This study addressed the problem of local patterns of host specificity among Ancyrocephalinae (Monogenoidea) on bass and sunfish species, when the hosts occur in different species combinations in separate ponds. One hundred fifty-three fish of the Centrarchidae, from 4 study sites in Nebraska, were collected. Host species included bluegill (Lepomis macrochirus), green sunfish (L. cyanellus), largemouth bass (Micropterus salmoides), black crappie (Pomoxis nigromaculatus), white crappie (P. annularis), and rock bass (Ambloplites rupestris). These fish occurred in different species combinations, depending on the pond sampled. Results indicated that several centrarchid species could inhabit the same pond and yet support distinct monogene communities. Clavunculus bursatus, Onchocleidus helicis, O. principalis, and Syncleithrum fusiformis were found only on largemouth bass, regardless of what other centrarchids were present in a particular pond. Haplocleidus dispar occurred on green sunfish, bluegill, largemouth bass, and black crappie, and H. furcatus occurred on both bluegill and largemouth bass. Onchocleidus cyanellus and O. ferox were found on both bluegill and green sunfish. Rock bass were present in only 1 of the 4 ponds, but were not infected with any monogenes, even though co-occurring centrarchids were often heavily infected. Largemouth bass had the most diverse ancyrocephaline communities. The degree of parasite host specificity among these monogenes was inversely related to the diversity of host species present in a particular pond. In general, the parasites were more host specific than might be inferred from the literature; parasite species did not necessarily colonize supposedly receptive host species even when the latter were present, and host relatedness was the major factor in determining whether host species shared a common parasite species.
The biochemical basis for the unexpected agonist-induced upregulation of the number of radioligand binding sites for two mutated ␣ 1B -adrenergic receptors reported previously was investigated. Up-regulation was independent of the expression vector used and was not prevented by cycloheximide or actinomycin D, eliminating several potential transcriptional mechanisms and new receptor protein synthesis. Antagonists were also able to induce up-regulation, suggesting that ligand occupancy without signal generation was sufficient to induce the increase in binding sites. Accordingly, we hypothesized that up-regulation results from ligand-induced protection from inherent instability of these mutated receptors. Studies with receptors in isolated membranes revealed that the two mutated receptors that exhibited up-regulation in intact cells also exhibited an inherent instability of their ligand binding capacity, and binding of either agonists or antagonists to these receptors could protect against the loss of binding. In contrast, the wildtype receptor and other mutated receptors that did not exhibit up-regulation in intact cells did not exhibit instability or ligandinduced protection in isolated membranes. The occurrence of instability and protection in isolated membranes for only those mutated receptors and ligands that exhibit up-regulation in intact cells provides compelling evidence that the apparent up-regulation of binding sites in intact cells results from ligandinduced protection from an inherent instability of these G protein coupling-defective receptors. Inclusion of protease inhibitors markedly reduced the loss of binding in isolated membranes, implicating membrane-localized proteolysis as the likely mechanism for the instability.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.