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A population genetic assessment of taxonomic species: The case of Lake Malawi cichlid fishes

Organisms sampled for population‐level research are typically assigned to species by morphological criteria. However, if those criteria are limited to one sex or life stage, or the organisms come from a complex of closely related forms, the species assignments may misdirect analyses. The impact of such sampling can be assessed from the correspondence of genetic clusters, identified only from patterns of genetic variation, to the species identified using only phenotypic criteria. We undertook this protocol with the rock‐dwelling mbuna cichlids of Lake Malawi, for which species within genera are usually identified using adult male coloration patterns. Given high local endemism of male colour patterns, and considerable allele sharing among species, there persists considerable taxonomic uncertainty in these fishes. Over 700 individuals from a single transect were photographed, genotyped and separately assigned: (a) to morphospecies using photographs; and (b) to genetic clusters using five widely used methods. Overall, the correspondence between clustering methods was strong for larger clusters, but methods varied widely in estimated number of clusters. The correspondence between morphospecies and genetic clusters was also strong for larger clusters, as well as some smaller clusters for some methods. These analyses generally affirm (a) adult male‐limited sampling and (b) the taxonomic status of Lake Malawi mbuna, as the species in our study largely appear to be well‐demarcated genetic entities. More generally, our analyses highlight the challenges for clustering methods when the number of populations is unknown, especially in cases of highly uneven sample sizes.     

Receptor activator of NF-[kappa]B ligand arrests bone growth and promotes cortical bone resorption in growing rats.

Receptor activator of NF-kappaB ligand (RANKL), produced by osteoblastic lineage cells and activated T cells, is an essential factor for osteoclast differentiation, activation, and survival. Therefore, RANKL is a focal point of therapies targeting bone diseases where there is an imbalance of bone metabolism in favor of bone resorption. The present study assesses the effects of exogenous RANKL on growing bone. RANKL (100 microg x kg-1x day-1 for 7 days) administered to Sprague-Dawley weanling rats caused major deficits in growth, appearance, and bone mineral densities (BMD). Urinary deoxypyridinoline crosslinks, a measure of bone turnover, were higher in the RANKL-treated rats (P = 0.031), and the bone mineral content was lower (P < 0.001). The final BMD in the RANKL-treated rats was lower (P = 0.039) than in the control rats (19 +/- 7 vs. 38 +/- 5 mg/cm3). Moreover, calculated cortical bone density in each bone slice (total BMD - trabecular BMD) indicated there was only 5% cortical bone remaining in RANKL-treated rats. We conclude that therapies targeting RANKL are likely to have effects on cortical as well as trabecular bone density.     

Nucleotide ectoenzyme activities of human and Chinese hamster fibroblasts in tissue culture

We have previously assigned human ecto-5'-nucleotidase (NT) to chromosome 6 on the basis of conversion of exogenously supplied [14C]AMP to adenosine by whole cells of human and Chinese hamster hybrids carrying chromosome 6. In this paper we demonstrate that the activity on human MRC-5 fibroblasts is typical of previously described and purified ecto-5'-nucleotidases. In contrast to MRC-5 cells, Chinese hamster V79A2 cells weakly express an AMPase activity that is not NT. The cytosolic form of NT in human and hybrid fibroblasts is similar to the ectoenzyme in substrate specificity. Hybrids that lack chromosome 6 express neither the ecto- nor the cytosolic enzyme, suggesting that both forms may be coded by the same gene on chromosome 6. Ecto-ATPase, ecto-ADPase, and ecto-ADP kinase activities are each expressed at similar levels in MRC-5 and V79A2. The ATPase, ADPase and NT activities of MRC-5 cells act sequentially to generate adenosine. A similar cascade acts on V79A2 cells but the lack of NT causes the accumulation of AMP.