Born to Cry: A Genetic Dissection of Infant Vocalization.

David George Ashbrook,Tobias Riede,Brittany G Clifford,Lu Lu,Robert W Williams,Snigdha Roy,Maria Luisa Scattoni,Detlef H Heck

doi:10.3389/fnbeh.2018.00250

Abstract

Infant vocalizations are one of the most fundamental and innate forms of behavior throughout avian and mammalian orders. They have a critical role in motivating parental care and contribute significantly to fitness and reproductive success. Dysregulation of these vocalizations has been reported to predict risk of central nervous system pathologies such as hypoxia, meningitis, or autism spectrum disorder. Here, we have used the expanded BXD family of mice, and a diallel cross between DBA/2J and C57BL/6J parental strains, to begin the process of genetically dissecting the numerous facets of infant vocalizations. We calculate heritability, estimate the role of parent-of-origin effects, and identify novel quantitative trait loci (QTLs) that control ultrasonic vocalizations (USVs) on postnatal days 7, 8, and 9; a stage that closely matches human infants at birth. Heritability estimates for the number and frequency of calls are low, suggesting that these traits are under high selective pressure. In contrast, duration and amplitude of calls have higher heritabilities, indicating lower selection, or their importance for kin recognition. We find suggestive evidence that amplitude of infant calls is dependent on the maternal genotype, independent of shared genetic variants. Finally, we identify two loci on Chrs 2 and 14 influencing call frequency, and a third locus on Chr 8 influencing the amplitude of vocalizations. All three loci contain strong candidate genes that merit further analysis. Understanding the genetic control of infant vocalizations is not just important for understanding the evolution of parent–offspring interactions, but also in understanding the earliest innate behaviors, the development of parent–offspring relations, and the early identification of behavioral abnormalities.

Highlights

Vocal communication is important for social interactions in all mammals, and it begins in rodents on the first postnatal day with the communication between an infant and its parents (Doty, 1974; Ehret and Haack, 1982; Maggio and Whitney, 1986; Oller et al, 2013; Arriaga, 2014)
Since we identified a clear effect of strain, and of genotype, on quantitative ultrasonic vocalizations (USVs) phenotypes above, we can examine whether these genetic effects are likely to be caused by a small number of loci with large effects, or a large number of loci of small effect
We found differences between by crossing C57BL/6J (B6) and D2 strains in four important acoustic features: (a) mean fundamental frequency is higher in B6, (b) sound amplitude is higher in D2 USVs, (c) ultrasonic calls are longer in D2 and (d) D2 pups vocalize at a higher rate (Figure 2)

Summary

Introduction

Vocal communication is important for social interactions in all mammals, and it begins in rodents on the first postnatal day with the communication between an infant and its parents (Doty, 1974; Ehret and Haack, 1982; Maggio and Whitney, 1986; Oller et al, 2013; Arriaga, 2014). Mouse pups produce high frequency ultrasonic vocalizations (USVs) when stressed by loss of body temperature (Okon, 1970a), by hunger or by separation from the mother (Noirot, 1966; Ehret, 2005). Pups vocalize in response to intense tactile stimulation (Okon, 1970b). Rodent USVs are prominent soon after birth and are useful as a phenotyping tool (Roubertoux et al, 1996; Scattoni et al, 2009; Roy et al, 2012; Wöhr, 2014; Riede et al, 2015)

Methods

Results

Conclusion