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Many populations of freshwater fishes are threatened with losses, and increasingly, the release of hatchery individuals is one strategy being implemented to support wild populations. However, stocking of hatchery individuals may pose long‐term threats to wild populations, particularly if genetic interactions occur between wild and hatchery individuals. One highly prized sport fish that has been heavily stocked throughout its range is the brook trout (Salvelinus fontinalis). In Nova Scotia, Canada, hatchery brook trout have been stocked since the early 1900s, and despite continued stocking efforts, populations have suffered declines in recent decades. Before this study, the genetic structure of brook trout populations in the province was unknown; however, given the potential negative consequences associated with hatchery stocking, it is possible that hatchery programs have adversely affected the genetic integrity of wild populations. To assess the influence of hatchery supplementation on wild populations, we genotyped wild brook trout from 12 river systems and hatchery brook trout from two major hatcheries using 100 microsatellite loci. Genetic analyses of wild trout revealed extensive population genetic structure among and within river systems and significant isolation‐by‐distance. Hatchery stocks were genetically distinct from wild populations, and most populations showed limited to no evidence of hatchery introgression (<5% hatchery ancestry). Only a single location had a substantial number of hatchery‐derived trout and was located in the only river where a local strain is used for supplementation. The amount of hatchery stocking within a watershed did not influence the level of hatchery introgression. Neutral genetic structure of wild populations was influenced by geography with some influence of climate and stocking indices. Overall, our study suggests that long‐term stocking has not significantly affected the genetic integrity of wild trout populations, highlighting the variable outcomes of stocking and the need to evaluate the consequences on a case‐by‐case basis.
brook trout, domestication, hatchery stocking, hybridization, introgression, microsatellites
Multiple decades of stocking has resulted in limited hatchery introgression in wild brook trout (Salvelinus fontinalis) populations of Nova Scotia
Sarah J. Lehnert,corresponding author 1 Shauna M. Baillie, 2 John MacMillan, 3 Ian G. Paterson, 2 Colin F. Buhariwalla, 3 Ian R. Bradbury, 1 , 2 and Paul Bentzen 2
Increased cyclooxygenase activity promotes progression of colorectal cancer, but the mechanisms behind COX-2 induction remain elusive. This study was therefore aimed to define external cell signaling and transcription factors relating to high COX-2 expression in colon cancer tissue.
Tumor and normal colon tissue were collected at primary curative operation in 48 unselected patients. COX-2 expression in tumor and normal colon tissue was quantified including microarray analyses on tumor mRNA accounting for high and low tumor COX-2 expression. Cross hybridization was performed between tumor and normal colon tissue. Methylation status of up-stream COX-2 promoter region was evaluated.
Tumors with high COX-2 expression displayed large differences in gene expression compared to normal colon. Numerous genes with altered expression appeared in tumors of high COX-2 expression compared to tumors of low COX-2. COX-2 expression in normal colon was increased in patients with tumors of high COX-2 compared to normal colon from patients with tumors of low COX-2. IL1β, IL6 and iNOS transcripts were up-regulated among external cell signaling factors; nine transcription factors (ATF3, C/EBP, c-Fos, Fos-B, JDP2, JunB, c-Maf, NF-κB, TCF4) showed increased expression and 5 (AP-2, CBP, Elk-1, p53, PEA3) were decreased in tumors with high COX-2. The promoter region of COX-2 gene did not show consistent methylation in tumor or normal colon tissue.
Transcription and external cell signaling factors are altered as covariates to COX-2 expression in colon cancer tissue, but DNA methylation of the COX-2 promoter region was not a significant factor behind COX-2 expression in tumor and normal colon tissue.
COX-2 gene expression in colon cancer tissue related to regulating factors and promoter methylation status
Annika Gustafsson Asting,1 Helena Caren,2 Marianne Andersson,1 Christina Lonnroth,1 Kristina Lagerstedt,1 and Kent Lundholmcorresponding author1
The Stubble-stubbloid (Sb-sbd) gene is required for ecdysone-regulated epithelial morphogenesis of imaginal tissues during Drosophila metamorphosis. Mutations in Sb-sbd are associated with defects in apical cell shape changes critical for the evagination of the leg imaginal disc and with defects in assembly and extension of parallel actin bundles in growing mechanosensory bristles. The Sb-sbd gene encodes a type II transmembrane serine protease (TTSP). Here we use a Sb-sbd transgenic construct to rescue both bristle and leg morphogenesis defects in Sb-sbd mutations. Molecular characterization of Sb-sbd mutations and rescue experiments with wild-type and modified Sb-sbd transgenic constructs show that the protease domain is required for both leg and bristle functions. Truncated proteins that express the noncatalytic domains without the protease have dominant effects in bristles but not in legs. Leg morphogenesis, but not bristle growth, is sensitive to Sb-sbd overexpression. Antibody localization of the Sb-sbd protein shows apical expression in elongating legs. Sb-sbd protein is found in the base and shaft in budding bristles and then concentrates at the growing tip when bristles are elongating rapidly. We propose a model whereby Sb-sbd helps coordinate proteolytic modification of extracellular matrix attachments with cytoskeletal changes in both legs and bristles.
Mutational Analysis of Stubble-stubbloid Gene Structure and Function in Drosophila Leg and Bristle Morphogenesis
Ann S. Hammonds and James W. Fristrom1