ScienceWeek

SCIENCEWEEK

December 29, 2006

Vol. 10 - Number 51

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Each piece, or part, of the whole of nature is always merely an approximation to the complete truth, or the complete truth so far as we know it. In fact, everything we know is only some kind of approximation, because we know that we do not know all the laws as yet.

-- Richard Feynman (1918-1988)

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Contents (full text below):

1. Evolution: On the Origin of Insects 2. Biochemistry: On Protein Small-World Interactions 3. Astrophysics: On Giant Gamma-Ray Bursts 4. Neuroscience: Botulinum Toxin and Nerve Terminals

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Also Noted:

Random Processes in Physics and Finance. Melvin Lax, Wei Cai, and Min Xu. Oxford University Press, Oxford, 2006. Hardback: 341 pp., illus. ISBN 0198567766. More information at: http://www.amazon.com/exec/obidos/ASIN/0198567766/scienceweek

The Problems of Physics. A. J. Leggett. Oxford University Press, Oxford, 2006. Paperback: 204 pp., illus. ISBN 0199211248. More information at: http://www.amazon.com/exec/obidos/ASIN/0199211248/scienceweek

The Mathematics of Behavior. Earl Hunt. Cambridge University Press, New York, 2006. Paperback: 356 pp., illus. ISBN 0521615224. More information at: http://www.amazon.com/exec/obidos/ASIN/0521615224/scienceweek

Encyclopedia of Evolution. Stanley A. Rice. Facts on File, New York, 2006. Hardback: 486 pp., illus. ISBN 0816055157. More information at: http://www.amazon.com/exec/obidos/ASIN/0816055157/scienceweek

CRC Handbook of Chemistry and Physics. A Ready-Reference Book of Chemical and Physical Data. 87th ed. David R. Lide, Ed. CRC Press (Taylor and Francis Group), Boca Raton, FL, 2006. Hardback: Variously paged, illus. ISBN 0849304873. More information at: http://www.amazon.com/exec/obidos/ASIN/0849304873/scienceweek

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1. EVOLUTION: ON THE ORIGIN OF INSECTS

The following points are made by H. Glenner et al (Science 2006 314:1883):

1) Although hexapods -- those arthropods having six legs, including insects -- are the most diverse group of contemporary animals in terms of biological niches and number of species, their origin is highly debated. A key problem is the almost complete absence of fossils that connect hexapods to the other major arthropod sub-phyla, namely Crustacea, Myriapoda (such as centipedes and millipedes), and Chelicerata (such as scorpions and spiders). Over the years, hexapods (insects, springtails, proturnas, and diplurans) have been phylogenetically linked to all of these major arthropod taxa (1).

2) Traditionally, hexapods and the multi-legged myriapods have been united in a group named Atelocerata on the basis of morphological similarities between their tracheal respiration systems and head appendages. However, recent evidence from phylogenetic analyses of molecular sequence data from a variety of genes, as well as from newer morphological studies, points to a relationship between hexapods and crustaceans (2-5), a grouping commonly referred to as Pancrustacea. Furthermore, studies on neurological development in the major arthropod groups have pointed out similarities between the myriapods and chelicerates. Hence, pancrustacean monophyly seems to be gaining more support. So, what does this view tell us about the possible origin of hexapods?

3) The crustaceans are recorded at least as far back as the Upper Cambrian, about 511 million years ago, where they are found in marine sediments. However, except for the debated Devonohexapodus bocksbergensis specimen, all hexapod remains are found only in freshwater or terrestrial strata no earlier than the Devonian, around 410 million years ago. This leaves a gap of 100 million years to the earliest crustaceans. The common explanation has been that earlier traces of hexapods have been erased from the fossil record and that hexapods, like other major groups of terrestrial animals, have closely related ancestors to be found in the marine environment.

