A survey of all the papers relating to life span in Drosophila melanogaster published in Experimental Gerontology from its origin in 1964 to 1981 shows that, contrary to a common belief, the mean life span of females exceeds that of males in only approximately 50% of the cases. It is shown that mean life span, as it is measured in most experiments, is a poor estimate of the potential life span of a Drosophila strain. However, the analysis of four extensive studies of Drosophila melanogaster life span strongly suggests that the potential (or maximal) life span is consistently higher for females than it is for males. That analysis also shows that, vis-à-vis the controlled or uncontrolled variations of the environment, the males have a broader norm of reaction or, in other words, a smaller homeostasis than the females. A model, mainly based on these two results, allows us to explain how the mean life span of males is so often higher than that of females.

No abstract

SummaryA large increase in the total phenotypic variance of thorax size was observed in a cage population of Drosophila melanogaster, maintained at 28 °C, a few months after it had been the victim of a naturally occuring population crash, the number of individuals in the population having, at a given moment, been reduced to half a dozen. In order to ascertain whether that increase in total phenotypic variance was due to an increase in environmental or in genetic variance that population was submitted, together with five other normally developing cage populations, to a selection programme for high and low bristle number. The additive genetic variance of these various populations was thereafter estimated. The additive genetic variance of the 28 °C cage population, victim of a population crash, was found to be highly significantly larger than all the other ones. The consequences of that unexpected observation on the theories of evolution are discussed. It is argued that that result confirms some of the predictions of the genetic revolution (genetic transilience) hypothesis of speciation.

Adequately localizing pain is crucial to protect the body against physical damage and react to the stimulus in external space having caused such damage. Accordingly, it is hypothesized that nociceptive inputs are remapped from a somatotopic reference frame, representing the skin surface, towards a spatiotopic frame, representing the body parts in external space. This ability is thought to be developed and shaped by early visual experience. To test this hypothesis, normally sighted and early blind participants performed temporal order judgment tasks during which they judged which of two nociceptive stimuli applied on each hand's dorsum was perceived as first delivered. Crucially, tasks were performed with the hands either in an uncrossed posture or crossed over body midline. While early blinds were not affected by the posture, performances of the normally sighted participants decreased in the crossed condition relative to the uncrossed condition. This indicates that nociceptive stimuli were automatically remapped into a spatiotopic representation that interfered with somatotopy in normally sighted individuals, whereas early blinds seemed to mostly rely on a somatotopic representation to localize nociceptive inputs. Accordingly, the plasticity of the nociceptive system would not purely depend on bodily experiences but also on crossmodal interactions between nociception and vision during early sensory experience.

No abstract