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ScienceWeek
SCIENCEWEEK
June 22, 2007
Vol. 11 - Number 24
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I would live to study, and not study to live.
-- Francis Bacon (1561-1626)
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Contents (full text below):
1. Genetics: A Breakthrough for Global Public Health
2. Psychology: Birth Order and Intelligence
3. Immunology: Short-Term Memory
4. Materials Science: Reflections on Ionic Liquids
5. Evolutionary Biology: Re-Crowning Mammals
6. Eukaryote Evolution: Engulfed by Speculation
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1.
Science 22 June 2007: Vol. 316. no. 5832, pp. 1703 - 1704 DOI: 10.1126/science.1138904
Genetics: A Breakthrough for Global Public Health
D.D. Chadee et al
The reemergence of dengue fever and urban yellow fever in the Americas during the past 20 years demonstrates that mosquito-borne diseases are threats even in the 21st century. Globally, about 50 million to 100 million cases of dengue and about 500,000 cases of dengue hemorrhagic fever occur annually (1). Recently, an unprecedented chikungunya virus outbreak occurred in countries bordering the Indian Ocean, with ~250,000 cases and 205 deaths. The threat of mosquito-borne pathogens is very real, with dengue, yellow fever, and chikungunya viruses all being transmitted by the mosquito Aedes aegypti.
Nene et al. report the complete genome sequence of Ae. aegypti (2). This comes about 4 years after the complete genome sequence of Anopheles gambiae, the primary mosquito vector of malaria in Africa (3). It is also a little over 100 years since Ae. aegypti was shown to transmit yellow fever. As the blueprint for the vector's biology, the Ae. aegypti genome sequence is another major advance in the history of combating mosquito-borne disease. Mosquito-borne disease control is currently based on clinical management of patients and mosquito control because efficient vaccines are unavailable. The challenge ahead is to use genome sequence information to understand gene and protein functions and the causes of mosquito diversity that determine the role of Ae. aegypti in pathogen transmission (4).
The completed sequence should greatly facilitate the identification of Ae. aegypti genes and proteins that control a wide range of traits such as vector competence and capacity for pathogen transmission, life history, olfactory cues that affect behavior, host seeking, mating behavior, and insecticide resistance. The genome sequence should also help identify new DNA markers and allow DNA fingerprinting for ecological studies. Such tools are essential to characterize both individual mosquitoes and natural populations of Ae. aegypti. Genetic characterization of mosquito populations should reveal how pathogen transmission is influenced by gene flow, geographic isolation, and population dynamics and dispersal. Moreover, characterizing gene variation in natural populations will provide a basis for understanding the risk for Ae. aegypti-borne epidemics. For example, yellow fever has never been reported in Asia, despite the presence of dengue and Ae. aegypti. Such an epidemic would be a catastrophe.
Tools for genetically altering Ae. aegypti (or An. gambiae) can now be more easily adapted for creating mosquitoes that are pathogen-resistant (5). In combination with new information on the effects of genes on the mosquito phenotype, deploying such resistant mosquitoes should be possible. Endosymbiotic bacteria could also be genetically modified to introduce desirable genes into mosquito populations that reduce vector competence for a pathogen or reduce their survival (6), a strategy guided by a deeper understanding of Ae. aegypti biology through its genome sequence.
The Ae. aegypti subspecies, Ae. aegypti aegypti and Ae. aegypti formosus, differ in appearance, geographical distribution, behavior, genetic diversity and relatedness, and vector competence for yellow fever virus (7) and dengue virus (8). The completed genome sequence is from Ae. aegypti aegypti because it is widely distributed, is the primary vector, and likely evolved from Ae. aegypti formosus (7). But the relationship between the geographic distribution and genetic diversity of Ae. aegypti must be clarified to ensure that control strategies are used that are appropriate for the specific location. Genetic mapping studies have implicated many genes in Ae. aegypti vector competence for dengue virus (8). However, specific genes have not yet been identified; the Ae. aegypti genome sequence should help in this characterization. The An. gambiae genome sequence has been essential to identifying candidate genes that control susceptibility to malaria infection. This was accomplished through the use of RNA interference, a technique that "knocks down" the expression of specific gene targets in the organism (9).
