Testicular Leydig cells, which are the predominant source of the male sex steroid hormone testosterone, express estrogen receptors (ESRs) and are subject to regulation by estrogen. Following ingestion, the two major isoflavones in soybeans, genistin and daidzin, are hydrolyzed by gut microflora to form genistein and daidzein, which have the capacity to bind ESRs and affect gene expression. Thus, the increasing use of soy-based products as nondairy sources of protein has raised concerns about the potential of these products to cause reproductive toxicity. In the present study, perinatal exposure of male rats to isoflavones induced proliferative activity in Leydig cells. Isoflavones have the capacity to act directly as mitogens in Leydig cells, because genistein treatment induced Leydig cell division in vitro. Genistein action regulating Leydig cell division involved ESRs, acting in concert with signaling molecules in the transduction pathway mediated by protein kinase B (AKT) and mitogen-activated protein kinase (MAPK). Enhanced proliferative activity in the prepubertal period increased Leydig cell numbers, which alleviated deficits in androgen biosynthesis and/or augmented serum and testicular testosterone concentrations in adulthood. Together, these observations indicate that the perinatal exposures of male rats to isoflavones affected Leydig cell differentiation, and they imply that including soy products in the diets of neonates has potential implications for testis function.

We applied an empirical model to predict hatching and emergence timing for 25 western Alaska sockeye salmon (Oncorhynchus nerka) populations in four lake-nursery systems to explore current patterns and potential responses of early life history phenology to warming water temperatures. Given the temperature regimes sockeye salmon experienced during development, we predicted hatching to occur in as few as 58 days to as many as 260 days depending on spawning timing and temperature. For a focal lake spawning population, our climate–lake temperature model predicted a water temperature increase of 0.7 to 1.4 °C from 2015 to 2099 during the incubation period, which translated to a hatching timing that was 16 to 30 days earlier. The most extreme warming scenarios shifted development to approximately 1 week earlier than historical minima and thus climatic warming may lead to only modest shifts in phenology during the early life history stage of this population. The marked variation in the predicted timing of hatching and emergence among populations in close proximity on the landscape may serve to buffer this metapopulation from climate change.

An important unresolved question is how populations of coldwater-dependent fishes will respond to rapidly warming water temperatures. For example, the culturally and economically important group, Pacific salmon (Oncorhynchus spp.), experience site-specific thermal regimes during early development that could be disrupted by warming. To test for thermal local adaptation and heritable phenotypic plasticity in Pacific salmon embryos, we measured the developmental rate, survival, and body size at hatching in two populations of sockeye salmon (Oncorhynchus nerka) that overlap in timing of spawning but incubate in contrasting natural thermal regimes. Using a split half-sibling design, we exposed embryos of 10 families from each of two populations to variable and constant thermal regimes. These represented both experienced temperatures by each population, and predicted temperatures under plausible future conditions based on a warming scenario from the downscaled global climate model (MIROC A1B scenario). We did not find evidence of thermal local adaptation during the embryonic stage for developmental rate or survival. Within treatments, populations hatched within 1 day of each other, on average, and among treatments, did not differ in survival in response to temperature. We did detect plasticity to temperature; embryos developed 2.5 times longer (189 days) in the coolest regime compared to the warmest regime (74 days). We also detected variation in developmental rates among families within and among temperature regimes, indicating heritable plasticity. Families exhibited a strong positive relationship between thermal variability and phenotypic variability in developmental rate but body length and mass at hatching were largely insensitive to temperature. Overall, our results indicated a lack of thermal local adaptation, but a presence of plasticity in populations experiencing contrasting conditions, as well as family-specific heritable plasticity that could facilitate adaptive change.