4) The recent morphological and molecular-based studies suggest an alternative interpretation -- that hexapods originated within the crustaceans rather than as a sister group. Although the morphological studies mainly favor a close phylogenetic connection between hexapods and malacostracan crustaceans (crabs and crayfish), recent molecular sequence data suggest that hexapods are closely related to branchiopods, a freshwater dwelling group of crustaceans that includes water fleas and fairy shrimp. This hypothesis is supported by analysis of Hox genes that demonstrates homology between development of the pregenital trunk region in insects and the thorax in branchiopods. The new molecular results correspond well with the fossil record and suggest an evolutionary origin of the hexapods in freshwater around 410 million years ago rather than in the marine Cambrian environment.

References (abridged):

1. G. Giribet, C. Ribera, Cladistics 16, 204 (2000).

2. J. M. Mallatt et al., Mol. Phy. Evol. 31, 178 (2004).

3. J. C. Regier, J. W. Shultz, Mol. Phy. Evol. 20, 136 (2001).

4. J. W. Shultz, J. C. Regier, Proc. R. Soc. London Ser. B 267, 1011 (2000).

5. U. W. Hwang et al., Nature 413, 154 (2001).

Science http://www.sciencemag.org

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2. BIOCHEMISTRY: ON PROTEIN SMALL-WORLD INTERACTIONS

The following points are made by T.O. Yeates and M. Beeby (Science 2006 314:1882):

1) Networks of interacting components have been put forward as models for understanding systems as diverse as food webs (1), the topology of the Internet, the social ties of guests at a cocktail party, and the collaboration networks of hip-hop acts in popular music (2). In the area of systems biology, networks of interacting proteins have been explored as models for understanding cellular processes (3-5). Many of these networks exhibit a "small world" property, meaning that a connection can be established between any two elements of the network by following only a small number of links. The small world property of some networks is due in part to the presence of hubs, which are elements connected to many other elements in the network. In protein interaction networks, hubs play an important role, and their properties have been investigated. New work (6) adds a new chapter to the analysis of hubs in protein interaction networks, clarifying some previously murky issues about how they operate in the cell and how they may have evolved.

2) In some protein networks, a link can denote a variety of different kinds of relationships between two proteins: direct physical interaction, correlated expression of proteins in the cell, performance of successive steps in a metabolic pathway, and so on. Kim et al (6) focus on direct physical interactions between proteins, but they take a further step by using the database of known three-dimensional structures to make inferences about what parts of the protein surfaces are involved in the various interactions.

3) This simple but elegant advance adds considerable information to the network view. With the added information it becomes possible to determine which of the multiple interactions or connections that are made to a given protein can occur simultaneously, and which are mutually exclusive due to overlapping binding surfaces. The thrust of their work is that they are able to distinguish between two different kinds of hubs in protein interaction networks. One type, referred to as a single-interface hub, makes interactions to numerous other proteins using just one binding surface; these interactions are mutually exclusive. The other type, a multi-interface hub, makes simultaneous interactions to multiple other proteins using multiple distinct binding surfaces. The distinction between the different kinds of hubs makes it possible to ask new questions and to see new features in protein networks. It also provides a way to begin to factor out spatial versus temporal complexities in networks, which are otherwise convoluted in generic protein interaction networks.

4) After discriminating between the two kinds of protein hubs, the authors are able to clarify a number of issues that had been examined previously. There has been some disagreement over whether hub proteins evolve at a slower rate than more peripheral proteins. Kim et al (6) clarify the topic by showing that the rate of mutation of a hub is constrained by the amount of the protein surface involved in interactions with other proteins, not simply by the number of proteins with which the hub interacts. Thus, multi-interface hubs evolve more slowly than typical cellular proteins, whereas single-interface hubs generally do not. They also note that, compared to single-interface hubs, multi-interface hubs show more highly correlated cellular expression with their interacting partners. This parallels the recent observation of a division of hubs into "date" hubs, which tend to be coexpressed with only one binding partner at a time, and "party" hubs that are co-transcribed alongside multiple partners. The interacting partners of multi-interface hubs are more often involved in stable multi-subunit complexes, whereas interactions to single-interface hubs are apparently more transient and temporally variable.

References (abridged):

1. R. J. Williams, E. L. Berlow, J. A. Dunne, A. L. Barabasi, N. D. Martinez, Proc. Natl. Acad. Sci. U.S.A 99, 12913 (2002).

