Exploring Ecoacoustic Trajectories in a Giant Sequoia Forest After Wildfire

Forest management strategies that create spatially diverse fire-caused disturbance outcomes, consistent with historic fire regimes, are a desired condition for fire adapted western United States forests. In this context, the temporal dynamics of forest response to fire can inform the tempo and scale of forest management, including prescribed burning. Here, we investigated the use of ecoacoustic methods to assess ecological condition in a four-year period (2016–2019) after wildfire in a giant sequoia forest landscape within Kings Canyon National Park, California, United States. Audio recorders at nine sites were deployed soon after the 2015 Rough Fire subsided. The monitoring sites were located in regions with different fire histories, representing five fire history categories. We used the Acoustic Complexity Index (ACI) to document biotic chorus complexity. This previously tested ecoacoustic index provided a daily indicator of biotic sound activity in frequencies dominated by avian calls. Patterns in ACI were evaluated using generalized additive mixed models to understand the relationship with time-since-fire and covariates that accounted for season, fire history category, and weather conditions. We showed that time-since fire and fire-history influenced patterns in ACI after accounting for season and air temperature effects. Monitoring sites where prescribed fire preceded the Rough Fire showed the highest predicted ACI and evidence for a relatively consistent seasonal pattern in ecoacoustic activity across subsequent seasons. Sites without prescribed fire and burned by the Rough Fire exhibited the most pronounced successive decreases in ACI in the first and second years after the fire. The daily temporal resolution of the ecoacoustic index also revealed phenological shifts related to time-since-fire and fire history. Sites unburned by the Rough Fire offered some context for how fire changed ecoacoustic activity post-wildfire, however evidence suggested they were also impacted by the presence of the nearby Rough Fire. The patterns in the ecoacoustic index when combined with vegetation surveys offered complementary insights into ecological dynamics of regeneration after fire. Our exploratory analysis showed that using ecoacoustic methods in wildfire monitoring offers a scalable approach to remote sensing of ecological trends. Archived recordings from the monitoring effort afford future opportunities for new or more detailed insights

Anthropogenic noise events perturb acoustic communication networks

Anthropogenic noise sources impact ecological processes by altering wildlife behavior and interactions with cascading impacts on community structure. The distribution and magnitude of such noise has grown exponentially over the past century, and now inundates even remote areas. Here we investigate biological responses to prolific, anthropogenic noise sources associated with the physical presence of the source (vehicle noise and human voices) and disconnected from it (aircraft overflight). Bioacoustic responses to these noise sources were documented at 103 sites in 40 U. S. National Park units. The presence of bird sounds was noted in 10-s audio samples every 2 min, for 8 days at each site and related to the presence of human voices, vehicle noise, and aircraft noise in the same and preceding samples. Generalized additive models were used to fit smoothing splines to weight the influence of noise in past samples on the probability of detecting bird sounds in the present sample. We found that the probability of hearing birds increased immediately following noise events, and decreased about 2 h after the event. The negative effects were persistent more than 3 h after a noise event. The persistence of these responses – especially for noise from jets that were many kilometers distant – raises questions about the functional significance and ecological consequences of this altered activity, particularly in light of the widespread and diverse habitats in this study and ubiquity of the noise sources evaluated

Why conservation biology can benefit from sensory ecology

Global expansion of human activities is associated with the introduction of novel stimuli, such as anthropogenic noise, artificial lights and chemical agents. Progress in documenting the ecological effects of sensory pollutants is weakened by sparse knowledge of the mechanisms underlying these effects. This severely limits our capacity to devise mitigation measures. Here, we integrate knowledge of animal sensory ecology, physiology and life history to articulate three perceptual mechanisms—masking, distracting and misleading—that clearly explain how and why anthropogenic sensory pollutants impact organisms. We then link these three mechanisms to ecological consequences and discuss their implications for conservation. We argue that this framework can reveal the presence of ‘sensory danger zones’, hotspots of conservation concern where sensory pollutants overlap in space and time with an organism’s activity, and foster development of strategic interventions to mitigate the impact of sensory pollutants. Future research that applies this framework will provide critical insight to preserve the natural sensory world

De novo CCND2 mutations leading to stabilization of cyclin D2 cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome

