Migratory neural crest-like cells form body pigmentation in a urochordate embryo

The neural crest, a source of many different cell types in vertebrate embryos, has not been identified in other chordates. Current opinion therefore holds that neural crest cells were a vertebrate innovation. Here we describe a migratory cell population resembling neural crest cells in the ascidian urochordate Ecteinascidia turbinata. Labelling of embryos and larvae with the vital lipophilic dye DiI enabled us to detect cells that emerge from the neural tube, migrate into the body wall and siphon primordia, and subsequently differentiate as pigment cells. These cells express HNK-1 antigen and Zic gene markers of vertebrate neural crest cells. The results suggest that migratory cells with some of the features of neural crest cells are present in the urochordates. Thus, we propose a hypothesis for neural crest evolution beginning with the release of migratory cells from the CNS to produce body pigmentation in the common ancestor of the urochordates and vertebrates. These cells may have gained additional functions or were joined by other cell types to generate the variety of derivatives typical of the vertebrate neural crest.     

Evolutionary genetics: CCR5 mutation and plague protection

A recent and prevalent mutation in the chemokine receptor CCR5 in humans of northern European ancestry has been proposed to provide protection against bubonic plague. Here we infect both normal and CCR5-deficient mice with the bacterium Yersinia pestis, the cause of the plague epidemics that wiped out one-third of Europeans in the Middle Ages, and find no difference in either bacterial growth or survival time between the two groups. Unless the pathogenesis of Yersinia infection differs markedly between mice and humans, our results indicate that CCR5 deficiency in people is unlikely to protect against plague.     

Stage-structured cycles promote genetic diversity in a predator-prey system of Daphnia and algae

Competition theory predicts that population fluctuations can promote genetic diversity when combined with density-dependent selection. However, this stabilizing mechanism has rarely been tested, and was recently rejected as an explanation for maintaining diversity in natural populations of the freshwater herbivore Daphnia pulex. The primary limitation of competition theory is its failure to account for the alternative types of population cycles that are caused by size- or stage-dependent population vital rates--even though such structure both explains the fluctuating dynamics of many species and may alter the outcome of competition. Here we provide the first experimental test of whether alternative types of cycles affect natural selection in predator-prey systems. Using competing Daphnia genotypes, we show that internally generated, stage-structured cycles substantially reduce the magnitude of selection (thereby contributing to the maintenance of genetic diversity), whereas externally forced cycles show rapid competitive exclusion. The change in selection is ecologically significant, spanning the observed range in natural populations. We argue that structured cycles reduce selection through a combination of stalled juvenile development and stage-specific mortality. This potentially general fitness-equalizing mechanism may reduce the need for strong stabilizing mechanisms to explain the maintenance of genetic diversity in natural systems.     

Cis-trans isomerization at a proline opens the pore of a neurotransmitter-gated ion channel

5-hydroxytryptamine type 3 (5-HT3) receptors are members of the Cys-loop receptor superfamily. Neurotransmitter binding in these proteins triggers the opening (gating) of an ion channel by means of an as-yet-uncharacterized conformational change. Here we show that a specific proline (Pro 8*), located at the apex of the loop between the second and third transmembrane helices (M2-M3), can link binding to gating through a cis-trans isomerization of the protein backbone. Using unnatural amino acid mutagenesis, a series of proline analogues with varying preference for the cis conformer was incorporated at the 8* position. Proline analogues that strongly favour the trans conformer produced non-functional channels. Among the functional mutants there was a strong correlation between the intrinsic cis-trans energy gap of the proline analogue and the activation of the channel, suggesting that cis-trans isomerization of this single proline provides the switch that interconverts the open and closed states of the channel. Consistent with this proposal, nuclear magnetic resonance studies on an M2-M3 loop peptide reveal two distinct, structured forms. Our results thus confirm the structure of the M2-M3 loop and the critical role of Pro 8* in the 5-HT3 receptor. In addition, they suggest that a molecular rearrangement at Pro 8* is the structural mechanism that opens the receptor pore.