Fidelity to foraging sites, consistency of migration routes and habitat modulation of home range by sea turtles

Aim  Resources can shape patterns of habitat utilization. Recently a broad foraging dichotomy between oceanic and coastal sites has been revealed for loggerhead sea turtles (Caretta caretta). Since oceanic and coastal foraging sites differ in prey availability, we might expect a gross difference in home-range size across these habitats. We tested this hypothesis by equipping nine adult male loggerhead sea turtles with GPS tracking devices. Location  National Marine Park of Zakynthos (NMPZ) Greece, central and eastern Mediterranean (Adriatic, Ionian and Aegean seas). Methods  In 2007, 2008 and 2009, Fastloc GPS-Argos transmitters were attached to nine male loggerheads. In addition, a Sirtrack PTT unit was attached to one male in 2007. Four of the turtles were tracked on successive years. We filtered the GPS data to ensure comparable data volumes. Route consistency between breeding and foraging sites of the four re-tracked turtles was conducted. Foraging site home range areas and within site movement patterns were investigated by the fixed kernel density method. Results  Foraging home range size ranged between circa 10 km2 at neritic habitats (coastal and open-sea on the continental shelf) to circa 1000 km2 at oceanic sites (using 90% kernel estimates), the latter most probably reflecting sparsely distributed oceanic prey. Across different years individuals did not follow exactly the same migration routes, but did show fidelity to their previous foraging sites, whether oceanic or neritic, with accurate homing in the final stages of migration. Main conclusions  The broad distribution and diverse life-history strategies of this population could complicate the identification of priority marine protected areas beyond the core breeding site.

Allosteric Modulation of the HIV-1 gp120-gp41 Association Site by Adjacent gp120 Variable Region 1 (V1) N-Glycans Linked to Neutralization Sensitivity

The HIV-1 gp120-gp41 complex, which mediates viral fusion and cellular entry, undergoes rapid evolution within its external glycan shield to enable escape from neutralizing antibody (NAb). Understanding how conserved protein determinants retain functionality in the context of such evolution is important for their evaluation and exploitation as potential drug and/ or vaccine targets. In this study, we examined how the conserved gp120-gp41 association site, formed by the N- and Cterminal segments of gp120 and the disulfide-bonded region (DSR) of gp41, adapts to glycan changes that are linked to neutralization sensitivity. To this end, a DSR mutant virus (K601D) with defective gp120-association was sequentially passaged in peripheral blood mononuclear cells to select suppressor mutations. We reasoned that the locations of suppressors point to structural elements that are functionally linked to the gp120-gp41 association site. In culture 1, gp120 association and viral replication was restored by loss of the conserved glycan at Asn136 in V1 (T138N mutation) in
conjunction with the L494I substitution in C5 within the association site. In culture 2, replication was restored with deletion of the N139INN sequence, which ablates the overlapping Asn141-Asn142-Ser-Ser potential N-linked glycosylation sequons in
V1, in conjunction with D601N in the DSR. The 136 and 142 glycan mutations appeared to exert their suppressive effects by altering the dependence of gp120-gp41 interactions on the DSR residues, Leu593, Trp596 and Lys601. The 136 and/or 142
glycan mutations increased the sensitivity of HIV-1 pseudovirions to the glycan-dependent NAbs 2G12 and PG16, and also pooled IgG obtained from HIV-1-infected individuals. Thus adjacent V1 glycans allosterically modulate the distal gp120-
gp41 association site. We propose that this represents a mechanism for functional adaptation of the gp120-gp41 association site to an evolving glycan shield in a setting of NAb selection.

Potassium channel modulation by a toxin domain in matrix metalloprotease

Peptide toxins found in a wide array of venoms block K+ channels, causing profound physiological and pathological effects. Here we describe the first functional K+ channel-blocking toxin domain in a mammalian protein. MMP23 (matrix metalloprotease 23) contains a domain (MMP23TxD) that is evolutionarily related to peptide toxins from sea anemones. MMP23TxD shows close structural similarity to the sea anemone toxins BgK and ShK. Moreover, this domain blocks K+ channels in the nanomolar to low micromolar range (Kv1.6 > Kv1.3 > Kv1.1 = Kv3.2 > Kv1.4, in decreasing order of potency) while sparing other K+ channels (Kv1.2, Kv1.5, Kv1.7, and KCa3.1). Full-length MMP23 suppresses K+ channels by co-localizing with and trapping MMP23TxD-sensitive channels in the ER. Our results provide clues to the structure and function of the vast family of proteins that contain domains related to sea anemone toxins. Evolutionary pressure to maintain a channel-modulatory function may contribute to the conservation of this domain throughout the plant and animal kingdoms.

