Becoming pure: identifying generational classes of admixed individuals within lesser and greater scaup populations.

Estimating the frequency of hybridization is important to understand its evolutionary consequences and its effects on conservation efforts. In this study, we examined the extent of hybridization in two sister species of ducks that hybridize. We used mitochondrial control region sequences and 3589 double-digest restriction-associated DNA sequences (ddRADseq) to identify admixture between wild lesser scaup (Aythya affinis) and greater scaup (A. marila). Among 111 individuals, we found one introgressed mitochondrial DNA haplotype in lesser scaup and four in greater scaup. Likewise, based on the site-frequency spectrum from autosomal DNA, gene flow was asymmetrical, with higher rates from lesser into greater scaup. However, using ddRADseq nuclear DNA, all individuals were assigned to their respective species with >0.95 posterior assignment probability. To examine the power for detecting admixture, we simulated a breeding experiment in which empirical data were used to create F1 hybrids and nine generations (F2-F10) of backcrossing. F1 hybrids and F2, F3 and most F4 backcrosses were clearly distinguishable from pure individuals, but evidence of admixed histories was effectively lost after the fourth generation. Thus, we conclude that low interspecific assignment probabilities (0.011-0.043) for two lesser and nineteen greater scaup were consistent with admixed histories beyond the F3 generation. These results indicate that the propensity of these species to hybridize in the wild is low and largely asymmetric. When applied to species-specific cases, our approach offers powerful utility for examining concerns of hybridization in conservation efforts, especially for determining the generational time until admixed histories are effectively lost through backcrossing.

Antlers on the Arctic Refuge: capturing multi-generational patterns of calving ground use from bones on the landscape.

Bone accumulations faithfully record historical ecological data on animal communities, and owing to millennial-scale bone survival on high-latitude landscapes, have exceptional potential for extending records on arctic ecosystems. For the Porcupine Caribou Herd, maintaining access to calving grounds on the Arctic National Wildlife Refuge (ANWR, Alaska) is a central management concern. However, variability in calving ground geography over the 30+ years of monitoring suggests establishing the impacts of climate change and potential petroleum development on future calving success could benefit from extended temporal perspectives. Using accumulations of female antlers (shed within days of calving) and neonatal skeletons, we test if caribou calving grounds develop measureable and characteristic bone accumulations and if skeletal data may be helpful in establishing a fuller, historically integrated understanding of landscape and habitat needs. Bone surveys of an important ANWR calving area reveal abundant shed antlers (reaching 10(3) km(-2)) and high proportional abundance of newborn skeletal individuals (up to 60% neonate). Openly vegetated riparian terraces, which compose less than 10 per cent of ANWR calving grounds, yield significantly higher antler concentrations than more abundant habitats traditionally viewed as primary calving terrain. Differences between habitats appear robust to potential differences in bone visibility. The distribution of antler weathering stages mirrors known multi-decadal calving histories and highlights portions of the antler accumulation that probably significantly extends records of calving activity. Death assemblages offer historically integrated ecological data valuable for the management and conservation of faunas across polar latitudes.

Progressive Cl- channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington's mice.

Huntington's disease (HD) patients suffer from progressive and debilitating motor dysfunction. Previously, we discovered reduced skeletal muscle chloride channel (ClC-1) currents, inwardly rectifying potassium (Kir) channel currents, and membrane capacitance in R6/2 transgenic HD mice. The ClC-1 loss-of-function correlated with increased aberrant mRNA processing and decreased levels of full-length ClC-1 mRNA (Clcn1 gene). Physiologically, the resulting muscle hyperexcitability may help explain involuntary contractions of HD. In this study, the onset and progression of these defects are investigated in R6/2 mice, ranging from 3 wk old (presymptomatic) to 9-13 wk old (late-stage disease), and compared with age-matched wild-type (WT) siblings. The R6/2 ClC-1 current density and level of aberrantly spliced Clcn1 mRNA remain constant with age. In contrast, the ClC-1 current density increases, and the level of aberrantly spliced Clcn1 mRNA decreases with age in WT mice. The R6/2 ClC-1 properties diverge from WT before the onset of motor symptoms, which occurs at 5 wk of age. The relative decrease in R6/2 muscle capacitance also begins in 5-wk-old mice and is independent of fiber atrophy. Kir current density is consistently lower in R6/2 compared with WT muscle. The invariable R6/2 ClC-1 properties suggest a disruption in muscle maturation, which we confirm by measuring elevated levels of neonatal myosin heavy chain (MyHC) in late-stage R6/2 skeletal muscle. Similar changes in ClC-1 and MyHC isoforms in the more slowly developing Q175 HD mice suggest an altered maturational state is relevant to adult-onset HD. Finally, we find nuclear aggregates of muscleblind-like protein 1 without predominant CAG repeat colocalization in R6/2 muscle. This is unlike myotonic dystrophy, another trinucleotide repeat disorder with similar ClC-1 defects, and suggests a novel mechanism of aberrant mRNA splicing in HD. These early and progressive skeletal muscle defects reveal much needed peripheral biomarkers of disease progression and better elucidate the mechanism underlying HD myopathy.