Abstract
Acoustic communication is fundamental to social interactions among animals, including humans. In fact, deficits in voice impair the quality of life for a large and diverse population of patients. Understanding the molecular genetic mechanisms of development and function in the vocal apparatus is thus an important challenge with relevance both to the basic biology of animal communication and to biomedicine. However, surprisingly little is known about the developmental biology of the mammalian larynx. Here, we used genetic fate mapping to chart the embryological origins of the tissues in the mouse larynx, and we describe the developmental etiology of laryngeal defects in mice with disruptions in cilia-mediated Hedgehog signaling. In addition, we show that mild laryngeal defects correlate with changes in the acoustic structure of vocalizations. Together, these data provide key new insights into the molecular genetics of form and function in the mammalian vocal apparatus.
Highlights
Vocal communication is fundamental to social interaction
Despite the fundamental role of the larynx and vocal folds in mammalian communication, we still understand little about the molecular genetic control of their development
We have explored the developmental basis for severe laryngeal defects in the ciliopathic Fuz mutant mice, and we describe qualitatively similar laryngeal defects, as well as vocalization defects, in mice mutant for the HH signal transduction protein Gli3
Summary
The voice is so crucial to our quality of life that the neurobiology of speech and language has been hotly studied for decades, as has the developmental biology of the ear These bodies of work stand in surprising contrast to our still rudimentary understanding of the developmental biology of the organs of vocalization, the larynx and vocal folds. Larynx and vocal fold morphology and elasticity are key factors influencing vocalization even in animals with widely divergent mechanisms of sound production (e.g. audible vocalizations in humans, ultrasound in rodents) This deficit in our understanding of laryngeal and vocal fold development is significant, because many people who are capable of normal speech still cannot communicate due to defects in voice (e.g. problems with pitch, loudness, etc.).
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