Activating mutations in genes encoding phosphatidylinositol 3-kinase (PI3K)-AKT pathway components cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome (MPPH, OMIM 603387). Here we report that individuals with MPPH lacking upstream PI3K-AKT pathway mutations carry de novo mutations in CCND2 (encoding cyclin D2) that are clustered around a residue that can be phosphorylated by glycogen synthase kinase 3β (GSK-3β). Mutant CCND2 was resistant to proteasomal degradation in vitro compared to wild-type CCND2. The PI3K-AKT pathway modulates GSK-3β activity, and cells from individuals with PIK3CA, PIK3R2 or AKT3 mutations showed similar CCND2 accumulation. CCND2 was expressed at higher levels in brains of mouse embryos expressing activated AKT3. In utero electroporation of mutant CCND2 into embryonic mouse brains produced more proliferating transfected progenitors and a smaller fraction of progenitors exiting the cell cycle compared to cells electroporated with wild-type CCND2. These observations suggest that cyclin D2 stabilization, caused by CCND2 mutation or PI3K-AKT activation, is a unifying mechanism in PI3K-AKT–related megalencephaly syndromes

The genetic landscape of high-risk neuroblastoma

Neuroblastoma is a malignancy of the developing sympathetic nervous system that often presents with widespread metastatic disease, resulting in survival rates of less than 50%1. To determine the spectrum of somatic mutation in high-risk neuroblastoma, we studied 240 cases using a combination of whole exome, genome and transcriptome sequencing as part of the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) initiative. Here we report a low median exonic mutation frequency of 0.60 per megabase (0.48 non-silent), and remarkably few recurrently mutated genes in these tumors. Genes with significant somatic mutation frequencies included ALK (9.2% of cases), PTPN11 (2.9%), ATRX (2.5%, an additional 7.1% had focal deletions), MYCN (1.7%, a recurrent p.Pro44Leu alteration), and NRAS (0.83%). Rare, potentially pathogenic germline variants were significantly enriched in ALK, CHEK2, PINK1, and BARD1. The relative paucity of recurrent somatic mutations in neuroblastoma challenges current therapeutic strategies reliant upon frequently altered oncogenic drivers

Escape from Autologous Neutralizing Antibodies in Acute/Early Subtype C HIV-1 Infection Requires Multiple Pathways

One aim for an HIV vaccine is to elicit neutralizing antibodies (Nab) that can limit replication of genetically diverse viruses and prevent establishment of a new infection. Thus, identifying the strengths and weaknesses of Nab during the early stages of natural infection could prove useful in achieving this goal. Here we demonstrate that viral escape readily occurred despite the development of high titer autologous Nab in two subjects with acute/early subtype C infection. To provide a detailed portrayal of the escape pathways, Nab resistant variants identified at multiple time points were used to create a series of envelope (Env) glycoprotein chimeras and mutants within the background of a corresponding newly transmitted Env. In one subject, Nab escape was driven predominantly by changes in the region of gp120 that extends from the beginning of the V3 domain to the end of the V5 domain (V3V5). However, Nab escape pathways in this subject oscillated and at times required cooperation between V1V2 and the gp41 ectodomain. In the second subject, escape was driven by changes in V1V2. This V1V2-dependent escape pathway was retained over time, and its utility was reflected in the virus's ability to escape from two distinct monoclonal antibodies (Mabs) derived from this same patient via introduction of a single potential N-linked glycosylation site in V2. Spatial representation of the sequence changes in gp120 suggested that selective pressure acted upon the same regions of Env in these two subjects, even though the Env domains that drove escape were different. Together the findings argue that a single mutational pathway is not sufficient to confer escape in early subtype C HIV-1 infection, and support a model in which multiple strategies, including potential glycan shifts, direct alteration of an epitope sequence, and cooperative Env domain conformational masking, are used to evade neutralization

Mutations in DCC cause isolated agenesis of the corpus callosum with incomplete penetrance

Brain malformations involving the corpus callosum are common in children with developmental disabilities. We identified DCC mutations in four families and five sporadic individuals with isolated agenesis of the corpus callosum (ACC) without intellectual disability. DCC mutations result in variable dominant phenotypes with decreased penetrance, including mirror movements and ACC associated with a favorable developmental prognosis. Possible phenotypic modifiers include the type and location of mutation and the sex of the individual