Franklin and Mesmer: an encounter.

In 1784, as the Enlightenment was on the wane, Paris faced a debate in which reason confronted the supernatural and the mysterious. Dr. Mesmer, a graduate of the medical school in Vienna, had been running a "magnetic clinic" based on the belief that magnetic fluid, flowing from the stars, permeated all living beings and that every disease was due to an obstruction in the flow. By manipulating that fluid, he launched the concept of animal as opposed to mineral magnetism and claimed to cure all ills. This got him into trouble with the medical faculty, and in 1778 he emigrated to Paris, creating secret societies all over France. Six years later, mesmerism was considered a threat, possibly deleterious to both mind and body. Louis XVI appointed two commissions to investigate this likely fraud. Dr. Guillotin headed one; the other, made up of five members of the Academy of Sciences, included an astronomer and was headed by Franklin, American Ambassador to France. Both commissions concluded that the success of mesmerism was due to the manipulation of the imagination. Mesmer protested vigorously but in vain. He left France and died in obscurity in 1815.     

Paramutation: from maize to mice

Paramutation is the epigenetic transfer of information from one allele of a gene to another to establish a state of gene expression that is heritable for generations. RNA has recently emerged as a prominent mediator of this remarkable phenomenon in both maize and mice.     

Unfinished business: an essay on finally leaving the bench

Spontaneous and induced chromosome aberrations have been studied over more than a century. The resolution of detection of aberrations has depended on the improvement of available techniques. An overview on the major high lights in this area of research, from the time of solid staining to fluorescence in situ hybridization technique is presented in this review.     

How FMN binds to anabaena apoflavodoxin: a hydrophobic encounter at an open binding site

Molecular recognition begins when two molecules approach and establish interactions of certain strength. The mechanisms of molecular recognition reactions between biological molecules are not well known, and few systems have been analyzed in detail. We investigate here the reaction between an apoprotein and its physiological cofactor (apoflavodoxin and flavin mononucleotide) that binds reversibly to form a non-covalent complex (flavodoxin) involved in electron transfer reactions. We have analyzed the fast binding reactions between the FMN cofactor (and shorter analogs) and wild type (and nine mutant apoflavodoxins where residues interacting with FMN in the final complex have been replaced). The x-ray structures of two such mutants are reported that show the mutations are well tolerated by the protein. From the calculated microscopic binding rate constants we have performed a Phi analysis of the transition state of complex formation that indicates that the binding starts by interaction of the isoalloxazine-fused rings in FMN with residues of its hydrophobic binding site. In contrast, the phosphate in FMN, known to contribute most to the affinity of the final holoflavodoxin complex, is not bound in the transition state complex. Both the effects of ionic strength and of phosphate concentration on the wild type complex rate constant agree with this scenario. As suggested previously by nmr data, it seems that the isoalloxazine-binding site may be substantially open in solution. Interestingly, although FMN is a charged molecule, electrostatic interactions seem not to play a role in directing the binding, unlike what has been reported for other biological complexes. The binding can thus be best described as a hydrophobic encounter at an open binding site.     

Patch leaving strategies and superparasitism: an asymmetric generalized war of attrition

When several competitors deplete a patch, it can be advantageous for each of them to stay provided that others leave, whereas, on the other hand, staying longer decreases the expected payoff for everyone. This situation can be considered as a generalized war of attrition. Previous studies have shown that optimal patch leaving strategies become stochastic and the expected leaving time is much larger than predicted by the marginal value theorem when competitors interfere. The possibility of superparasitism, as occurs for example in parasitoids, induces such interference. In addition, it gives several complications. First, the payoff of females that have left the patch is affected by the ovipositions of the remaining individuals. Second, differences in the arrival time of females cause payoff-relevant asymmetries, since females that arrived early on have parasitized more hosts in a patch at the moment superparasitism starts than those that arrived later. We show that this can be modelled as an asymmetric generalized war of attrition, and derive global characteristics of the ESS for simultaneous decisions on when to start superparasitism and when to leave a patch.     

Endocytosis and signaling cascades: a close encounter.

Internalization of receptors and other cell surface components is well known to occur via clathrin-mediated endocytosis, although other less well characterized pathways are also involved. Internalized receptors are then delivered to early endosomes, where they are sorted to be recycled back to the plasma membrane for reutilization or transported to late endosomes/lysosomes for degradation. Endocytosis has long been considered as a constitutive, housekeeping function of animal cells that occurs independently of the cellular environment in contrast to regulated secretion. Here, we will discuss recent studies that are uncovering the existence of cross-talk between signaling molecules and components of the transport machinery, indicating that endocytosis can be modulated by signaling pathways.     

Use of an encounter model to predict size-selective predation by a stream-dwelling cyprinid

1. The increased probability of detection of larger prey in the drift appeared to be the major determinant of prey consumption by red roach (Rutilus arcasi) in an Iberian stream. We developed a model of prey encounter incorporating this factor that explained 68% of the overall variation in the consumption of prey of different size. When the same model was applied to benthic size distributions the variance explained was 16%. 2. Gape-limited ingestion also was a significant factor influencing prey consumption and, when added to the model, the variance explained increased to 85% (32% for the benthos), but its importance was strongly dependent on both: (i) the maximum prey size available and (ii) fish size. 3. The exact shape of red roach reactive fields and, as a consequence, their degree of size-selectivity appeared to vary seasonally and ontogenetically. In summer, younger fish exhibited apparently reduced reactive fields. We hypothesize that this can be the result of factors such as microhabitat shifts or a reduced range of prey sizes.     

Liver injury after an aggressive encounter in male mice

Acute and intense psychological stressors induce cell damage in several organs, including the heart and the liver. Much less is known about social stress. In male mice, aggressive behavior is the most common social stressor. It is remarkable that upon fighting, submandibular salivary glands release a number of peptides into the bloodstream including epidermal growth factor (EGF). We showed previously that released EGF protects the heart from cell damage in this particular stressful situation. Here, we studied the effect of an aggressive encounter on the liver and whether EGF has a similar effect on this organ. An aggressive encounter in male mice caused inflammatory response and a transient increase in plasma alanine and aspartate transaminase activities. At 3 h, focal infiltration of neutrophils was observed in liver parenchyma. These cells accumulate on eosinophilic hepatocytes, which may correspond to dying cells. A few hours later, evidence of necrotic lesion was observed. Surgical excision of submandibular glands, sialoadenectomy, did not prevent the rise in plasma EGF concentration and did not affect the increase in plasma transaminase activities. Neither did the administration of tyrphostin AG-1478 (inhibitor of EGF receptor kinase) alter the increase in plasma alanine transaminase activity. However, it did enhance the rise in both aspartate transaminase and creatine kinase activity, suggesting heart damage. We conclude that an aggressive encounter causes mild liver damage and that released EGF does not protect this organ, in contrast to its effect on the heart.