that do not rely on nonlinear optical effects. This is an important advantage given that heat dissipation is becoming the key limiting parameter in microelectronics. A fascinating feature of this work is the use of the p-i-n junction, which combines the nonlinear-optical and semiconducting properties of silicon in the same device. Rong et al. show that this design enables control of the optical power emitted by the laser, which in principle should also be possible at a very high frequency and could therefore be used for information processing. Last but not least, this work demonstrates that techno- logical advances in microelectronics, in this case the silicon-on-insulator and nanolitho- graphy techniques used to fabricate the waveguide ridge structure, can be applied to create advances in an apparently unrelated research field such as optoelectronics. ■ Jerome Faist is at the Physics Institute, University of Neuchâtel, CH-2000 Neuchâtel, Switzerland. e-mail: jerome.faist@unine.ch 1. Rong, H. et al. Nature 433, 725–728 (2005). 2. Rosencher, E. & Vinter, B. Optoelectronics (Cambridge Univ. Press, 2002). 3. Shen, Y. R. The Principles of Nonlinear Optics (Wiley, New York, 1984). 4. Spillane, S. M., Kippenberg, T. J. & Vahala, K. J. Nature 415, 621–623 (2002). 5. Kippenberg, T. J., Spillane, S. M., Armani, D. K. & Vahala, K. J. Optics Lett. 29, 1224–1227 (2004). 6. Luryi, S., Xu, J. & Zaslavsky, A. (eds) Future Trends in Microelectronics (Wiley-IEEE, New York, 2004). 7. Boyraz, O. & Jalali, B. Optics Express 12, 5269–5273 (2004). 8. Rong, H. et al. Nature 433, 292–294 (2005). and is mediated by several protein families 2 . In mammals, most apoptotic cell deaths are mediated by a specific signalling pathway known as the mitochondrial pathway. As its name implies, this pathway requires the active participation of mitochondria — the organelles better known for their role in cellular respiration and the generation of the high-energy molecule ATP. In cells con- demned to die, mitochondria release several dozen proteins into the cytosol, and they can then wreak havoc in the rest of the cell. The best known of these mitochondrial expatriates — cytochrome c — interacts in the cytosol with the Apaf-1 protein, ulti- mately activating a group of proteases (pro- tein-digesting enzymes) known as caspases 3 . These enzymes then cleave a selected set of target proteins, resulting in the controlled ‘implosion’ of the cell. How cytochrome c et al. manage to cross the outer lipid bilayer of the mitochondria to reach the cytosol is still hotly debated. What is clear, however, is that this release is regulated by proteins of the Bcl-2 family,many of which can bind directly to the outer mitochondrial membrane. Recently, several groups have reported a second peculiar behaviour of mitochondria during apoptosis: not only do they release proteins, but they also fragment into smaller pieces 4 . That mitochondria can fragment is nothing new in itself — like bacteria, mitochondria divide by a process of fission, in which one long organelle is pinched in the middle to produce two shorter daugh- ters. Unlike bacteria, mitochondria can also undergo the reverse process, and fuse together to form long filaments. Fission and fusion are tightly controlled, and are important for the proper distribution of mitochondria during cell division. But why mitochondria should fragment during apoptosis is not clear. One possibility is that the release of mitochondrial proteins stimulates mitochondrial division. Indeed, conditions that compromise mitochondrial function have been reported to result in short, round mitochondria. An attractive alterna- tive would be that fission is necessary (directly or indirectly) for the release of cytochrome c. Consistent with this idea, interfering with the fission process has been reported to delay cytochrome c release during apopto- sis 5 . Whether this is a general phenomenon remains to be seen. Furthermore, given that mitochondrial fission occurs continuously in living cells, there must be more to the story than fission simply promoting death. Enter C. elegans. Genetic studies in this species showed that most components of the apoptotic pathway have been conserved throughout evolution 6 . For example, C. ele- gans has a Bcl-2 counterpart (CED-9), an Apaf-1-like molecule (CED-4) and a caspase (CED-3). Surprisingly, however, mitochon- drial proteins have so far played at best a minor role in the apoptosis saga in C. elegans. news and views 692 NATURE | VOL 433 | 17 FEBRUARY 2005 | www.nature.com/nature Figure 2 Cross-section of the silicon laser designed by Rong et al. 1 . A ridge-shaped waveguide made of silicon is surrounded by silica (SiO 2 ). The large difference in refractive index between silicon and silica ensures that the light intensity is tightly confined within the waveguide so that a large Raman amplification can be obtained. This structure is embedded within a semiconductor device, which enhances the laser output by draining off unwanted electrons and holes that are created by the two-photon absorption shown in Fig. 1b. Cell biology Divide and conquer Michael Hengartner The discovery that cell death in nematode worms induces fragmentation of mitochondria reveals a new parallel to the death process in mammals, and may shed light on why mitochondria divide in death. W hen mammalian cells die by the process of apoptosis, their mito- chondria fragment into smaller pieces. Why these power-generating com- partments should divide as the cell around them dies, and whether this fragmentation is important for the death process or simply an epiphenomenon, has so far largely remained unclear. But an answer is suggested by the paper from Conradt and colleagues on page 754 of this issue 1 .The authors show that mito- chondria also fragment during apoptosis in the small nematode worm Caenorhabditis elegans. Moreover, experimental induction or prevention of mitochondrial fragmenta- tion could respectively enhance or partially prevent apoptosis. These observations hint that mitochondrial fragmentation has an evolutionarily conserved, causative role in promoting apoptotic cell death. The term apoptosis refers to a specific type of programmed cell death that occurs in all multicellular animals, from the lowly worm to the highly complex human. Apoptosis is characterized by specific morphological changes in the dying cell, Nature Publishing Group ©2005