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The best of all worlds or the best possible world? Developmental constraint in the evolution of beta-tubulin and the sperm tail axoneme.

Through evolutionary history, some features of the phenotype show little variation. Stabilizing selection could produce this result, but the possibility also exists that a feature is conserved because it is developmentally constrained--only one or a few developmental mechanisms can produce that feature. We present experimental data documenting developmental constraint in the assembly of the motile sperm tail axoneme. The 9+2 microtubule architecture of the eukaryotic axoneme has been deeply conserved. We argue that the quality of motility supported by axonemes with this morphology explains their long conservation, rather than a developmental necessity for the 9+2 architecture. However, our functional tests in Drosophila spermatogenesis reveal considerable constraint in the coevolution of testis-specific beta-tubulin and the sperm tail axoneme. The evolution of testis beta-tubulins used in insect sperm tail axonemes is highly punctuated, indicating some pressure acting on their evolution. We provide a mechanistic explanation for their punctuated evolution by testing structure-function relationships between testis beta-tubulin and the motile axoneme in D. melanogaster. We discovered that a highly conserved sequence feature of beta-tubulins used in motile axonemes is needed to specify central pair formation. Second, our data suggest that cooperativity in the function of internal beta-tubulin amino acids is needed to support the long axonemes characteristic of Drosophila sperm tails. Thus, central pair formation constrains the evolution of the axoneme motif, and intramolecular cooperativity makes the evolution of the internal residues path dependent, which slows their evolution. Our results explain why a highly specialized beta-tubulin is needed to construct the Drosophila sperm tail axoneme. We conclude that these constraints have fixed testis-specific beta-tubulin identity in Drosophila.

Animals↗
PubMed2005

From the Old World to the New World: an ecologic study of population susceptibility to HIV infection.

It remains unclear why the global distribution of human immunodeficiency virus (HIV), between and within continents, is so heterogeneous. This ecologic study of 34 populations of the Americas explored the hypothesis that populations differ in their intrinsic, biological susceptibility to HIV which, together with exposure, might determine the ultimate 'mature' prevalence. If true, national HIV prevalence in populations of the Americas should be predictable from each country's ethnic mosaic, inter-racial admixture and HIV prevalence in regions of Africa, Europe and Asia from where their ancestors migrated. For each country, the adult population (15-49 years) was multiplied by the proportion corresponding to each ethnic group by HIV prevalence in the country/region of origin of each group, yielding the predicted prevalences, which were then compared with observed prevalences documented by UNAIDS for 2001. Predicted and observed HIV prevalences were highly correlated (r = 0.70, P < 0.001). In North America, predicted prevalences were within 0.5% of the observed values, except for African-Americans and African-Canadians. In Central and South America, differences between predicted and observed prevalences were <1.0% except in Honduras and Guyana. Some Caribbean countries had a predicted prevalence identical to the observed one, but there were outliers. Overall, predicted prevalence was 0.93% and observed prevalence 0.64%; two-thirds of this difference was attributed to Brazil. Although it was not possible to adjust to the confounding effects of sexual behaviour and cofactors of transmission (such as sexually transmitted infections) because of the lack of nationally representative data for each and every country, a number of arguments reviewed in the paper suggest that confounders cannot explain all this association and that differential susceptibility might be an important determinant of steady-state HIV prevalence.

Adolescent↗
PubMed2005

Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture: presented at the third World Congress of World Institute of Pain, Barcelona 2004.

The neuromatrix theory of pain proposes that pain is a multidimensional experience produced by characteristic "neurosignature" patterns of nerve impulses generated by a widely distributed neural network-the "body-self neuromatrix"-in the brain. These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them. Acute pains evoked by brief noxious inputs have been meticulously investigated by neuroscientists, and their sensory transmission mechanisms are generally well understood. In contrast, chronic pain syndromes, which are often characterized by severe pain associated with little or no discernable injury or pathology, remain a mystery. Furthermore, chronic psychological or physical stress is often associated with chronic pain, but the relationship is poorly understood. The neuromatrix theory of pain provides a new conceptual framework to examine these problems. It proposes that the output patterns of the body-self neuromatrix activate perceptual, homeostatic, and behavioral programs after injury, pathology, or chronic stress. Pain, then, is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation, or other pathology. The neuromatrix, which is genetically determined and modified by sensory experience, is the primary mechanism that generates the neural pattern that produces pain. Its output pattern is determined by multiple influences, of which the somatic sensory input is only a part, that converge on the neuromatrix.

Journal Article↗
PubMed2005

Pain: disease or dis-ease? The John Bonica Lecture: presented at the third World Congress of World Institute of Pain, Barcelona 2004.

Chronic pain has only recently been recognized as an important health care issue. There is no widely shared agreement as to the best ways to diagnose and treat chronic pain patients. Pain management is a chaotic component of contemporary medicine. I argue that we need to think of chronic pain as a disease in its own right and develop our specialty of pain management on the basis of evidence for treatment outcomes. The current chaotic state confuses patients, health care providers, and payers. It is possible that pain management may disappear from health care if we do not improve our understanding of chronic pain and how to best treat those who suffer.

Journal Article↗