Mónica Bettencourt-Dias

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Publications in Refereed Journals of biology taught by renowned international scientists in each research field. Oct 1991-Oct 1996 FCUL Lisboa, PT 5 year degree in Biochemistry Final classification 18/20. Research performed at ITQB (Oeiras) with Prof. Helena Santos & University of Konstanz (Germany) with Prof. Winfried Boos. • Carvalho-Santos Z, Azimzadeh J, Pereira-Leal JB, Bettencourt-Dias M. Evolution: Tracing the origins of centrioles, cilia, and flagella. J Cell Biol. 2011 Jul 25;194(2):165-75. • Bettencourt-Dias M, Hildebrandt F, Pellman D, Woods G, Godinho SA. Centrosomes and cilia in human disease. Trends Genet. 2011 Aug;27(8):307-15. • Dzhindzhev NS, Yu QD, Weiskopf K, Tzolovsky G, Cunha-Ferreira I, Riparbelli M, Rodrigues-Martins A, Bettencourt-Dias M, Callaini G, Glover DM. (2010) Asterless is a scaffold for the onset of centriole assembly. Nature. 2010 Oct 7;467(7316):714-8. • Otto EA, Hurd TW, Airik R, Chaki M, Zhou W, Stoetzel C, Patil SB, Levy S, Ghosh AK, Murga-Zamalloa CA, van Reeuwijk J, Letteboer SJ, Sang L, Giles RH, Liu Q, Coene KL, Estrada-Cuzcano A, Collin RW, McLaughlin HM, Held S, Kasanuki JM, Ramaswami G, Conte J, Lopez I, Washburn J, Macdonald J, Hu J, Yamashita Y, Maher ER, Guay-Woodford LM, Neumann HP, Obermller N, Koenekoop RK, Bergmann C, Bei X, Lewis RA, Katsanis N, Lopes V, Williams DS, Lyons RH, Dang CV, Brito DA, Dias MB, Zhang X, Cavalcoli JD, Nrnberg G, Nrnberg P, Pierce EA, Jackson PK, Antignac C, Saunier S, Roepman R, Dollfus H, Khanna H, Hildebrandt F. (2010) Candidate exome capture identifies mutation of SDCCAG8 as the cause of a retinal-renal ciliopathy.Nat Genet. 2010 Oct;42(10):840-50. • Carvalho-Santos Z, Machado P, Branco P, Tavares-Cadete F, Rodrigues-Martins A, Pereira-Leal JB, Bettencourt-Dias M. Stepwise evolution of the centriole-assembly pathway. J Cell Sci. 2010 May 1;123(Pt 9):1414-26. Using computational and experimental studies we proposed that a conserved group of proteins explains the conservation of centriole architecture, and that taxon and tissuespecific molecular innovations, gained through emergence, or duplication and divergence, play important roles in coordinating centriole biogenesis to different cellular contexts. This work contextualises the biogenesis and functions of the centriole structure, providing us with a conceptual, evolutionary framework, and suggesting strategies that we are now using to identify novel players in those processes. • Debec A, Sullivan W, Bettencourt-Dias M. Centrioles: active players or passengers during mitosis? Cell Mol Life Sci. 2010 Mar 19. • Kuriyama R, Bettencourt-Dias M, Hoffmann I, Arnold M, Sandvig L. Gamma-tubulincontaining abnormal centrioles are induced by insufficient Plk4 in human HCT116 colorectal cancer cells. J Cell Sci. 2009 Jun 15;122:2014-23. • Cunha-Ferreira I, Bento I, Bettencourt-Dias M. From Zero to Many: Control of Centriole Number in Development and Disease. Traffic. 2009¸10(5):482-98 • Bettencourt-Dias and Glover. SnapShot: centriole biogenesis. Cell. 2009 Jan 9;136(1):188-188.e1. • Cunha-Ferreira I, Rodrigues-Martins A, Bento I, Riparbelli M, Zhang W, Laue E, Callaini G, Glover DM, Bettencourt-Dias M. The SCF/Slimb Ubiquitin Ligase Limits Centrosome Amplification through Degradation of SAK/PLK4. Curr Biol. 2009 Jan 13;19(1):43-9. We show that centrosome amplification is normally inhibited by degradation of SAK/PK4 degradation, mediated by the SCF/Slimb ubiquitin ligase. This complex physically 2/9 2
