An international multi‐laboratory project was conducted to develop a standardized DNA database for Chinook salmon (Oncorhynchus tshawytscha). This project was in response to the needs of the Chinook Technical Committee of the Pacific Salmon Commission to identify stock composition of Chinook salmon caught in fisheries during their oceanic migrations. Nine genetics laboratories identified 13 microsatellite loci that could be reproducibly assayed in each of the laboratories. To test that the loci were reproducible among laboratories, blind tests were conducted to verify scoring consistency for the nearly 500 total alleles. Once standardized, a dataset of over 16,000 Chinook salmon representing 110 putative populations was constructed ranging throughout the area of interest of the Pacific Salmon Commission from Southeast Alaska to the Sacramento River in California. The dataset differentiates the major known genetic lineages of Chinook salmon and provides a tool for genetic stock identification of samples collected from mixed fisheries. A diverse group of scientists representing the disciplines of fishery management, genetics, fishery administration, population dynamics, and sampling theory are now developing recommendations for the integration of these genetic data into ocean salmon management.

Single nucleotide polymorphisms (SNPs) are appealing genetic markers due to several beneficial attributes, but uncertainty remains about how many of these bi-allelic markers are necessary to have sufficient power to differentiate populations, a task now generally accomplished with highly polymorphic microsatellite markers. In this study, we tested the utility of 37 SNPs and 13 microsatellites for differentiating 29 broadly distributed populations of Chinook salmon (n = 2783). Information content of all loci was determined by In and , and the top 12 markers ranked by In were microsatellites, but the 6 highest, and 7 of the top 10 ranked markers, were SNPs. The mean ratio of random SNPs to random microsatellites ranged from 3.9 to 4.1, but this ratio was consistently reduced when only the most informative loci were included. Individual assignment test accuracy was higher for microsatellites (73.1%) than SNPs (66.6%), and pooling all 50 markers provided the highest accuracy (83.2%). When marker types were combined, as few as 15 of the top ranked loci provided higher assignment accuracy than either microsatellites or SNPs alone. Neighbour-joining dendrograms revealed similar clustering patterns and pairwise tests of population differentiation had nearly identical results with each suite of markers. Statistical tests and simulations indicated that closely related populations were better differentiated by microsatellites than SNPs. Our results indicate that both types of markers are likely to be useful in population genetics studies and that, in some cases, a combination of SNPs and microsatellites may be the most effective suite of loci. Fig. 2 Chord distance (D CSE ) neighbour-joining dendrograms and self-assignment matrices of populations of Chinook salmon from North America as determined with (a) 13 microsatellites, (b) 37 SNPs, and (c) all 50 markers combined. The diagonal represents the percentage of self-assigned individuals from a population and shaded blocks above and below the diagonal indicate percentage of mis-assignments to populations corresponding with the dendrogram. Grey grid lines correspond to regional clusters in the neighbour-joining dendrogram. Shading scale at the right of each figure depicts percentage assignment in 10% increments. 3472 S . R . N A R U M E T A L .

Inverted DNA repeats are known to cause genomic instabilities. Here we demonstrate that double-strand DNA breaks (DSBs) introduced a large distance from inverted repeats in the yeast (Saccharomyces cerevisiae) chromosome lead to a burst of genomic instability. Inverted repeats located as far as 21 kb from each other caused chromosome rearrangements in response to a single DSB. We demonstrate that the DSB initiates a pairing interaction between inverted repeats, resulting in the formation of large dicentric inverted dimers. Furthermore, we observed that propagation of cells containing inverted dimers led to gross chromosomal rearrangements, including translocations, truncations, and amplifications. Finally, our data suggest that break-induced replication is responsible for the formation of translocations resulting from anaphase breakage of inverted dimers. We propose a model explaining the formation of inverted dicentric dimers by intermolecular single-strand annealing (SSA) between inverted DNA repeats. According to this model, anaphase breakage of inverted dicentric dimers leads to gross chromosomal rearrangements (GCR). This "SSA-GCR" pathway is likely to be important in the repair of isochromatid breaks resulting from collapsed replication forks, certain types of radiation, or telomere aberrations that mimic isochromatid breaks.Genetic instability is associated with most tumor cells, and fusions between chromosomes or chromatids is a common source of chromosome aberrations found in such cells. Fusions between chromatids can be initiated by simultaneous breakage of the two chromatids or by the loss of telomere capping (13,35). The outcome of fusions depends on the location of the fusion site. Thus, fusions between acentric fragments lead to gene amplifications due to missegregation (21,36). Fusions between fragments containing centromeres lead to the formation of dicentric chromosomes that break during anaphase, when the two centromeres are pulled in opposite directions (breakage-fusion bridge [BFB] events). BFB events often lead to BFB cycles characterized by continued breakages and fusions. The BFB cycle, which was originally described by McClintock for maize (32), is repeated until newly acquired telomeres stabilize the broken chromosomes (13, 35). The process of broken chromosomes acquiring telomeres (the exit from BFB) creates different chromosomal rearrangements, including translocations, deletions, and amplifications (25,35,39,46).The mechanisms responsible for initiating chromosome or chromatid fusions are not clear. Although several studies indicate an important role for nonhomologous end joining in this process (33, 41), fusions can efficiently occur in a number of nonhomologous end joining-defective mutants (11), implicating the involvement of alternative mechanisms. Junctions of chromatid fusions sometimes have short regions of homology (26), suggesting the possible involvement of a homology-driven repair mechanism. Our present knowledge of fusions is based mainly on cells with defects in telomere ...

The number of greater prairie-chickens in Wisconsin has decreased by 91% since 1932. The current population of approximately 1500 birds exists primarily in four isolated management areas. In previous studies of the Wisconsin populations we documented low levels of genetic variation at microsatellite loci and the mitochondrial DNA control region. Here we investigate changes in genetic structure between the four management areas in Wisconsin over the last 50 years. We estimated the harmonic mean effective population size (Ne) over the last 50 years by comparing allele frequencies from the early 1950s with those from contemporary samples. Using a pseudo-likelihood approach that accounted for migration, estimates of Ne (15-32 prairie-chickens within each management area) were 10 times lower than census numbers from booming-ground counts. These low estimates of Ne are consistent with increased habitat fragmentation and an increase in genetic isolation between management areas over the last 50 years. The reduction of gene flow between areas has reduced Ne, increased genetic drift and, consequently, reduced genetic variation. These results have immediate consequences for the conservation of the prairie-chicken, and highlight the importance of how mating systems and limited dispersal may exacerbate the loss of genetic variation in fragmented populations.