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.
Subject(s)
Cilia/physiology , Hedgehog Proteins/metabolism , Larynx/embryology , Signal Transduction , Animals , Larynx/abnormalities , MiceABSTRACT
Vocalizations transmit information to social partners, and mice use these signals to exchange information during courtship. Ultrasonic vocalizations from adult males are tightly associated with their interactions with females, and vary as a function of male quality. Work in the last decade has established that the spectrotemporal features of male vocalizations are not learned, but that female attention toward specific vocal features is modified by social experience. Additionally, progress has been made on elucidating how mouse vocalizations are encoded in the auditory system, and on the olfactory circuits that trigger their production. Together these findings provide us with important insights into how vocal communication can contribute to social interactions.