Kinetochores: if you build it, they will come

Successful mitosis depends critically on the segregation of chromosomes by kinetochore microtubules. A recent paper describes a conserved protein network from Caenorhabditis elegans that is composed of three classes of molecules, each of which contributes uniquely to the building of the kinetochore-microtubule attachment site.     

The evolution of obligate mutualism: if you can't beat 'em, join 'em

Wolbachia is best known as a facultative endosymbiotic parasite, manipulating host reproduction. However, it has also evolved as an obligate mutualist at least twice. In a recent paper, Pannebakker et al. identify a possible mechanism for such a transition from facultative parasitism to obligate mutualism in a parasitic wasp in which Wolbachia are required for producing eggs (oogenesis). Their proposed mechanism suggests that compensatory evolution in the host to counter the harmful effects of Wolbachia is the basis of this evolutionary transition.     

It's all who you know: the evolution of socially cued anticipatory plasticity as a mating strategy

Selection has led to the evolution of a variety of different mating strategies, each adapted to different competitive challenges. But what happens if the competitive challenges depend on the social environment? Here we discuss and review examples of socially cued anticipatory plasticity: irreversible developmental tactics in which resource allocation during the juvenile stage is altered to develop an appropriate phenotype for the competitive or mate choice environment that an individual encounters when mature. There are numerous theoretical and empirical examinations of the role of the social environment on the strength and direction of selection. However, only a handful of empirical studies examine how the social environment affects juvenile allocation and whether such tactics are adaptive. The goal of this review is to synthesize current knowledge about socially cued anticipatory plasticity, including the sensory modalities that individuals use to predict the adult competitive and mating environment. We then outline the various factors that are necessary for the evolution of socially cued anticipatory plasticity and discuss how this can affect phenotypic evolution. We conclude by suggesting some directions that future studies should take in order to understand how social variation can alter selection and the evolution of development.     

Brains, islands and evolution: breaking all the rules

The announcement in 2004 that a small-brained hominin, Homo floresiensis, had been discovered on the island of Flores, Indonesia, was hailed as a major scientific breakthrough because it challenged preconceptions about the evolution of our closest relatives. Now, just over two years later, questions raised by the interpretation of the fossil abound. In a series of recent papers, critics have questioned the interpretation of the small brain volume of the fossil as that of a new hominin species, suggesting instead that it was due to microcephaly. The arguments raised by critics and advocates alike prompt a re-examination of ideas about what is possible during the evolution of the brain.     

Striatal D2 receptors and LTD: yes, but not where you thought they were

D1 and D2 dopamine receptors are expressed in disjoint subsets of striatal projection neurons, the direct and indirect pathways, respectively. This differential distribution of receptors forms the basis for explanations of many aspects of basal ganglia function and dysfunction, but it seems incompatible with some other important properties of striatal neurons. In this issue of Neuron, Wang et al. discover the mechanism of D2 sensitivity of long term depression at synapses on the striatal projection neuron. They show that D2 dependence of LTD does not depend on dopamine receptors of on the projection cell but is mediated by dopamine-induced changes in release of acetylcholine by interneurons that contact projection cells of both types.     

Gates,GAVI, the glorious global funds and more: all you ever wanted to know

Global immunization programmes have achieved some remarkable successes. In 1977, Frank Fenner's Commission declared smallpox to have been eradicated by an 11-year-long intensive campaign. The Expanded Programme on Immunization encompassed six important childhood vaccines and reached over three-quarters of the world's children. Polio eradication has gone remarkably well, with only 10 out of 200 countries reporting residual cases. But amidst all the good news, there is also bad news. Coverage is variable; infrastructure is crumbling; and newer vaccines are not being incorporated in many country programmes. The Bill and Melinda Gates Foundation has introduced a new dynamic here. From their initial gift of $100 million in December 1998, their commitment to date is US$1.5 billion - and rising. At the centre is a Global Children's Vaccine Fund which permitted the launch, in January 2000, of the Global Alliance for Vaccines and Immunization. This is targeted to the 74 poorest countries of the world and is designed to improve vaccination infrastructure, to purchase newer vaccines and to support research and development. Even before we know how successful this programme will be, it has had its imitators. The Global Fund to Fight AIDS, TB and Malaria borrowed many concepts from GAVI. The Global Alliance for Improved Nutrition announced in May 2002 does so as well, and is heavily supported by Gates. Highly effective parasite control programmes antedate all this but will be much strengthened. However, we still face a sizeable budgetary gap both for research and for bringing the best advances to all people who need them.     

