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Scent of a woman. Like the blind retired Marine colonel played by Al Pacino in Scent of a Woman, mammals respond to odor cues in a variety of social situations. CAS Biology Professor Michael Baum and colleagues at the University of Cambridge and at the Babraham Institute in Cambridge, UK, have found what they believe to be a "hard-wired" genetic mechanism that leads mice to avoid the urinary odor of their parent-of-origin, an adaptive characteristic that minimizes inbreeding.

"Mammals use odor to recognize kin, select mates, and avoid inbreeding, thereby helping to maximize the diversity of the gene pool," says Baum. Because the mice avoid areas where maternal odors are prevalent, as they mature they are also driven to move away from the area where they were born. This helps to control population density and leaves resources -- food and habitats -- available for parents to nurture succeeding generations.

To eliminate the possibility that the mice were exhibiting a learned response, Baum and his colleagues conducted their research on a cohort group of mice transferred as embryos from their genetic mothers to genetically unrelated surrogates. They found that both adult males and adult females preferred the urine odor of females from an unrelated strain of mice to the odor of their genetic mother's urine.

The researchers attribute this behavior to the expression of imprinted genes, which comprise only a small percentage of the mouse genome. Only the copy of an imprinted gene inherited from an individual's mother or from its father is expressed, whereas for most genes there is no parent-of-origin effect on its expression. Baum and his coworkers suggest that the expression of imprinted genes somehow affects the development of the olfactory nervous system of the mice, causing them to avoid areas where the scent of their mother is prevalent.

This research was reported in the February 15 issue of the journal Nature.


The "stronger" sex weaker? ex weaker? Do strong muscles actually leave men more vulnerable? Benjamin Campbell, a CAS assistant professor of anthropology, is one of a group of scientists interested in the relationship between testosterone, the hormone that defines maleness, and immune function in males.

"The differences in immune response between males and females suggest that testosterone is a significant cause of male susceptibility to disease," write Campbell and his coauthors in a chapter in the forthcoming book Reproductive Ecology and Human Evolution. And, they posit, this greater susceptibility may be related to trade-offs between the immune system and the muscle system.

Testosterone, the authors argue, focuses the energy resources of the male body toward the development of skeletal muscle mass, increased bone density, higher concentration of red blood cells, and a higher metabolic rate. These things enhance certain aspects of male survival and reproduction at the expense of the immune response.

To better understand this relationship, Campbell and his colleagues studied the Turkana, a group of pastoral nomads in northeast Kenya. The Turkana have minimal energy resources. They tend to be chronically undernourished and depend largely on their animals -- goats, sheep, cattle, and camels -- for subsistence. They are also subject to intestinal parasites such as tapeworms, and diseases such as tuberculosis, malaria, diarrhea, and acute respiratory infection. The researchers collected data on the nutritional status, testosterone levels, and health complaints of the men in the community. Although the analysis of the results was not conclusive, the authors found that Turkana males with elevated testosterone levels were more likely to complain of respiratory-related chest pain and may be at greater risk for cumulative damage to their lungs. If this is so, they write, "the costs of testosterone-mediated immunosuppression may be evident in its long-term effects on health and mortality."

"Research Briefs" is written by Joan Schwartz in the Office of the Provost. To read more about BU research, visit http://www.bu.edu/research.

       

15 May 2003
Boston University
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