19. Walter, F., Murchie, A. I., Duckett, D. R. & Lilley, D. M. Global structure of four-wayRNA junctions studied using ¯uorescence resonance energy transfer. RNA 4, 719±728 (1998). 20. Liautard, J. -P., Sri-Widada, J., Brunel, C. & Jeanteur, P. Structural organisation of ribonucleoproteins containing small nuclear RNAs from HeLa cells. J. Mol. Biol. 162, 623±643 (1982). 21. Hartmuth, K., Raker, V. A., Huber, J., Branlant, C. & Lu È hrmann, R. An unusual chemical reactivity of Sm site adenosines strongly correlates with proper assembly of core U snRNP particles. J. Mol. Biol. 285, 133±147 (1999). 22. Hoet, R. M., Kastner, B., Lu Èhrmann, R. & van Venrooij, W. J. Puri®cation and characterization of human autoantibodies directed to speci®c regions on U1RNA; recognition of native U1RNP complexes. Nucleic Acids Res. 21, 5130±5136 (1993). 23. Lin, W. -L. & Pederson, T. Ribonucleoprotein organization of eukaryotic RNA. XXXI. Structure of the U1 small nuclear ribonucleoprotein. J. Mol. Biol. 180, 947±960 (1984). 24. Urlaub, H., Raker, V., Kostka, S. & Lu Èhrmann, R. Sm protein±Sm site RNA interactions within the inner ring of the spliceosomal snRNP core structure. EMBO J. 20, 1±10 (2001). 25. Heinrichs, V., Bach, M., Winckelmann, G. & Lu È hrmann, R. U1-speci®c protein C needed for ef®cient complex formation of U1 snRNP with a 59 splice site. Science 247, 69±72 (1990). 26. Adrian, M., Dubochet, J., Lepault, J. & McDowall, A. W. Cryo-electron microscopy of viruses. Nature 308, 32±36 (1984). 27. van Heel, M., Harauz, G. & Orlova, E. V. A new generation of the IMAGIC image processing system. J. Struct. Biol. 116, 17±24 (1996). 28. van Heel, M. & Frank, J. Use of multivariate statistics in analysing the images of biological macromolecules. Ultramicroscopy 6, 187±194 (1981). 29. van Heel, M. & Harauz, G. Resolution criteria for three-dimensional reconstruction. Optik 73, 119± 122 (1986). Acknowledgements We thank F. Mu Èller for the modelling software ERNA-3D; K. Nagai and C. Kambach for the Sm protein ring model; and M. Golas and B. Sander for assistance in electron microscopy. This work was supported by the Gottfried Wilhelm Leibniz Program and a grant from the Deutsche Forschungsgemeinschaft. Correspondence and requests for materials should be addressed to H.S. (e-mail: Holger.Stark@mpibpc.mpg.de). letters to nature 542 NATURE | VOL 409 | 25 JANUARY 2001 | www.nature.com ................................................................. addendum A one-hit model of cell death in inherited neuronal degenerations G. Clarke, R. A. Collins, B. R. Leavitt, D. F. Andrews, M. R. Hayden, C. J. Lumsden & R. R. McInnes Nature 406, 195±199 (2000). .................................................................................................................................. It has been questioned whether our neurodegeneration model was anticipated by Calne and co-workers 1±4 . Both groups related expo- nential neuronal loss to pathogenesis, but the models are radically different. We recognized that in neurodegeneration, exponential death kinetics mean that the risk of cell death remains constant with age. To accommodate constant risk, we proposed a one-hit model: the hit is a consequence of a neuron being in a high-risk (for example, mutant) state; a hit is a biochemical reaction within each single neuron, committing it to death at a random time. We noted that constant risk excludes cumulative intracellular damage as a disease mechanism. Calne et al. proposed that in idiopathic Parkinsonism ``An event [for example, infection] acts on the neuronal population over a brief period ¼[to initiate disease]'' 2 . They excluded ongoing processes as causing idiopathic Parkinsonism 2,4 , but the role of cumulative intracellular damage was not addressed. Their focus on whole neuron populations and on events that act on them is notable, and complementary to but different from our model. M 1. Lee, C. S. et al. Clinical observations on the rate of progression of idiopathic parkinsonism. Brain 117, 501±507 (1994). 2. Schulzer, M., Lee, C. S., Mak, E. K., Vingerhoets, F. J. G. & Calne, D. B. A mathematical model of pathogenesis in idiopathic parkinsonism. Brain 117, 509±516 (1994). 3. Calne, D. B. Is idiopathic parkinsonism the consequence of an event or a process? Neurology 44, 5±10 (1994). 4. Lee, C. S. et al. Patterns of asymmetry do not change over the course of idiopathic parkinsonism: implications for pathogenesis. Neurology 45, 435±439 (1995). ................................................................. corrections Kainate receptors are involved in synaptic plasticity Zuner A. Bortolotto, Vernon R. J. Clarke, Caroline M. Delany, Michael C. Parry, Ilse Smolders, Michel Vignes, Ken H. Ho, Peter Miu, Bradford T. Brinton, Robert Fantaske, Ann Ogden, Mary Gates, Paul L. Ornstein, David Lodge, David Bleakman & Graham L. Collingridge Nature 402, 297±301 (1999). .................................................................................................................................. In this paper, the authors omitted the reference to the published synthetic pathway 1 by which the selective GluR5 kainate receptor antagonist LY382884 may be made. M 1. Bleisch, T. J. et al. Structure activity studies of aryl-spaced decahydroisoquinoline-3-carboxylic acid AMPA receptor antagonists. Bioorg. Med. Chem. Lett. 7, 1161±1166 (1997). ................................................................. correction Error and attack tolerance of complex networks Re  ka Albert, Hawoong Jeong & Albert-La  szlo  Barabasi Nature 406, 378±382 (2000). .................................................................................................................................. In this paper, the error tolerance curves for the exponential network were affected by a software error. This did not impact the attack curves nor the measurements and conclusions regarding the error/ atack tolerance of scale-free networks, the World-Wide Web and the Internet. The corrected Figs 2a and 3a are shown below. M SF E Attack Failure 0 0.2 0.4 0.6 0.8 1.0 0 20 40 60 d 0 0.2 0.4 0.6 0.8 1.0 f 0 0.5 1.0 1.5 2.0 S and <s> <s> S Failure Attack 2a 3a © 2001 Macmillan Magazines Ltd