A navigational guide to variable fitness: common methods of analysis,where they break down,and what you can do instead

Our methods for analyzing stochastic fitness are mostly approximations, and the assumptions behind these approximations are not always well understood. Furthermore, many of these approximations break down when fitness variance is high. This review covers geometric mean growth, diffusion approximations, and Markov processes. It discusses where each is appropriate, the conditions under which they break down, and their advantages and disadvantages, with special attention to the case of high fitness variance. A model of sessile and site-attached coastal species is used as a running example, and fully worked calculations and code are provided. Summary: The logarithm of geometric mean growth is usually only appropriate when (a) an invader growth rate is needed and (b) fitness variability is driven by environmental fluctuations. The usual approximation breaks down when fitness variance is high. Diffusion approximations can provide a reasonable guide to the expected change in frequency over a time step if expected fitnesses and fitness variances are appropriately scaled by the average expected fitness. Diffusion approximations can perform less well for fixation probabilities, especially since further approximations may be required. Fixation probabilities can be calculated exactly using a Markov process, regardless of how large fitness variance is, although an analytic expression is frequently not possible. If an analytic expression is desired, it may be worth using a diffusion approximation and checking it with a Markov process calculation.     

Polymorphism in heterogeneous environments,evolution of habitat selection and sympatric speciation: Soft and hard selection models

Summary The adaptation to a variable environment has been studied within soft and hard selection frameworks. It is shown that an epistatically determined habitat preference, following a Markovian process, always leads to the maintenance of an adaptive polymorphism, in a soft selection context. Although local mating does not alter the conditions for polymorphism maintenance, it is shown that, in that case, habitat selection also leads to the evolution of isolated reproductive units within each available habitat. Habitat selection, however, cannot evolve in the total absence of adaptive polymorphism. This represents a theoretical problem for all models assuming habitat selection to be an initially fixed trait, and means that within a soft selection framework, all the available habitats will be exploited, even the less favourable ones.On the other hand, polymorphism cannot be maintained when selection is hard, even when all individuals select their habitat. Here, the evolution of habitat selection does not need any prerequisite polymorphism, and always leads to the exploitation of only one habitat by the most specialized genotype. It appears then that hard selection can account for the existence of empty habitat and for an easier evolution of habitat specialization.     

Teaching evolution (and all of biology) more effectively: Strategies for engagement, critical reasoning, and confronting misconceptions

The strength of the evidence supporting evolution has increased markedly since the discovery of DNA but, paradoxically, public resistance to accepting evolution seems to have become stronger. A key dilemma is that science faculty have often continued to teach evolution ineffectively, even as the evidence that traditional ways of teaching are inferior has become stronger and stronger. Three pedagogical strategies that together can make a large difference in students' understanding and acceptance of evolution are extensive use of interactive engagement, a focus on critical thinking in science (especially on comparisons and explicit criteria) and using both of these in helping the students actively compare their initial conceptions (and publicly popular misconceptions) with more fully scientific conceptions. The conclusion that students' misconceptions must be dealt with systematically can be difficult for faculty who are teaching evolution since much of the students' resistance is framed in religious terms and one might be reluctant to address religious ideas in class. Applications to teaching evolution are illustrated with examples that address criteria and critical thinking, standard geology versus flood geology, evolutionary developmental biology versus organs of extreme perfection, and the importance of using humans as a central example. It is also helpful to bridge the false dichotomy, seen by many students, between atheistic evolution versus religious creationism. These applications are developed in detail and are intended to be sufficient to allow others to use these approaches in their teaching. Students and other faculty were quite supportive of these approaches as implemented in my classes.     

Isolation of null alleles of the Caenorhabditis elegans gly-12, gly-13 and gly-14 genes,all of which encode UDP-GlcNAc: alpha-3-D-mannoside beta1,2-N-acetylglucosaminyltransferase I activity

UDP-GlcNAc: alpha-3-D-mannoside beta1,2-N-acetylglucosaminyltransferase I (GnT I) is a Golgi-resident enzyme which transfers a GlcNAc residue in beta1,2 linkage to the Manalpha1,3Manbeta-terminus of (Manalpha1,6(Manalpha1,3)Manalpha1,6)(Manalpha1,3)Manbeta1,4GlcNAcbeta1,4GlcNAc-Asn-protein, thereby initiating the synthesis of hybrid N-glycans. Three Caenorhabditis elegans genes homologous to mammalian GnT I (designated gly-12, gly-13 and gly-14) have been cloned. All three cDNAs encode proteins with GnT I enzyme activity. We report in this paper the preparation by ultra-violet (UV) light irradiation in the presence of trimethylpsoralen, of mutants lacking either gly-12, gly-13 or gly-14. A double null mutation in the gly-12 and gly-14 genes (gly-14; gly-12) has also been prepared. These mutations are intragene deletions, removing large portions of the GnT I catalytic domain, and are therefore, all molecular nulls. The gly-12 and gly-14 mutants as well as the gly-14; gly-12 double mutant all displayed wild-type phenotypes, indicating that neither gly-12 nor gly-14 is necessary for worm development under standard laboratory conditions. In contrast, about 60% of the mutants lacking the gly-13 gene arrested as L1 larvae at 20 degrees C and the remaining 40% homozygous worms grew to adulthood but displayed severe morphological and behavioral defects despite the presence of the other two GnT I genes, gly-12 and gly-14. Attempts to rescue the gly-13 null phenotype with the wild type transgene were not successful. However, lethality co-segregated with the gly-13 deletion within 0.02 map units (mu) in genetic mapping experiments, suggesting that the gly-13 mutation is responsible for the phenotype.