Why does allometry evolve so slowly?

Morphological allometry is striking due to its evolutionary conservatism, making it an example of a certain sort of evolutionary stasis. Organisms that vary in size, whether for developmental, environmental, or evolutionary reasons, adopt shapes that are predictable from that size alone. There are two major hypotheses to explain this. It may be that natural selection strongly favors each allometric pattern, or that organisms lack the development and genetic capacity to produce variant shapes for selection to act on. Using a high-throughput system for measuring the size and shape of Drosophila wings, we documented an allometric pattern that has been virtually unchanged for 40 million years. We performed an artificial selection experiment on the static allometric slope within one species. In just 26 generations, we were able to increase the slope from 1.1 to 1.4, and decrease it to 0.8. Once artificial selection was suspended, the slope rapidly evolved back to a value near the initial static slope. This result decisively rules out the hypothesis that allometry is preserved due to a lack of genetic variation, and provides evidence that natural selection acts to maintain allometric relationships. On the other hand, it seems implausible that selection on allometry in the wing alone could be sufficiently strong to maintain static allometries over millions of years. This suggests that a potential explanation for stasis is selection on a potentially large number of pleiotropic effects. This seems likely in the case of allometry, as the sizes of all parts of the body may be altered when the allometric slope of one body part is changed. Unfortunately, hypotheses about pleiotropy have been very difficult to test. We lay out an approach to begin the systematic study of pleiotropic effects using genetic manipulations and high-throughput phenotyping.

Changes in Gene Expression and Metabolism in the Testes of the Rat following Spinal Cord Injury.

Spinal cord injury (SCI) results in devastating changes to almost all aspects of a patient's life. In addition to a permanent loss of sensory and motor function, males also will frequently exhibit a profound loss of fertility through poorly understood mechanisms. We demonstrate that SCI causes measureable pathology in the testis both acutely (24 h) and chronically up to 1.5 years post-injury, leading to loss in sperm motility and viability. SCI has been shown in humans and rats to induce leukocytospermia, with the presence of inflammatory cytokines, anti-sperm antibodies, and reactive oxygen species found within the ejaculate. Using messenger RNA and metabolomic assessments, we describe molecular and cellular changes that occur within the testis of adult rats over an acute to chronic time period. From 24 h, 72 h, 28 days, and 90 days post-SCI, the testis reveal a distinct time course of pathological events. The testis show an acute drop in normal sexual organ processes, including testosterone production, and establishment of a pro-inflammatory environment. This is followed by a subacute initiation of an innate immune response and loss of cell cycle regulation, possibly due to apoptosis within the seminiferous tubules. At 1.5 years post-SCI, there is a chronic low level immune response as evidenced by an elevation in T cells. These data suggest that SCI elicits a wide range of pathological processes within the testes, the actions of which are not restricted to the acute phase of injury but rather extend chronically, potentially through the lifetime of the subject. The multiplicity of these pathological events suggest a single therapeutic intervention is unlikely to be successful.