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2.
Science 22 June 2007: Vol. 316. no. 5832, pp. 1711 - 1712 DOI: 10.1126/science.1144749
Psychology: Birth Order and Intelligence
Frank J. Sulloway
Research on birth order and intellectual performance is replete with contradictory findings and long-standing conceptual disagreements. In the wake of these ongoing controversies, a new study that has profited from past debates is especially welcome. In an elegantly designed analysis of 241,310 Norwegian 18- and 19-year-olds that appears on page 1717 of this issue, Kristensen and Bjerkedal show that older siblings have higher intelligence test scores than younger siblings (1). In addition, these two researchers demonstrate that how study participants were raised, not how they were born, is what actually influences their IQs.
In a companion study, Bjerkedal et al. (2) show that birth-order differences in their Norwegian sample are nearly identical for a subset of adjacent siblings who were raised together (127,902 individuals) and for a between-family sample (112,799 individuals). Critics have long argued that such birth-order effects, which typically emerge in between-family studies, are spurious--phantom artifacts of uncontrolled differences in family size, socioeconomic status, parental IQ, and other background factors (3-5). At least in the domain of intellectual ability, the new Norwegian findings rule out this alternative explanation.
Critics might still argue that the mean IQ difference documented between a Norwegian firstborn and a secondborn is only 2.3 points. Such a modest difference, however, can have far greater consequences than most people realize. For example, if Norway's educational system had only two colleges--a more prestigious institution for students with IQs above the mean, and a less desirable institution for all other students--an eldest child would be about 13% more likely than a secondborn to be admitted to the better institution (the relative risk ratio), and the odds of a firstborn being admitted would be 1.3 times as great. In medicine, new therapeutic benefits of this magnitude often make front-page headlines. In addition, such differences in opportunities gained or lost inevitably accumulate over one's lifetime.
One puzzle highlighted by these latest findings is why certain other within-family studies have failed to show equally consistent results. Some of these previous null findings, which have all been obtained in much smaller samples, may be explained by inadequate statistical power, as Bjerkedal et al. themselves suggest. But most previous researchers have overlooked another intriguing reason for such inconsistent outcomes, which are generally found in studies of children rather than adults. As has been noted by Zajonc and colleagues, younger siblings tend to score higher than older siblings when tests of intellectual ability are conducted under the age of about 12 (6, 7). In more than 50 previous samples, there is a significant tendency for IQ disparities by birth order to reverse direction as children get older.
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3.
Nature 447, 916-917 (21 June 2007) | doi:10.1038/447916a; Published online 20 June 2007
Immunology: Short-Term Memory
Benjamin N. Gantner & Harinder Singh
Chemical modification of histone proteins can affect the expression of their associated genes. Some immune cells seem to exploit this process to avoid excessive inflammation while fighting invading pathogens.
The innate immune system has several essential roles: it must detect infectious pathogens, initiate antimicrobial mechanisms to remove them and trigger inflammation to activate additional immune responses such as fever. This last function is tricky because too little inflammation will lead to an ineffective response and too much can lead to septic shock and death. So how does the innate immune system prevent excessive responses while repeatedly encountering the same pathogen during an infection?
It has been appreciated for some time that particular innate immune cells — macrophages — can dampen their reactions; however, on page 972 of this issue, Foster et al.1 suggest a more complex change in the sensitivity of these cells to pathogens. They find that macrophages selectively modify the histone proteins that package the genes activated in response to pathogens, to adapt to repeated exposure.
More than a century ago, Richard Pfeiffer discovered2 that components of dead bacteria, which he called endotoxins, could kill test animals; this is now known to be due to an excessive inflammatory response. Endotoxins are highly conserved components of pathogens that are recognized by the innate immune system. Among the most potent endotoxins is lipopolysaccharide (LPS), which is a component of the outer membrane of bacterial cells. It is recognized by Toll-like receptor 4 (TLR4) on the surface of macrophages, where it initiates the molecular signalling pathways that lead to the activation of proinflammatory and antimicrobial genes.
