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Page, B.

Publications and source records attributed to Page, B..

3 recordsLinked to original sources

Stochastic population models to identify optimal and cost-effective harvest strategies for feral pig eradication

Eradicating feral pigs from island ecosystems can assist in restoring damaged biodiversity values and protect commercial industries such as agriculture. Although many feral pig eradications have been attempted, management decisions are often led by practitioner experience rather than empirical evidence. Few interventions have been guided by population models to identify harvest rates necessary to achieve eradication within a specified time frame, nor have they applied data on control effort and cost to evaluate the relative cost-effectiveness of proposed control strategies. We used effort and cost data from a feral pig-control program on Kangaroo Island, South Australia over 17 months to derive functional-response relationships between control effort (hours pig-1) and pig abundance for four control methods: (i) ground-based shooting, (ii) trapping with remote triggers, (iii) poison baiting, and (iv) thermal-assisted aerial culling. We developed a stochastic Leslie matrix with compensatory density feedback on survival and fertility to project population trajectories from an initial population (N0) of 250 female pigs with an estimated island-wide carrying capacity (K) of 2500 over 3 and 10 years for populations subjected to an annual harvest of 35% to 95%. We built functional-response models to calculate annual effort and cost for six cull scenarios across all harvest rates. We derived total cost and effort over 3- and 10-year projections from the sum of annual cost and effort within the projection intervals. Pig populations were reduced to < 10% N0 based on harvest rates > 70% and 50% for culls of 3- and 10-year duration, respectively. In all scenarios except trapping only, the total cost to reduce population to [&le;] 10% of N0 decreased with increasing harvest proportion, with lower total costs incurred over 3 years compared to 10 years. The simulations suggest that the most cost-effective approach for most scenarios is to maximise annual harvest and complete eradication effort over the shortest periods.

ecology↗

Heterogeneity in human hippocampal CaMKII transcripts reveals an allosteric role for the hub domain in activity regulation

Ca2+-calmodulin dependent protein kinase II (CaMKII) plays a central role in Ca2+ signaling throughout the body. Specifically in the hippocampus, CaMKII is required for learning and memory. CaMKII is encoded by four highly conserved genes in vertebrates: , {beta}, {gamma}, and {delta}. AllCaMKIIs are comprised of a kinase domain, regulatory segment, variable linker region, and hub domain responsible for oligomerization. The four genes differ primarily in linker length and composition due to extensive alternative splicing. Here, we unambiguously report the heterogeneity of CaMKII transcripts in 3 complex samples of human hippocampus using Illumina sequencing. Our results show that hippocampal cells contain a diverse collection of 70 CaMKII transcripts from all four CaMKII genes. We characterized the Ca2+/CaM sensitivity of hippocampal CaMKII variants spanning a broad range of linker lengths and compositions. We demonstrate that the effect of the variable linker on Ca2+/CaM sensitivity is conditional on kinase and hub domains. Moreover, we reveal a novel role for the hub domain as an allosteric regulator of kinase activity, which may provide a new pharmacological target for modulating CaMKII activity. Using small angle X-ray scattering and single-particle electron cryo-microscopy, we present evidence for extensive interaction between the kinase and the hub domain, even in the presence of a 30-residue linker. Taken together, we propose that Ca2+/CaM sensitivity in CaMKII is gene-dependent and includes significant contributions from the hub. Our sequencing approach combined with biochemistry provides new insights into understanding the complex pool of endogenous CaMKII. One Sentence SummaryCaMKII is a well-conserved protein that is essential for learning and memory. When CaMKII is mutated in a mouse, this mouse has difficulty learning and remembering how to get through a maze. The hippocampus is the part of the brain required for memory. Here, we used a specific experiment to determine every type of CaMKII that is in a human hippocampus. We found 70 different types and then asked how these differences affect CaMKII function. These data provide evidence that an assembly domain of CaMKII plays an unexpected role regulating its activity. This new finding helps us better understand endogenous CaMKII in the brain and provides a new mechanism for modulating CaMKII activity.

biochemistry↗

Disabling Gβγ SNARE interaction in transgenic mice disrupts GPCR-mediated presynaptic inhibition leading to physiological and behavioral phenotypes.

Gi/o-coupled G-protein coupled receptors modulate neurotransmission presynaptically through inhibition of exocytosis. Release of G{beta}{gamma} subunits decreases the activity of voltage-gated calcium channels (VGCC), decreasing excitability. A less understood G{beta}{gamma}-mediated mechanism downstream of calcium entry is the binding of G{beta}{gamma} to SNARE complexes. Here, we create a mouse partially deficient in this interaction. SNAP25{Delta}3 homozygote animals are developmentally normalbut impaired gait and supraspinal nociception. They also have elevated stress-induced hyperthermia and impaired inhibitory postsynaptic responses to 2A-AR, but normal inhibitory postsynaptic responses to Gi/o-coupled GABAB receptor activation. SNAP25{Delta}3 homozygotes have deficits in inhibition of hippocampal postsynaptic responses to 5 HT1b agonists that affect hippocampal learning. These data suggest that Gi/o-coupled GPCR inhibition of exocytosis through the G{beta}{gamma}-SNARE interaction is a crucial component of numerous physiological and behavioral processes.

neuroscience↗