Field Application of Sustained-Yield Harvest Management for Northern Bobwhite in Texas

Sustained-yield harvest (SYH) is considered a potentially viable strategy for managing harvest of northern bobwhites (Colinus virginianus). However, application of SYH has not been evaluated for northern bobwhites. We evaluated the application of using SYH as a harvest management strategy for bobwhite during the 2007 2008 and 2008 2009 hunting seasons in 2 ecoregions of Texas (Rolling Plains, South Texas Plains). We collected field data at 3 study sites/ecoregion (900 1,900 ha each; 2 hunted sites and 1 control) to estimate 4 demographic parameters (fall and spring density, overwinter survival in the absence of hunting, and harvest rate). We used these data to parameterize the additive harvest model for bobwhites and compare predictions of spring abundance of the model with field estimates. The additive harvest model, compared to field estimates, consistently underestimated spring population density (mean 6 SE) by 55.7 6 17.8% (2007 2008) and 34.1 6 4.9% (2008 2009) in the Rolling Plains, and by 26.4 6 25.3% (2007 2008) and 49.1 6 2.1% (2008 2009) in the South Texas Plains. Implementing SYH in the field, despite its potential benefits, will be challenging given the need for reliable estimates of 3 key population parameters (fall and spring density, and natural mortality in the absence of hunting) and the high variation often associated with them. Conservative harvest prescriptions based on the lower 95% CIs of fall density estimates may permit sustainable harvest despite variation in density estimates

A Simulation Model of Sustained-Yield Harvest for Northern Bobwhite in South Texas

Recommended sustainable harvest rates for northern bobwhite (Colinus virginianus) vary greatly and range from 25% to 70% of the prehunt population. Because northern bobwhite populations have declined across their geographic range, determining sustainable harvest levels is critical for effective management. Our objectives were to use simulation modeling to identify sustainable rates of bobwhite harvest, probability of population persistence, and minimum viable population estimates. We also conducted a sensitivity analysis to evaluate the impacts of harvest on northern bobwhite populations in Texas, USA. We constructed a simulation model using Program STELLA 9.0 for a hypothetical northern bobwhite population on 800 ha in the South Texas Plains USA and modeled population dynamics to 100 years over a range of harvest rates (0–40%). A 20% harvest rate produced the greatest average yields (mean ± standard error = 231 ± 10 bobwhites harvested/year). Given a quasi-extinction criterion of ≤40 bobwhites (≤0.05 bobwhite/ha), a 30% harvest rate resulted in a high probability of quasi-extinction (PE = 0.75) within 47.8 ± 2.3 years. A 40% harvest rate was not sustainable (PE = 1.0), with quasi-extinction occurring within 15.5 ± 2.6 years. Harvesting northern bobwhite populations in the South Texas Plains at rates of 20−25% of the prehunt population should maximize long-term harvest while minimizing the probability of population extinction. Spring densities of 0.60−0.80 bobwhite/ha may represent minimum viable spring densities for northern bobwhite populations in the South Texas Plains as these are the densities associated with sustainable 20-25% harvest rates. Harvest rates \u3e30% are likely to be excessive with respect to long-term population persistence for northern bobwhite populations in the South Texas Plains

Adaptor protein complex 4 deficiency: a paradigm of childhood-onset hereditary spastic paraplegia caused by defective protein trafficking