Paul Beeson's seminal work3 in the 1940s uncovered a fascinating twist to the endotoxin response in humans. The typhoid vaccine was used in patients with syphilitic infection of the nervous system to slow disease progression. Although initial exposure to this vaccine caused fever, repeated daily exposures suppressed the induction of fever and led to a state of tolerance. Similarly, macrophages, which underpin many of the physiological responses to endotoxins, exhibit LPS tolerance on repeated stimulation4. Consequently, through limiting the production of proinflammatory molecules, tolerance is thought to provide a mechanism for restraining systemic inflammation and avoiding septic shock4.
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4.
Nature 447, 917-918 (21 June 2007) | doi:10.1038/447917a; Published online 20 June 2007
Materials Science: Reflections on Ionic Liquids
Robin D. Rogers
Ionic liquids are generally regarded as solvents, but these modular, tunable compounds have far greater technological potential. With a coat of silver, they become ideal materials for the liquid mirror of a space telescope.
Ionic liquids seem to defy common sense. Most ionic compounds are crystalline solids with high melting points, but these fascinating salts melt at temperatures below 100 °C; indeed, many are liquids at room temperature. Their melt forms are composed of discrete cations and anions1 that can be individually customized, allowing the synthesis of a wide range of liquid materials with tunable physical, chemical and biological properties.
There are thought to be about a million possible pure ionic liquids, and 1018 ternary liquid mixtures, so anyone designing the perfect liquid material for a given application has a lot of room for manoeuvre. A particularly striking example is described by Borra et al.2 on page 979 of this issue. They have coated an ionic liquid with colloidal silver particles, yielding a material that could be used as a liquid mirror in a telescope.
Ionic liquids are not new3, but they have recently received intense worldwide scrutiny as possible environmentally friendly solvents4 because many are non-volatile. This has fuelled a technological revolution, powered by the sheer number of unstudied liquids that might be fine-tuned for specific purposes (although the 'green' credentials of ionic liquids have been questioned by reports that some of these compounds are toxic5). It was, therefore, inevitable that new applications would emerge from the growing number of scientific and technological disciplines studying these liquids.
Ionic liquids are known for their distinct physical properties (such as low or non-volatility, thermal stability and large ranges of temperatures over which they are liquids6), chemical properties (such as resistance to degradation, antistatic behaviour, chirality and high energy density) and biological activities (such as antimicrobial and analgesic properties7). But what is less appreciated is that these properties in individual ionic liquids can be combined in composite materials to afford multifunctional designer liquids. It is therefore refreshing to see a study2 that focuses on the unique attributes and uses of ionic liquids, rather than on whether they are green or toxic.
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5.
Nature 447, 918-920 (21 June 2007) | doi:10.1038/447918a; Published online 20 June 2007
Evolutionary Biology: Re-Crowning Mammals
Richard L. Cifelli & Cynthia L. Gordon
The evolutionary history of mammals is being tackled both through molecular analyses and through morphological studies of fossils. The 'molecules versus morphology' debate remains both vexing and vibrant.
On page 1003 of this issue, Wible and co-authors1 announce the discovery of a well-preserved mammal from Mongolia dated at between 71 million and 75 million years old. The fossil, dubbed Maelestes gobiensis, is noteworthy in its own right: finds of this sort are exceptional in view of the generally poor record of early mammals.
More interesting, though, is what this fossil and others from the latter part of the age of dinosaurs (the Cretaceous period, about 145 million to 65 million years ago) have to say about the rise of mammalian varieties that populate Earth today. The authors have gone much further than describing an ancient fossil specimen, and present a genealogical tree depicting relationships among the main groups of living and extinct mammals. Here, all Cretaceous fossil mammals are placed near the base of the tree, as dead 'side branches', well below the major tree 'limbs' leading to living mammals. These results differ strikingly from those of other recent palaeontological studies2, 3.
