To determine effects of pulp mill effluent on population genetic structure, redbreast sunfish (Lepomis auritus) were collected from several sites along the Pigeon River, NC, as well as from reference sites. Previous studies found effects on molecular, biochemical, physiological, population, and community level endpoints in these populations. The population genetic structure of these fish was determined using the randomly amplified polymorphic DNA (RAPD) technique. The level of genetic diversity was higher in the Pigeon River populations than in the reference populations. Genetic distances among populations could not be explained by drainage patterns and may have been altered by contaminant exposure. Phylogeographic analysis, maximum likelihood analysis, and assignment tests suggested that there were fewer emigrants and more immigrants in the contaminated sites than in the reference sites, suggesting that the contaminated sites may harbor "sinklike" populations. Finally, a "terminal branch amplitype" analysis (neighbor-joining and minimum-spanning trees) and maximum likelihood analysis indicated that there may be an elevated mutation rate in the polluted sites. Thus, the genetic diversity (within and among populations) in the Pigeon River populations may have been affected by altered gene flow and mutational processes as a result of pulp mill effluent discharge.

Expression of the hepatic enzyme tyrosine aminotransferase was analyzed in the perinatal period of development in the rat, when this expression undergoes significant changes associated with hepatocyte differentiation. In late prenatal liver both enzyme and functional mRNA gene products are present at levels 10- to 15-fold below those in the fully differentiated adult liver. This low level of expression in fetal liver is refractory to induction by glucocorticoids, but both gene products are increased to a limited extent by cyclic AMP. This induction by cyclic AMP (cAMP) does not confer glucocorticoid-responsiveness on expression. By 3 hr after birth both functional mRNA and enzyme levels are significantly increased, an increase which continues until a peak is reached at 12 hr that is appreciably above the adult levels. Both gene products then decline until adult levels are reached by 24 hr. The postnatal shift in aminotransferase expression is accompanied by acquisition of the capacity to respond to glucocorticoids. Treatment of newborns with an antiglucocorticoid steroid or with glucose suppresses the postnatal overshoot of expression, but neither treatment affects the increase from fetal to adult levels of expression. The results indicate that prior to birth, expression of the aminotransferase gene is partially repressed, a repression that is lifted essentially immediately upon birth. The hormones capable of inducing aminotransferase synthesis have no apparent necessary role in this process.

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