Deficiency of the adaptor protein complex 4 (AP-4) leads to childhood-onset hereditary spastic paraplegia (AP-4-HSP): SPG47 (AP4B1), SPG50 (AP4M1), SPG51 (AP4E1) and SPG52 (AP4S1). This study aims to evaluate the impact of loss-of-function variants in AP-4 subunits on intracellular protein trafficking using patient-derived cells. We investigated 15 patient-derived fibroblast lines and generated six lines of induced pluripotent stem cell (iPSC)-derived neurons covering a wide range of AP-4 variants. All patient-derived fibroblasts showed reduced levels of the AP4E1 subunit, a surrogate for levels of the AP-4 complex. The autophagy protein ATG9A accumulated in the trans-Golgi network and was depleted from peripheral compartments. Western blot analysis demonstrated a 3-5-fold increase in ATG9A expression in patient lines. ATG9A was redistributed upon re-expression of AP4B1 arguing that mistrafficking of ATG9A is AP-4-dependent. Examining the downstream effects of ATG9A mislocalization, we found that autophagic flux was intact in patient-derived fibroblasts both under nutrient-rich conditions and when autophagy is stimulated. Mitochondrial metabolism and intracellular iron content remained unchanged. In iPSC-derived cortical neurons from patients with AP4B1-associated SPG47, AP-4 subunit levels were reduced while ATG9A accumulated in the trans-Golgi network. Levels of the autophagy marker LC3-II were reduced, suggesting a neuron-specific alteration in autophagosome turnover. Neurite outgrowth and branching were reduced in AP-4-HSP neurons pointing to a role of AP-4-mediated protein trafficking in neuronal development. Collectively, our results establish ATG9A mislocalization as a key marker of AP-4 deficiency in patient-derived cells, including the first human neuron model of AP-4-HSP, which will aid diagnostic and therapeutic studies

Defining the clinical, molecular and imaging spectrum of adaptor protein complex 4-associated hereditary spastic paraplegia

Abstract Bi-allelic loss-of-function variants in genes that encode subunits of the adaptor protein complex 4 (AP-4) lead to prototypical yet poorly understood forms of childhood-onset and complex hereditary spastic paraplegia: SPG47 (AP4B1), SPG50 (AP4M1), SPG51 (AP4E1) and SPG52 (AP4S1). Here, we report a detailed cross-sectional analysis of clinical, imaging and molecular data of 156 patients from 101 families. Enrolled patients were of diverse ethnic backgrounds and covered a wide age range (1.0–49.3 years). While the mean age at symptom onset was 0.8 ± 0.6 years [standard deviation (SD), range 0.2–5.0], the mean age at diagnosis was 10.2 ± 8.5 years (SD, range 0.1–46.3). We define a set of core features: early-onset developmental delay with delayed motor milestones and significant speech delay (50% non-verbal); intellectual disability in the moderate to severe range; mild hypotonia in infancy followed by spastic diplegia (mean age: 8.4 ± 5.1 years, SD) and later tetraplegia (mean age: 16.1 ± 9.8 years, SD); postnatal microcephaly (83%); foot deformities (69%); and epilepsy (66%) that is intractable in a subset. At last follow-up, 36% ambulated with assistance (mean age: 8.9 ± 6.4 years, SD) and 54% were wheelchair-dependent (mean age: 13.4 ± 9.8 years, SD). Episodes of stereotypic laughing, possibly consistent with a pseudobulbar affect, were found in 56% of patients. Key features on neuroimaging include a thin corpus callosum (90%), ventriculomegaly (65%) often with colpocephaly, and periventricular white-matter signal abnormalities (68%). Iron deposition and polymicrogyria were found in a subset of patients. AP4B1-associated SPG47 and AP4M1-associated SPG50 accounted for the majority of cases. About two-thirds of patients were born to consanguineous parents, and 82% carried homozygous variants. Over 70 unique variants were present, the majority of which are frameshift or nonsense mutations. To track disease progression across the age spectrum, we defined the relationship between disease severity as measured by several rating scales and disease duration. We found that the presence of epilepsy, which manifested before the age of 3 years in the majority of patients, was associated with worse motor outcomes. Exploring genotype-phenotype correlations, we found that disease severity and major phenotypes were equally distributed among the four subtypes, establishing that SPG47, SPG50, SPG51 and SPG52 share a common phenotype, an ‘AP-4 deficiency syndrome’. By delineating the core clinical, imaging, and molecular features of AP-4-associated hereditary spastic paraplegia across the age spectrum our results will facilitate early diagnosis, enable counselling and anticipatory guidance of affected families and help define endpoints for future interventional trials.</jats:p