Space vector modulation based fast speed response field-orientation control of induction motor drive with adaptive neural integrator

This paper presents a novel fast speed response control strategy for the poly-phase induction motor drive system based on flux angle. The control scheme is derived in rotor field coordinates and employs the estimation of the rotor flux and its position. An adaptive notch filter is proposed to eliminate the dc component of the integration of signals used for the rotor flux estimation. To improve the performance of the rotor flux estimator, derivative term of the back emf is incorporated in the system. The voltage components in the synchronous reference frame are generated in the controllers which are transformed to stationary reference frame for driving the motor. Space vector modulation technique is used here. Simulation of the drive system was carried out and the results were compared with those obtained for a system that produces the above mentioned voltage components using the conventional PI controller. It is observed that the proposed control methodology provides faster response than the conventional PI controller incorporated system.

Lack of seasonal and moult-related stress modulation in an opportunistically breeding bird: the white-plumed honeyeater (Lichenostomus penicillatus).

In most vertebrate species, glucocorticoid levels and stress sensitivity vary in relation to season and life-history stage. In birds, baseline corticosterone (CORT) and stress sensitivity are typically highest while breeding and decrease substantially during moult. Because elevated CORT adversely affects protein synthesis, moult-related CORT suppression is thought to be necessary for forming high-quality feathers. Surprisingly, some passerine species lack moult-related CORT suppression, but these are distinguished by having slow rates of moult and being opportunistic breeders. We examined baseline and stress-induced CORT levels in an opportunistically breeding Australian passerine, the white-plumed honeyeater (Lichenostomus penicillatus). Although this species has a slower moult rate than high-latitiude breeders, it differs little from north-temperate passerines. Neither baseline nor stress-induced CORT levels varied with season (winter, spring or summer), sex or moult status in adult birds. While breeding tended to be highest in early spring through late summer, laparotomies revealed only limited reduction in testicular size in males the year round. In all but one sampling period, at least some females displayed follicular hierarchy. Breeding usually coincides with outbreaks of phytophagous insects, which can happen at any time of the year. This results in moult/breeding overlap when infestations occur in late spring or summer. The ability of this species to moult and breed at the same time while having breeding-levels of CORT demonstrates that CORT suppression is not a prerequisite for synthesis of high-quality feathers. An experimental design incorporating moulting and non-moulting phenotypes is suggested to test the functional significance of CORT suppression in other species.

miRNA modulation of SOCS1 using an influenza A virus delivery system

Difficulties associated with efficient delivery and targeting of miRNAs to cells is hampering the real world application of miRNA technology. This study utilized an influenza A-based delivery system to express miR-155 in order to knockdown SOCS1 mRNA. Using qPCR and dual luciferase technology we show that miR-155 delivery resulted in a significant increase in cellular miR-155 which facilitated a downregulation of SOCS1 gene expression and a functional increase in IL-6 and IFN-β cytokines.

Breakdown in central motor control can be attenuated by motor practice and neuro-modulation of the primary motor cortex

The performance of a repetitive index finger flexion–extension task at maximal voluntary rate (MVR) begins to decline just a few seconds into the task and we have previously postulated that this breakdown has a central origin. To test this hypothesis, we have combined two objectives; to determine whether motor practice can lessen the performance deterioration in an MVR task, and whether further gains can be achieved with a transcranial magnetic stimulation (TMS) protocol that increases corticomotor excitability (CME). Eleven right-handed subjects participated in a randomized crossover study design that consisted of a 15-min interventional TMS at I-wave periodicity (ITMS) and single-pulsed Sham intervention prior to six 10-s practice sets of a repetitive finger flexion–extension task at MVR. Motor-evoked potentials (MEPs) were recorded from the first dorsal interosseous muscle. The starting movement rate, and the percentage decline in rate by the end of the MVR were quantitated. Training of the MVR task improved the sustainability of the task by reducing the decline in movement rate. CME increased steadily after each training bout, and this increase was maintained up to 20 min after the last bout. ITMS further increased CME, and was associated with an increase in both the starting rate of the MVR task and its sustainability, when compared to Sham. The results implicate central motor processes in the performance and sustainability of the MVR task, and indicate that MVR kinematics can improve with short-term training and with non-invasive neuro-modulation.

Modulation of corticomotor excitability after maximal or sustainable-rate repetitive finger movement is impaired in Parkinson’s disease and is reversed by levodopa

Objectives: In healthy subjects, fatiguing exercises induce a period of post-exercise corticomotor depression (PECD) that is absent in Parkinson’s disease (PD). Our objective is to determine the time-course of corticomotor excitability changes following a 10-s repetitive index finger flexion–extension task performed at maximal voluntary rate (MVR) and a slower sustainable rate (MSR) in PD patients OFF and ON levodopa.
Methods: In 11 PD patients and 10 healthy age-matched controls, motor evoked potentials (MEPs) were recorded from the extensor indicis proprius (EIP) and first dorsal interosseous (FDI) muscles of the dominant arm immediately after the two tasks and at 2-min intervals for 10 min.
Results: In the OFF condition the PECD was absent in the two test muscles after both the MVR and MSR tasks. In the ON condition finger movement kinematics improved and a period of PECD comparable to that in controls was present after both tasks.
Conclusion: The absence of PECD in PD subjects off medication indicates a persisting increase in corticomotor excitability after non-fatiguing repetitive finger movement that is reversed by levodopa.