Roxanne J. Larsen

Mist netting bias, species accumulation curves, and the rediscovery of two bats on Montserrat (Lesser Antilles)

ABSTRACT Mist nets are commonly used to survey bat populations and to estimate bat biodiversity, but several studies have found that mist net capture data and methods are biased due to a number of factors, including size and placement of nets, and the frequency at which investigators check their nets. Despite the wealth of literature and anecdotal reports, few investigators have quantified the interactions of bats with mist nets directly. We employed night vision camcorders to monitor bat behavior when bats encountered a mist net and then utilized these data to reevaluate years of survey data collected on Montserrat, Lesser Antilles. We recorded 2,523 bat passes during 43.3 hours of videotaping in July 2005 and June 2006. Observations conducted on successive nights provide evidence of avoidance-learning behavior in bats. When a mist net was present, 5.4% of bats in the airspace came into contact with the net giving an overall capture rate of 3.2% (range 0–10.3%). Mist nets are not accurately sampling bats that utilize flyways on Montserrat and such fieldwork thereby generates potentially misleading data. Biodiversity assessments and conservation guidelines based on short-term mist net surveys alone are not sufficient or reliable in regards to bats. A pragmatic solution to reduce mist net bias is to repeatedly sample a target region, utilize a variety of netting sites, use variable net sets, and carefully analyze species accumulation curves.

Genetic Diversity of Neotropical Myotis (Chiroptera: Vespertilionidae) with an Emphasis on South American Species

Background Cryptic morphological variation in the Chiropteran genus Myotis limits the understanding of species boundaries and species richness within the genus. Several authors have suggested that it is likely there are unrecognized species-level lineages of Myotis in the Neotropics. This study provides an assessment of the diversity in New World Myotis by analyzing cytochrome-b gene variation from an expansive sample ranging throughout North, Central, and South America. We provide baseline genetic data for researchers investigating phylogeographic and phylogenetic patterns of Myotis in these regions, with an emphasis on South America. Methodology and Principal Findings Cytochrome-b sequences were generated and phylogenetically analyzed from 215 specimens, providing DNA sequence data for the most species of New World Myotis to date. Based on genetic data in our sample, and on comparisons with available DNA sequence data from GenBank, we estimate the number of species-level genetic lineages in South America alone to be at least 18, rather than the 15 species currently recognized. Conclusions Our findings provide evidence that the perception of lower species richness in South American Myotis is largely due to a combination of cryptic morphological variation and insufficient sampling coverage in genetic-based systematic studies. A more accurate assessment of the level of diversity and species richness in New World Myotis is not only helpful for delimiting species boundaries, but also for understanding evolutionary processes within this globally distributed bat genus.

Warning SINEs: Alu elements, evolution of the human brain, and the spectrum of neurological disease

Alu elements are a highly successful family of primate-specific retrotransposons that have fundamentally shaped primate evolution, including the evolution of our own species. Alus play critical roles in the formation of neurological networks and the epigenetic regulation of biochemical processes throughout the central nervous system (CNS), and thus are hypothesized to have contributed to the origin of human cognition. Despite the benefits that Alus provide, deleterious Alu activity is associated with a number of neurological and neurodegenerative disorders. In particular, neurological networks are potentially vulnerable to the epigenetic dysregulation of Alu elements operating across the suite of nuclear-encoded mitochondrial genes that are critical for both mitochondrial and CNS function. Here, we highlight the beneficial neurological aspects of Alu elements as well as their potential to cause disease by disrupting key cellular processes across the CNS. We identify at least 37 neurological and neurodegenerative disorders wherein deleterious Alu activity has been implicated as a contributing factor for the manifestation of disease, and for many of these disorders, this activity is operating on genes that are essential for proper mitochondrial function. We conclude that the epigenetic dysregulation of Alu elements can ultimately disrupt mitochondrial homeostasis within the CNS. This mechanism is a plausible source for the incipient neuronal stress that is consistently observed across a spectrum of sporadic neurological and neurodegenerative disorders.

Mechanisms for regulating step length while running towards and over an obstacle

The ability to run across uneven terrain with continuous stable movement is critical to the safety and efficiency of a runner. Successful step-to-step stabilization while running may be mediated by minor adjustments to a few key parameters (e.g., leg stiffness, step length, foot strike pattern). However, it is not known to what degree runners in relatively natural settings (e.g., trails, paved road, curbs) use the same strategies across multiple steps. This study investigates how three readily measurable running parameters - step length, foot placement, and foot strike pattern - are adjusted in response to encountering a typical urban obstacle - a sidewalk curb. Thirteen subjects were video-recorded as they ran at self-selected slow and fast paces. Runners targeted a specific distance before the curb for foot placement, and lengthened their step over the curb (p<0.0001) regardless of where the step over the curb was initiated. These strategies of adaptive locomotion disrupt step cycles temporarily, and may increase locomotor cost and muscle loading, but in the end assure dynamic stability and minimize the risk of injury over the duration of a run.

Alu elements, evolution of the human brain, and the spectrum of neurological disease

Alu elements are a highly successful family of primate-specific retrotransposons that have fundamentally shaped primate evolution, including the evolution of our own species. Alus play critical roles in the formation of neurological networks and the epigenetic regulation of biochemical processes throughout the central nervous system (CNS), and thus are hypothesized to have contributed to the origin of human cognition. Despite the positive aspects of Alus, deleterious Alu activity is associated with a number of neurological and neurodegenerative disorders. In particular, neurological networks are potentially vulnerable to the epigenetic dysregulation of Alu elements operating across the suite of nuclear-encoded mitochondrial genes that are critical for both mitochondrial and CNS function. Here, we highlight the beneficial neurological aspects of Alu elements as well as their potential to cause disease by disrupting key cellular processes across the CNS. We identify at least 37 neurological and neurodegenerative disorders wherein deleterious Alu activity has been implicated as a contributing factor for the manifestation of disease and, for many of these disorders, this activity is operating on genes that are essential for proper mitochondrial function. We conclude that the epigenetic dysregulation of Alu elements can ultimately disrupt mitochondrial homeostasis within the CNS. This mechanism is a plausible source for the incipient neuronal stress that is consistently observed across a spectrum of sporadic neurological and neurodegenerative disorders.