2. R. D. Smith, J. Stat. Mech. P02006, 10.1088/1742-5468/2006/02/P02006 (2006).

3. A. L. Barabasi, Z. N. Oltvai, Nat. Rev. Genet. 5, 101 (2004).

4. E. M. Marcotte, M. Pellegrini, M. J. Thompson, T. O. Yeates, D. Eisenberg, Nature 402, 83 (1999).

5. L. Salwinski et al., Nucleic Acids Res. 32, D449 (2004).

6. P. M. Kim, L. J. Lu, Y. Xia, M. B. Gerstein, Science 314, 1938 (2006).

Science http://www.sciencemag.org

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3. ASTROPHYSICS: ON GIANT GAMMA-RAY BURSTS

The following points are made by Bing Zhang (Nature 2006 444:1010):

1) The events known as gamma-ray bursts (GRBs) are the most violent and luminous explosions observed in the Universe. In the early 1990s, it became clear that they come in two distinct flavours: longer-duration bursts, typically longer than 2 seconds, with a spectrum of emitted radiation that peaks at lower ("softer") energy; and shorter-duration bursts with a more energetic, "harder" spectrum (1). Observations of burst afterglows in the past decade -- particularly in the past year (2-4) -- have seemed to show that this division is a clean one, and is firmly rooted in the progenitor of each type of burst. According to this picture, long bursts are associated with a young stellar population, marking the deaths of massive stars whose lifetime is short (5). Short bursts, on the other hand, are associated with an old stellar population, and are probably powered by mergers of compact objects such as neutron stars or black holes (6).

2) New work (7-10) blows a hole in this cosy paradigm. The new work contains observations of a bright gamma-ray burst, GRB 060614, that triggered NASA's GRB sentinel, the Swift satellite, at 12:43:48 UT on 14 June 2006. The burst defies pigeonholing within the current scheme. Gehrels et al (7) detail the circumstances of this peculiar burst's discovery. It is one of the brightest ever seen, and was soon located precisely not only by Swift's instrumentation, but also by other space- and ground-based telescopes. The burst is situated in the suburbs of a faint and relatively nearby dwarf galaxy (8). Its duration, recorded by Swift as 102 seconds (7), characterizes it unambiguously as a long GRB. According to previous experience, evidence for the death of a star in a stellar explosion -- a supernova -- should have been spotted in the burst's neighbourhood before too long. But the many optical telescopes around the world trained on the target, waiting for yet another confirmation of the connection between GRBs and supernovae, saw nothing.

3) Three further papers (8-10) provide independent reports of the stringent upper limits on the radiation flux from a possible supernova underlying GRB 060614. Gal-Yam and colleagues (8) made a series of observations with the Hubble Space Telescope in the weeks after the burst trigger. These set an upper limit more than 100 times fainter than the faintest supernova previously associated with a GRB — and indeed considerably fainter than any supernova ever observed. Della Valle et al (9) report complementary observations from the European Southern Observatory's Very Large Telescope in the Atacama desert in northern Chile. This survey started 15 hours and ended 65 days after the burst, and provides an upper limit on the flux that is about three times higher than that of Gal-Yam and colleagues', but still well below the luminosity of any known supernova over an unprecedentedly long time span. Fynbo et al (10) use a range of telescopes to arrive at a similar result -- and also discover a second long burst with no apparent supernova signature.

4) The absence of a supernova need not in itself be revolutionary. The production of a significant amount of nickel-56, which is a prerequisite for a supernova, is not guaranteed in a collapsing star (7,8), and the earliest model to connect GRBs with the massive-star collapses indeed characterized the bursts as "failed supernovae" (5). A supernova might also precede its associated GRB. Nevertheless, the weight of evidence from the past decade is consistent with there being no significant gap between a GRB and its supernova, as well as with the hypothesis that every long GRB has a supernova accompanying it. What makes the story more intriguing is that every property of GRB 060614 places it in the short-burst category -- except, that is, for its duration.

