Segregation of infectious pancreatic necrosis resistance QTL in the early life cycle of Atlantic Salmon (Salmo salar)

In a previous study, three significant quantitative trait loci (QTL) associated with resistance to Infectious Pancreatic Necrosis (IPN) disease were identified by analysing challenge data from one sub-population of Landcatch Atlantic salmon (Salmo salar) smolt. While these QTL were shown to affect the resistance in seawater, their effect in freshwater was unknown. This study investigates the effect of these QTL on IPN resistance in salmon fry in freshwater. Twenty families with intermediate levels of IPN mortality were analysed from a freshwater challenge trial undertaken on a different sup-population of LNS salmon to that studied previously. Only the QTL from linkage group 21 (LG21) appeared to have a significant and large effect on resistance in freshwater; the same QTL was found to have the largest effect in seawater in the previous study. Variance component analysis showed a high heritability for the QTL: 0.45 ± 0.07 on the liability scale and 0.25 ± 0.05 on the observed scale. In a family where both parents were segregating for the QTL, there was a 0% vs. 100% mortality in homozygous offspring for resistant and susceptible QTL alleles. The finding that the same QTL has major effect in both freshwater and seawater has important practical implications, as this will allow the improvement of resistance in both phases through marker assisted selection by targeting this QTL. Moreover, the segregation of the LG21 QTL in a different sub-population gives further evidence of its association with IPN-resistance.     

RFLP and linkage analysis of the porcine casein loci—CASAS1, CASAS2, CASB and CASK

Restriction fragment length polymorphisms (RFLPs) were revealed at the porcine casein loci with the following combinations of restriction endonucleases and porcine cDNA clones: α_s1,-casein (TaqI); α_s2-casein (BamHI); and ß-casein (Sacl). These RFLPs were shown to be under simple monogenic control by segregation analysis of two- and three-generation families. The CASAS1, CASAS2 and CASB casein loci were also shown to be linked with no recombinant haplotypes observed amongst 77 meioses in Large White and Meishan F₁ and F₂ crosses. No recombinants were observed in a further 106 meioses that were informative for linkage between CASAS1 and CASAS2.     

Decreased 8N3-[gamma-32P]GTP photolabeling of Gs alpha in tumorigenic lung epithelial cell lines: association with decreased hormone responsiveness and loss of contact-inhibited growth

The 45-kDa alpha subunit of the signal transducing Gs protein complex, which stimulates receptor-coupled adenylate cyclase, incorporated less of the photoaffinity probe, 8N3-[gamma-32P]GTP, in extracts from tumorigenic cell lines in comparison with nontumorigenic cell lines derived from mouse lung epithelium. Immunoblotting experiments using anti-Gs alpha antibodies demonstrated that tumor cells do not have a decreased amount of Gs alpha and photolabeling of tumor cell Gs alpha increased when the rate of nucleotide exchange was promoted. Therefore, tumor cell Gs alpha function may be altered. Consistent with this hypothesis is the observation that the tumor cells exhibited decreased responsiveness to the beta-adrenergic agonist, isoproterenol. Gs alpha photolabeling in growing nontumorigenic cells was reduced to a level resembling that observed in tumor cells, but photolabeling increased when cells became contact-inhibited. This increase in 8N3-[gamma-32P]GTP incorporation into Gs alpha by normal cells at confluence was not seen in the tumorigenic cells. Since Gs alpha photolabeling was inversely proportional to the percentage of [3H]thymidine-labeled nuclei at confluence, we suggest that the altered Gs alpha in tumor cells is involved in the loss of cell growth regulation.     

Variation in human limb joint articular morphology

Objectives

Synovial joints in human limbs strike a balance between mobility, stability, and articular fit, yet little is known about how these conflicting demands pattern intraspecific variation in articular shape. In this study, we use geometric morphometrics to establish the apportionment and magnitude of morphological variance of the articular surfaces of the human shoulder, elbow, hip, and knee. We hypothesize that variances will be comparable between articulating surfaces within a joint and will be larger in joints with smaller ranges of motion, given their plurality of functional demands.

Materials and Methods

Three-dimensional landmarks were taken on the articular surfaces of the glenohumeral, humeroulnar, acetabulofemoral, and tibiofemoral joints from CT scans of 200 skeletons from the University of Tennessee Donated Skeletal Collection (84 females, 116 males). Root mean-squared distances between articulations calculated from Procrustes shape coordinates were used to determine variance distributions.

Results

We found no difference in variances for each articular surface between the sexes or between left and right articular surfaces. A high range of motion is associated with greater morphological variance; however, this pattern is largely driven by the concave articular surfaces of each joint, which consistently exhibit statistically greater variance than their convex counterparts.

Discussion

The striking pattern of differential variance between articulating morphologies points to potential disparities in development between them. Consistently higher variance in concave surfaces may relate to chondral modeling theory for the formation of joints. Establishing intraspecific morphological variance patterns is a first step in understanding coordinated evolution among articular features.     

Marker-assisted introgression using non-unique marker alleles I: selection on the presence of linked marker alleles

This paper investigates marker-assisted introgression of a major gene into an outbred line, where identification of the introgressed gene is incomplete because marker alleles are not unique to the base populations (the same marker allele can occur in both donor and recipient population). Those markers are used to identify the introgressed allele as well as the background genotype. The effect of using those markers, as if they were completely informative on the retention of the introgressed allele, was examined over five generations of backcrossing by using a single marker or a marker bracket for different starting frequencies of the marker alleles. Results were calculated by using both a deterministic approach, where selection is only for the desired allele, and by a stochastic approach, where selection is also on background genotype. When marker allele frequencies in donor and recipient population diverged from 1 and 0 (using a diallelic marker), the ability to retain the desired allele rapidly declined. Marker brackets performed notably better than single markers. If selection on background marker genotype was applied, the desired allele could be lost even more quickly than expected at random because the chance that the allele, which is common in the donor line, is present on the locus identifying the introgressed allele and is surrounded by alleles common in the recipient line on the background marker loci, will descend from the donor line (double recombination has taken place), is a lot smaller than the chance that this allele will stem from the recipient line (in which the allele occurs in low frequency). Marker brackets again performed better. Preselection against marker homozygotes (producing uninformative gametes) gave a slightly better retention of the introgressed allele.     

GTPase from rod outer segments: characterization by photoaffinity labeling and tryptic peptide mapping

The photoaffinity label [γ-³²P]8-N₃GTP has been used to identify GTP-binding components in highly purified preparations of GTPase from bovine rod outer segments. These preparations contain two major polypeptides of 37,000 and 39,000 daltons. In the presence of photolyzing radiation, [γ-³²P]8-N₃GTP is covalently attached to the 37,000 dalton polypeptide. Tryptic peptide mapping of this polypeptide indicates that it is highly related to the 39,000 dalton species that has been previously identified as a GTP-binding component.     

The human mineralocorticoid receptor gene (MLR) is located on chromosome 4 at q31.2

The gene for the human mineralocorticoid receptor (MLR) was previously localized to chromosome 4. Here, we have localized this gene to 4q31.2 by in situ hybridization. This precise mapping of MLR will assist in the linkage analysis and genetic characterization of pseudohypoaldosteronism, an autosomal recessive disorder which likely results from a defect in the MLR gene.