Introduced and invasive species make excellent natural experiments for investigating rapid evolution. Here, we describe the effects of genetic drift and rapid genetic adaptation in pink salmon (Oncorhynchus gorbuscha) that were accidentally introduced to the Great Lakes via a single introduction event 31-generations ago. Using whole-genome resequencing for 134 fish spanning five sample groups across the native and introduced range, we estimate that the progenitor population’s effective population size was 146,886 at the time of introduction, whereas the founding population’s effective population size was just 72—a 2040-fold decrease. As expected with a severe bottleneck, we show reductions in genome-wide measures of genetic diversity, specifically a 37.7% reduction in the number of SNPs and an 8.2% reduction in observed heterozygosity. Despite this decline in genetic diversity, we provide evidence for putative selection at 47 loci across multiple chromosomes in the introduced populations, including missense variants in genes associated with circadian rhythm, immunological response, and maturation, which match expected or known phenotypic changes in the Great Lakes. For one of these genes, we use a species-specific agent-based model to rule out genetic drift and conclude that a strong response to selection occurred in a period gene (per2) that plays a predominant role in determining an organism’s daily clock, matching large day length differences experienced by introduced salmon during important phenological periods. Together, these results inform how populations might evolve rapidly to new environments, even with a small pool of standing genetic variation.

1The resistance of bacteria, disease vectors, and pests to chemical controls has vast ecological, 2 economic, and human-health costs. In most cases, resistance is only detected after non-3 susceptible phenotypes have spread throughout the entire population. Detecting resistance in its 4 incipient stages, by comparison, provides time to implement preventative strategies. Incipient 5 resistance (IR) can be detected by coupling standard toxicology assays with large-scale gene 6 expression experiments. We apply this approach to a system where an invasive parasite, sea 7 lamprey (Petromyzon marinus), has been treated with the highly-effective pesticide 3-8 trifluoromethyl-4-nitrophenol (TFM) for 60 years. Toxicological experiments revealed that 9 lamprey from treated populations did not have higher survival to TFM exposure than lamprey 10 from their native range, demonstrating that full-fledged resistance has not yet evolved. In stark 11 contrast, we find hundreds of genes differentially expressed in response to TFM in the 12 population with the longest history of exposure, many of which relate to TFM's primary mode of 13 action, the uncoupling of oxidative phosphorylation. One gene critical to oxidative 14 phosphorylation, ATP5PB, which encodes subunit b of ATP synthase, was nearly fixed for 15 alternative alleles in comparisons between native and treated populations (FST > 9 SD from the 16 mean). A gene encoding an additional subunit of ATP synthase, ATP5F1B, was canalized for 17 high expression in treated populations, but remained plastic in response to treatment in sea 18 lamprey from the native range. These combined genomic and transcriptomic results illustrate that 19 an adaptive, genetic response to TFM is driving incipient resistance in a damaging pest species. 20 S3). Remarkably, when comparing samples treated with 0.3 mg/L TFM to control samples, we 113 found 336 genes that were differentially expressed (275 upregulated, 61 downregulated in 114 comparison to control individuals) in muscle tissue in the Lake Michigan population, dwarfing 115 the number of differentially expressed genes (DEGs) found in both the Lake Champlain (n = 21) 116 and the Connecticut River (n = 68) populations (Fig. 3A-C; Table S4). No DEGs were shared 117 among all three populations and different population responses were observed when lower 118 concentrations (i.e., 0.2 mg/L) of TFM were applied and when different tissues were examined 119 (Figures S2-S5). 120The primary mode of action for TFM is to uncouple oxidative phosphorylation in the 121 mitochondria resulting in severe ATP depletion and eventual death (25, 26, 32). Of the 336 122 DEGs identified in Lake Michigan, several genes were directly related to this mode of action 123 including CRCM1 (LogFC = 2.60), a calcium release-activated channel protein that controls the 124 influx of calcium into cells when depleted, and PLCD4 (LogFC = 2.41), an enzyme responsible 125 for hydrolyzing phosphatidylinositol 4,5-bisphosphate into two secondary messenger molecules, 126 one of which (...