Multiple variants in subtelomeric regions of normal karyotypes

We describe a human genomic cosmid clone, 56.1.1, that contains subtelomeric sequences present on multiple human chromosomes. In particular, using fluorescence in situ hybridization, we have identified 16 sites of hybridization on 12 chromosomes. In a sample of 8 unrelated individuals, 10 of these sites showed interindividual variation. Co-hybridization with other polymorphic probes allowed us to demonstrate cytologically heterozygosity at three sites in six individuals. The chromosomal distribution of hybridization sites in a family strongly suggests that these variants are inherited in a Mendelian fashion. These data show that subtelomeric repeats are a rich source of genetic variability. Possible mechanisms of generation of such variants are discussed.     

Foraging habits in a generalist predator: Sex and age influence habitat selection and resource use among bottlenose dolphins (Tursiops truncatus)

This study examines resource use (diet, habitat use, and trophic level) within and among demographic groups (males, females, and juveniles) of bottlenose dolphins (Tursiops truncatus). We analyzed the δ¹³C and δ¹⁵N values of 15 prey species constituting 84% of the species found in stomach contents. We used these data to establish a trophic enrichment factor (TEF) to inform dietary analysis using a Bayesian isotope mixing model. We document a TEF of 0‰ and 2.0‰ for δ¹³C and δ¹⁵N, respectively. The dietary results showed that all demographic groups relied heavily on low trophic level seagrass‐associated prey. Bayesian standard ellipse areas (SEA_b) were calculated to assess diversity in resource use. The SEA_b of females was nearly four times larger than that of males indicating varied resource use, likely a consequence of small home ranges and habitat specialization. Juveniles possessed an intermediate SEA_b, generally feeding at a lower trophic level compared to females, potentially an effect of natal philopatry and immature foraging skills. The small SEA_b of males reflects a high degree of specialization on seagrass associated prey. Patterns in resource use by the demographic groups are likely linked to differences in the relative importance of social and ecological factors.     

Myosin heavy chain isoforms regulate muscle function but not myofibril assembly.

Myosin heavy chain (MHC) is the motor protein of muscle thick filaments. Most organisms produce many muscle MHC isoforms with temporally and spatially regulated expression patterns. This suggests that isoforms of MHC have different characteristics necessary for defining specific muscle properties. The single Drosophila muscle Mhc gene yields various isoforms as a result of alternative RNA splicing. To determine whether this multiplicity of MHC isoforms is critical to myofibril assembly and function, we introduced a gene encoding only an embryonic MHC into Drosophila melanogaster. The embryonic transgene acts in a dominant antimorphic manner to disrupt flight muscle function. The transgene was genetically crossed into an MHC null background. Unexpectedly, transformed flies expressing only the embryonic isoform are viable. Adult muscles containing embryonic MHC assemble normally, indicating that the isoform of MHC does not determine the dramatic ultrastructural variation among different muscle types. However, transformed flies are flightless and show reduced jumping and mating ability. Their indirect flight muscle myofibrils progressively deteriorate. Our data show that the proper MHC isoform is critical for specialized muscle function and myofibril stability.     

Ecological and behavioural correlates of intracellular buffering capacity in the muscles of antarctic fishes

Summary Five species of antarctic fishes can be arranged in order of increasing anaerobic capacity of the white muscles for burst swimming: Rhigophila dearborni (Zoarcidae), icefish (Channichthyidae), Dissostichus mawsoni, Trematomus centronotus, and Pagothenia borchgrevinki (Nototheniidae). This order reflects increasing dependence on anaerobic work done during short bursts of speed during prey capture or predator avoidance. Buffer capacity () for white muscle was lower than that of behaviourally equivalent fish from lower latitudes and is itself temperature-dependent.     

H2 histaminic receptors in rat cerebral cortex. 3. Inhibition of [3H]histamine by H2 agonists

The binding of [3H]histamine to H2 receptors in homogenates of rat cerebral cortex is inhibited by 11 H2 agonists in a characteristic and unique manner. At low concentrations of the radioligand (less than 1.5 nM), the inhibitory profiles of individual agonists (A) are distinctly biphasic; specific binding is well described in most cases by the empirical expression Y = F1K1/(K1 + [A]) + F2K2/(K2 + [A]), in which F1 and F2 sum to 1. Maximal inhibition is the same for all agonists. Since values of F2 vary from 0.42 to 0.90, the agonist appears to determine the equilibrium distribution of receptors between two states of affinity. Ratios of apparent affinity (K2/K1) vary from 204 to 3 090 000, and there is no correlation between values of K1 and K2. Compounds lacking H2 activity, including structural analogues of histamine and dimaprit, reveal a Hill coefficient of 1 and inhibit the radioligand only weakly. For six agonists, values of K2 agree and correlate well (P = 0.00047) with H2 pharmacological potency (EC50) in the guinea pig right atrium; for the others, K2 is less than EC50 by 15-61-fold. Four observations suggest that the inhibition corresponding to F1 is allosteric and cooperative: the dissociation constant of the radioligand appears to vary in the presence of an unlabeled agonist, absolute levels of binding corresponding to F1, as defined by dimaprit, decrease at higher concentrations of [3H]histamine, F1 for dimaprit is reduced from 0.48 to 0.32 by 2-methylhistamine (F1 = 0.27) at a concentration of 20 nM (approximately K1(0.5) K2(0.5) for 2-methylhistamine), but the increase in K1 for dimprit is at least 100-fold less than expected from competitive effects, and 1 equiv of some agonists appears to preclude access of [3H]histamine to more than 1 equiv of receptors, with no evidence that an appreciable fraction of the unlabeled drug is bound. Noncompetitive effects also may account in part for the inhibition corresponding to F2.     

Developmental changes in the response of larval Manduca sexta fat body glycogen phosphorylase to starvation, stress and octopamine

Fasting or starvation of 1(st)- and 2(nd)-day fifth instar Manduca sexta larvae leads to rapid activation of fat body glycogen phosphorylase. Under feeding conditions, 21-29% of the phosphorylase was found in the active form. However, after only one hour of starvation, the active form increased to 55-65%. In larvae on the 3(rd)-day there was a slower increase in the activation, requiring three hours of starvation to reach a maximum of 60-65%. No activation was observed in 4(th)-day larvae after three hours of starvation. When 1(st)- or 2(nd)-day larvae were decapitated, the time-course of activation of glycogen phosphorylase was very similar to that observed in intact insects. However, activation of glycogen phosphorylase following decapitation was only observed in 1(st)- and 2(nd)-day larvae. In 2(nd)-day larvae, octopamine promoted activation of glycogen phosphorylase and 100-pmol of octopamine promoted maximum activation. Higher amounts of injected octopamine caused a decrease in activation. The injection of 100 pmol of octopamine caused a 50-55% activation of phosphorylase within 30 minutes. The simultaneous injection of the alpha-adrenergic receptor antagonist phentolamine with octopamine blocked the octopamine effect in 1(st)- and 2(nd)-day feeding larvae. However, the activation of glycogen phosphorylase observed in ligated/decapitated larvae on the 1(st)- and 2(nd)-day was not abolished by injection of phentolamine. All of these data suggest that factors other than adipokinetic hormone and octopamine may be involved in the activation of glycogen phosphorylase during fasting or starvation in the early part of the fifth larval stage of M. sexta.