair-rule gene product Ten-m. Dev. Biol. 216, 195–209.
Schöler, J., Ferralli, J., Thiry, S., Chiquet-Ehrismann, R. The intracellular domain of teneurin-1 induces the activity of microphthalmia-associated transcription factor by binding to transcriptional repressor HINT1. J Biol Chem. 290, 8154–65.