References (abridged):

1. Kouveliotou, C. et al. Astrophys. J. 413, L101–L104 (1993).

2. Gehrels, N. et al. Nature 437, 851–854 (2005).

3. Fox, D. B. et al. Nature 437, 845–851 (2005).

4. Barthelmy, S. D. et al. Nature 438, 994–996 (2005).

5. Woosley, S. E. Astrophys. J. 405, 273–277 (1993).

6. Paczynski, B. Astrophys. J. 308, L43–L46 (1986).

7. Gehrels, N. et al. Nature 444, 1044–1046 (2006).

8. Gal-Yam, A. et al. Nature 444, 1053–1055 (2006).

9. Della Valle, M. et al. Nature 444, 1050–1052 (2006).

10. Fynbo, J. P. U. et al. Nature 444, 1047–1049 (2006).

Nature http://www.nature.com/nature

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4. NEUROSCIENCE: BOTULINUM TOXIN AND NERVE TERMINALS

The following points are made by Giampietro Schiavo (Nature 2006 444:1019):

1) Botulinum neurotoxins (BoNTs) are some of the most deadly substances known to mankind. By blocking nerve function, they cause botulism, a severe condition that may ultimately lead to muscular and respiratory paralysis. These sophisticated bacterial proteins owe their toxicity to their extraordinary specificity for neurons and to their enzymatic activity. New work (1,2) describes the mechanisms by which BoNT/B -- a toxin that causes human botulism -- recognizes the surface of neuron junctions (synapses). This work provides insight into how other BoNTs may exert their lethal action, and describes a mode of binding that might be used by other biological compounds.

2) Once inside a neuron, a single molecule of BoNT is, in principle, capable of deactivating the whole synapse. BoNTs consist of two protein segments, known as the heavy and light chains. It is the light chain that deactivates neuromuscular junctions -- the synapses that connect muscles to their controlling neurons -- by specifically inhibiting members of the SNARE protein family (3). SNARE proteins are distributed over the membranes of all animal and plant cells and are also found on the membranes of synaptic vesicles, the bubble-shaped organelles that store and release neurotransmitter chemicals at neuron terminals. SNARE proteins are essential for membrane fusion, during which vesicles merge with the cell membrane and release their load. Once the synaptic vesicles have done this, they are recycled by the neuron for further use.

3) So how do BoNTs enter neurons? The heavy chain is most likely to be responsible. One half of the heavy chain mediates binding to neurons by interacting with lipid molecules (polysialogangliosides, PSGs) in the cell membrane, and with either one of two integral membrane proteins -- synaptotagmin I or synaptotagmin II -- found in synaptic vesicles. A dual-receptor model for these toxins was proposed long ago (4), but experimental validation of this theory has required a worldwide effort. The model predicts that the interaction of BoNTs with both PSGs and protein receptors is necessary to explain their awesome potency (3), with a different protein receptor being recognized by each BoNT.

4) Evidence for protein involvement in BoNT binding was scarce until it was discovered (5) that BoNT/B binds to both PSGs and the part of synaptotagmins that lies inside synaptic vesicles, in the area known as the lumen. More recently, the specific regions of synaptotagmins that bind BoNT/B have been identified6, as have those bound by the closely related BoNT/G. Taken together, these results suggest that BoNTs enter neurons by stowing away inside recycled synaptic vesicles, binding simultaneously to PSGs and to the luminal domain of synaptic-vesicle proteins. The toxins then escape from the vesicle lumen when the vesicles are acidified as they reload with neurotransmitters. Another BoNT family member, BoNT/A, has been shown to bind to the synaptic vesicle protein SV2, in agreement with the prediction that each type of BoNT interacts with a different protein.

References (abridged):

1. Jin, R., Rummel, A., Binz, T. & Brunger, A. T. Nature 444, 1092–1095 (2006).

2. Chai, Q. et al. Nature 444, 1096–1100 (2006).

3. Schiavo, G., Matteoli, M. & Montecucco, C. Physiol. Rev. 80, 717–766 (2000).

4. Montecucco, C. Trends Biochem. Sci. 11, 314–317 (1986).

5. Nishiki, T. et al. FEBS Lett. 378, 253–257 (1996).

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