Application of molecular markers to mixed-stock analysis of Yukon River fall chum salmon

Thesis (M.S.) University of Alaska Fairbanks, 2004Country of origin provides the basis for allocating harvests of Yukon River chum salmon. The genetic divergence among Yukon River chum salmon populations adjacent to the international border as revealed by allozyme and micro satellite variation is insufficient to determine the country of origin of returning fish using mixed-stock analysis (MSA). Consequently, we investigated the resolution provided by alternative genetic markers in an attempt to detect levels of divergence that would be sufficient for MSA. We analyzed 10 Yukon River chum salmon populations for variation at 30 variable amplified fragment length polymorphism (AFLP) loci and for mitochondrial DNA (mtDNA) restriction site variation. We assessed these markers for their utility in MSA and, for mtDNA, phylogeographic analysis. The AFLP results show that MSA was most successful when mixtures were allocated to regions. The AFLP data were able to provide improved country of origin MSA estimates for the border populations with a 6.5% improvement for the Canadian populations over micro satellite analysis. No divergence in mtDNA haplotype frequency distributions was detected (P>0.05) within the Yukon River. Lack of mtDNA divergence likely resulted from a Pleistocene bottleneck that led to panmixia of the mtDNA genome.Ch. 1. Mitochondrial DNA variation within and among Yukon River chum salmon populations -- Ch. 2. Application of amplified fragment length polymorphism (AFLP) to mixed-stock analysis of Yukon River fall chum salmon, Oncorhynchus keta

These Unequal States: Corporate Organization and Income Inequality in the United States

In an analysis of data on employment in the 48 contiguous United States from 1978 to 2008, we examine the connection between organizational demography and rising income inequality at the state level. Drawing on research on social comparisons and firm boundaries, we argue that large firms are susceptible to their employees making social comparisons about wages and that firms undertake strategies, such as wage compression, to help ameliorate their damaging effects. We argue that wage compression affects the distribution of wages throughout the broader labor market and that, consequently, state levels of income inequality will increase as fewer individuals in a state are employed by large firms. We hypothesize that the negative relationship between large-firm employment and income inequality will weaken when large employers are more racially diverse and their workers are dispersed across a greater number of establishments. Our results show that as the number of workers in a state employed by large firms declines, income inequality in that state increases. When these firms are more racially diverse, however, the negative relationship between large-firm employment and income inequality weakens. These results point to the importance of considering how corporate demography influences the dispersion of wages in a labor market

Looking within for Vision

Channelrhodopsin-2 (ChR2), a directly light-gated cation channel from the green alga Chlamydomonas reinhardtii has been shown to be a directly light-switched cation-selective ion channel, which employs 11-cis retinal as its chromophore. This is the same chromophore as the mammalian photoreceptor's visual pigment—rhodopsin. Previously, investigators demonstrated that ChR2 can be used to optically control neuronal firing by depolarizing the cell. In this issue of Neuron, Bi et al. apply viral-mediated gene transfer to deliver ChR2 to retinal ganglion cells (RGC) in a rodent model of inherited blindness. In this way, the authors have genetically engineered surviving retinal neurons to take on the lost photoreceptive function. The conversion of light-insensitive retinal interneurons into photosensitive cells introduces an entirely new direction for treatments of blinding retinal degeneration

Retinal degeneration is rescued in transgenic rd mice by expression of the cGMP phosphodiesterase ß subunit

The ß subunit of the cGMP phosphodiesterase (PDE) gene has been identified as the candidate gene for retinal degeneration in the rd mouse. To study the molecular mechanisms underlying degeneration and the potential for gene repair, we have expressed a functional bovine cGMP PDE ß subunit in transgenic rd mice. One transgenic mouse line showed complete photoreceptor rescue across the entire span of the retina. A second independently derived line showed partial rescue in which photoreceptors in the superior but not the inferior hemisphere of the retina were rescued. In the latter animals, intermediate stages of degeneration were observed in the transition zone between rescued and diseased photoreceptors. Pathologic changes in the retina ranged from vesiculation of the basalmost outer segment discs in otherwise structurally intact rod cells to photoreceptors with highly disorganized outer segments and intact inner segments. Totally or partially rescued retinas showed a corresponding restoration of cGMP PDE activity, whereas nonrescued retinas had minimal enzyme activity, characteristic of the rd phenotype. These transgenic animals provide models for studying the molecular basis of retinal degenerative disease and conclusively demonstrate that the phenotype of rd mice is produced by a defect in the ß subunit of cGMP PDE

Translational Retinal Research and Therapies.

The following review summarizes the state of the art in representative aspects of gene therapy/translational medicine and evolves from a symposium held at the School of Veterinary Medicine, University of Pennsylvania on November 16, 2017 honoring Dr. Gustavo Aguirre, recipient of ARVO's 2017 Proctor Medal. Focusing on the retina, speakers highlighted current work on moving therapies for inherited retinal degenerative diseases from the laboratory bench to the clinic

Müller cell activation, proliferation and migration following laser injury.

PurposeMüller cells are well known for their critical role in normal retinal structure and function, but their reaction to retinal injury and subsequent role in retinal remodeling is less well characterized. In this study we used a mouse model of retinal laser photocoagulation to examine injury-induced Müller glial reaction, and determine how this reaction was related to injury-induced retinal regeneration and cellular repopulation.MethodsExperiments were performed on 3-4-week-old C57BL/6 mice. Retinal laser photocoagulation was used to induce small, circumscribed injuries; these were principally confined to the outer nuclear layer, and surrounded by apparently healthy retinal tissue. Western blotting and immunohistochemical analyses were used to determine the level and location of protein expression. Live cell imaging of green fluorescent protein (GFP)-infected Müller cells (AAV-GFAP-GFP) were used to identify the rate and location of retinal Müller cell nuclear migration.ResultsUpon injury, Müller cells directly at the burn site become reactive, as evidenced by increased expression of the intermediate filament proteins glial fibrillary acidic protein (GFAP) and nestin. These reactive cells re-enter the cell cycle as shown by expression of the markers Cyclin D1 and D3, and their nuclei begin to migrate toward the injury site at a rate of approximately 12 microm/hr. However, unlike other reports, evidence for Müller cell transdifferentiation was not identified in this model.ConclusionsRetinal laser photocoagulation is capable of stimulating a significant glial reaction, marked by activation of cell cycle progression and retinal reorganization, but is not capable of stimulating cellular transdifferentiation or neurogenesis