Presentations

Abstract

Bats have a sophisticated audio-vocal system that allows them t
o orientate in the dark, acoustically
discriminate prey and surface structures, and identify conspeci
fics. To date, research into this area has
largely focused on bat echoloca
tion. However, their highly soci
al nature and complex communication calls
make them a well-suited animal model for studying vocal communi
cation: several bat species have been
found to have extensive call repertoires and to exhibit a rich
palette of acoustic social interactions.
Sophisticated song and syllable formation, the ability for voca
l learning, and complex social interactions
such as turn-taking (antiphonal vocalizations) have all been ob
served. Given the importance of vocal
learning in humans for spoken language and turn-taking for ling
uistic interactions, we are investigating
these abilities in the lesser spear-nosed bat
Phyllostomus discolor.
To assess turn-taking behavior we are
evaluating vocal interactions between groups of animals in audi
o/video recordings. To verify vocal
learning, and specifically production learning, we have develop
ed a multistage training plan, in which adult
San Antonio, Texas
44 | P a g e
bats will be trained via an ultrasonic intercom to adjust their
calls according to electronically transmitted
calls of conspecifics. Adult bats will be trained with food rew
ard to adjust the spectral and/or temporal
parameters of their calls to match playbacks of modified conspe
cific calls (assessed via spectro-temporal
analyses before and after the training period). These studies w
ill demonstrate fundamental aspects of vocal
communicative behaviour in
Phyllostomus discolor
, including behaviors that may ultimately be relevant
for our understanding of the evol
ution of spoken language in hu
mans.

Abstract

The capacity for speech and language is a fundamental trait of humankind, but its genetic encoding is poorly understood. I will present a range of diverse but complementary approaches to study the genetic underpinnings of speech and language including; clinical studies that investigate the molecular mechanisms underlying speech and language disorders; neuromolecular studies that demonstrate how such genes influence neuronal development and function; and work in animal models linking gene function to behaviours relevant for speech and language

Abstract

The ability to use language is a uniquely human trait involving one of the most complex and poorly understood biological processes. This is particularly true when considering the encoding of human language at the molecular level. Disorders of speech and language are highly heritable and widely prevalent in the general population. Approximately 7% of school age children display specific language impairment (SLI) and language deficiencies are known to feature in a range of common neurodevelopmental disorders such as autism spectrum disorders. The first direct insights into the molecular basis of language were given by the identification of the FOXP2 gene. Mutations in this gene were shown to be causative of a rare speech and language disorder in a large pedigree. Since then, a number of FOXP2 disruptions in unrelated patients displaying a similar phenotype have been reported. However FOXP2 remains the only known monogenic cause of language disorder and little progress has been made via traditional genetic approaches to understanding the molecular basis of language and language impairment. Given that FOXP2 acts as a transcription factor to regulate target gene expression, we hypothesized that understanding the downstream regulatory pathways would give insight into the molecular basis of normal language development and language disorder. We have identified gene networks regulated by FOXP2 that have been implicated in language development and demonstrated that new candidates for involvement in common language disorders can be found by identifying genes that act in these pathways. Our recent findings modeling Foxp2 pathways in the brain, suggest that neuronal connectivity and circuit formation is disturbed in particular types of language disorder due to neurite outgrowth defects during development. We are currently studying how effects on this and other FOXP2 related pathways that we have identified (including Wnt signalling and non-coding RNA pathways) are involved in neural circuit formation and language development, and investigating genetic risk factors from these pathways in patients via genome based screening studies. This novel approach will help us to understand the fundamental neurodevelopmental basis of language and pinpoint genetic risk factors for language impairments.

Abstract

The ability to use language is a uniquely human trait involving one of the most complex and poorly understood biological processes. This is particularly true when considering the encoding of human language at the molecular level. Disorders of speech and language are highly heritable and widely prevalent in the general population. Approximately 7% of school age children display specific language impairment (SLI) and language deficiencies are known to feature in a range of common neurodevelopmental disorders such as autism spectrum disorders. The first direct insights into the molecular basis of language were given by the identification of the FOXP2 gene. Mutations in this gene were shown to be causative of a rare speech and language disorder in a large pedigree. Since then, a number of FOXP2 disruptions in unrelated patients displaying a similar phenotype have been reported. However FOXP2 remains the only known monogenic cause of language disorder and little progress has been made via traditional genetic approaches to understanding the molecular basis of language and language impairment. Given that FOXP2 acts as a transcription factor to regulate target gene expression, we hypothesized that understanding the downstream regulatory pathways would give insight into the molecular basis of normal language development and language disorder. We have identified gene networks regulated by FOXP2 that have been implicated in language development and demonstrated that new candidates for involvement in common language disorders can be found by identifying genes that act in these pathways. Our recent findings modeling Foxp2 pathways in the brain, suggest that neuronal connectivity and circuit formation is disturbed in particular types of language disorder due to neurite outgrowth defects during development. We are currently studying how effects on this and other FOXP2 related pathways that we have identified (including Wnt signalling and non-coding RNA pathways) are involved in neural circuit formation and language development, and investigating genetic risk factors from these pathways in patients via genome based screening studies. This novel approach will help us to understand the fundamental neurodevelopmental basis of language and pinpoint genetic risk factors for language impairments.