Chronologically speaking, this new analysis1 is eye-popping because it places direct ancestry of today's mammals near the Cretaceous–Tertiary (K/T) boundary about 65 million years ago. This is much younger than dates based on molecular biology — for example, a recent and comprehensive analysis by Bininda-Emonds et al.4 pushed that ancestry back more than twice as far into the geological past, to some 148 million years ago. The conflicting results of these palaeontological1 and molecular4 studies have profound implications for understanding the evolutionary history of mammals, and for understanding the pace and nature of evolution generally.
Three main groups of living mammal are recognized: the egg-laying monotremes such as the platypus; marsupials (kangaroos, koalas, opossums and so on); and placentals, which constitute the most varied and diverse group, including everything from bats to whales and accounting for more than 5,000 of the 5,400 or so living mammals. Fossils can be placed within one of these three 'crown' groups only if anatomical features show them to be nested among living species5.
The placental crown group, which is of primary interest here, represents the living members of a more encompassing group, Eutheria, which includes extinct allied species, the oldest of which dates to about 125 million years ago6. Herein lies a central problem: because of inadequate preservation and/or non-comparability with living species, the affinities of many early mammals have been contentious. Certain Cretaceous fossils have been previously recognized as members of the placental crown group; some analyses suggest the presence of placental superorders in the Cretaceous2, 3, but referral of such ancient fossils to living orders is dubious5. For context, placentals encompass four major divisions, or superorders, each containing one to six orders, such as Cetacea (whales), Primates and Rodentia.
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6.
Nature 447, 913 (21 June 2007) | doi:10.1038/447913a; Published online 20 June 2007
Eukaryote Evolution: Engulfed by Speculation
Anthony Poole & David Penny
The notion that eukaryotes evolved via a merger of cells from the other two domains — archaea and bacteria — overlooks known processes.
In the absence of direct evidence, science should proceed cautiously with conjecture. Geologist Charles Lyell (1797–1875) warned us not to proceed like medieval scholars, who "often preferred absurd and extravagant positions, because greater skill was required to maintain them". Scientific speculation, Lyell emphasized, must take known processes into account. This has not happened with the debate on how eukaryotes (animals, plants, fungi, protists) arose. The conflicting hypotheses currently on offer show a curious disregard for mechanism.
One thing at least is agreed: the mitochondrion, powerhouse of the eukaryote cell, evolved from an engulfed bacterium. The question is 'who' did the engulfing. Did an archaeon engulf a bacterium? Did a bacterium, bacterial consortium, or RNA cell engulf first an archaeon (which became the nucleus) and then the mitochondrial ancestor? Perhaps nuclei emerged in a virus-infected archaeon, which then engulfed mitochondria. Which, if any of these, is right?
In the mid-1990s, a somewhat pedestrian view of eukaryotic origins, the 'archezoa hypothesis', held sway. This maintained that a protoeukaryote (with nucleus) engulfed the mitochondrial ancestor. Supporting the theory were 'archezoa', anaerobic eukaryotes with no mitochondria. Archezoa apparently populated the oldest branches of the eukaryote tree, suggesting that eukaryotes began diversifying before mitochondria entered the picture.
The archezoa hypothesis is thus composed of two independent hypotheses: (a) that a protoeukaryote host (PEH) engulfed the mitochondrial ancestor, and (b) that modern archezoa are 'missing links' that never possessed mitochondria. Hypothesis (b) is now unanimously rejected: every archezoan examined bears vestigial mitochondria, or genes inherited from mitochondria. Thus, all modern eukaryotes evolved from a mitochondrion-bearing ancestor.
But the baby was thrown out with the bath-water. Hypothesis (a) was also rejected, and because eukaryotes and archaea share a number of similar genes, the deposed PEH was replaced with archaea. Consequently, incorporation of the mitochondrion — not the origin of the nucleus — was hailed as the defining event in eukaryotic origins. This opened the floodgates of speculation, and numerous new hypotheses emerged. None is supported by observation: no archaea reside within bacteria, no bacteria reside within archaea, viruses have preposterously few similarities to the nucleus, and no RNA cells exist.
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