Ears achieve their exquisite sensitivity by means of mechanical feedback: motile mechanosensory cells through their active motion boost the mechanical input from the ear. Examination of the auditory mechanics in Drosophila melanogaster mutants shows that the transient receptor potential (TRP) channel NompC is required to promote this feedback, whereas the TRP vanilloid (TRPV) channels Nan and Iav serve to control the feedback gain. The combined function of these channels specifies the sensitivity of the fly auditory organ.

Hearing relies on dedicated mechanotransducer channels that convert sound-induced vibrations into electrical signals [1]. Linking this transduction to identified proteins has proven difficult because of the scarcity of native auditory transducers and their tight functional integration into ears [2-4]. We describe an in vivo paradigm for the noninvasive study of auditory transduction. By investigating displacement responses of the Drosophila sound receiver, we identify mechanical signatures that are consistent with a direct mechanotransducer gating in the fly's ear. These signatures include a nonlinear compliance that correlates with electrical nerve responses, shifts with adaptation, and conforms to the gating-spring model of vertebrate auditory transduction. Analyzing this gating compliance in terms of the gating-spring model reveals striking parallels between the transducer mechanisms for hearing in vertebrates and flies. Our findings provide first insights into the mechanical workings of invertebrate mechanotransducer channels and set the stage for using Drosophila to specifically search for, and probe the roles of, auditory transducer components.

Circadian clocks are synchronized by the natural day/night and temperature cycles. Our previous work demonstrated that synchronization by temperature is a tissue autonomous process, similar to synchronization by light. We show here that this is indeed the case, with the important exception of the brain. Using luciferase imaging we demonstrate that brain clock neurons depend on signals from peripheral tissues in order to be synchronized by temperature. Reducing the function of the gene nocte in chordotonal organs changes their structure and function and dramatically interferes with temperature synchronization of behavioral activity. Other mutants known to affect the function of these sensory organs also interfere with temperature synchronization, demonstrating the importance of nocte in this process and identifying the chordotonal organs as relevant sensory structures. Our work reveals surprising and important mechanistic differences between light- and temperature-synchronization and advances our understanding of how clock resetting is accomplished in nature.