interacts with SAK/PLK4, and in its absence, SAK/PLK4 accumulates, leading to the striking formation of multiple daughter centrioles surrounding each mother. This interaction is mediated via a conserved Slimb binding motif in SAK/PLK4, mutations of which leads to centrosome amplification. This regulation is likely to be conserved, because knockout of the ortholog of Slimb, beta-Trcp1 in mice, also leads to centrosome amplification. Because the SCF/beta-Trcp complex plays an important role in cell-cycle progression, our results lead to new understanding of the control of centrosome number and how it may go awry in human disease. • Rodrigues-Martins A, Riparbelli M, Callaini G, Glover D and Bettencourt-Dias M. From centriole biogenesis to cellular function: centrioles are essential for cell division at critical developmental stages. Cell Cycle. 2008. Jan;7(1):11- 6. The identification of mutants impaired in centriole biogenesis has permitted the study of the physiological consequences of their absence in the whole organism. In Drosophila, centrioles are not necessary for somatic cell divisions. We showed here that centrioles are needed for proper male meiosis and early embryonic divisions. These results show diversity in the need for centrioles in cell division. This suggests that tissue specific constraints selected for different contributions of centrosome-independent and dependent mechanisms in spindle function. This heterogeneity should be taken into account both in reaching an understanding of spindle function and when designing drugs that target cell division. • Mónica Bettencourt-Dias & Zita Carvalho-Santos (2008) The double life of centrioles: CP110 hits the spotlight, Trends in Cell Biology, Research Focus, Jan;18(1):8-11. • A Rodrigues-Martins, M Riparbelli, G Callaini, DM Glover and M Bettencourt- Dias (2007) Revisiting the role of the mother centriole in centriole duplication, Science, May 18;316(5827):1046-50. Recommended by Faculty of 1000 Biology: http://www.f1000biology.com/article/id/1086061/evaluation We showed that overexpression of SAK/PLK4, a conserved kinase, is sufficient to make centrioles de novo, suggesting centriole biogenesis is a template-free self-assembly process locally triggered by SAK/PLK4. This suggested the mother centriole is not a bona-fide “template” but a platform for regulatory molecules in centriole biogenesis, hence catalyzing it. Implications for Biomedicine: misregulation of molecules involved in centriole duplication may be sufficient to generate centrosome abnormalities observed in cancer. Those molecules may be used in the diagnostic, prognostic and perhaps as targets for drugs in cancer treatment. §� M Bettencourt-Dias and DM Glover (2007), Centrosome Biogenesis And Function, Nature Reviews in Molecular and Cellular Biology, Jun;8(6):451-63. §� A Rodrigues-Martins*, M Bettencourt-Dias*, M Riparbelli*, C Ferreira, I Ferreira, G Callaini & DM Glover (2007). DSAS-6 organizes a tube-like centriole precursor and its absence suggests modularity in centriole assembly. Curr Biol . Sep 4;17(17):1465-72. Our work points to the universality of the role of SAS-6 and of a tube-like scaffold in centriole assembly. Additionally, loss of function and overexpression of Drosophila SAS- 6, highlights a new concept in centriole biology: that its assembly is modular. Implications for Biomedicine: High levels of DSAS-6 trigger the formation of supernumerary abnormal centrosomes, a condition existent in cancer, alerting for negative outcomes of misregulation of SAS-6. §� M Bettencourt-Dias, A Rodrigues-Martins, L Carpenter, M Riparbelli, L Lehmann, MK Gatt, N Carmo, F Balloux, G Callaini & DM Glover (2005) SAK/PLK4 Is Required for Centriole Duplication and Flagella Development, Curr Biol. 15, 2199-207. 3/9 3
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Mónica Bettencourt-Dias

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