Silent sounds in the Andes: underwater vocalizations of three frog species with reduced tympanic middle ears (Anura: Telmatobiidae: Telmatobius)

Underwater vocalization in anurans is restricted to a few, distantly related species. In some of them, sound is transmitted through tympanic and extra-tympanic pathways. Members of the Andean genus Telmatobius Wiegmann, 1834 lack a tympanic membrane, and earlier reports assumed the absence of vocalizations in the genus. We recorded underwater vocalizations and examined the middle-ear morphology in three species of Telmatobius with different lifestyles: Telmatobius oxycephalus Vellard, 1946 (semiaquatic, riverine); Telmatobius hintoni Parker, 1940 (markedly aquatic, riverine); Telmatobius culeus (Garman 1876) (fully aquatic, lacustrine). Males emit underwater calls, which in the three species are simple and stereotyped; they consist of a repeated train of notes, with a low fundamental frequency (309–941 Hz). In each of the three species, the tympanic membrane is absent and the tympanic cavity is extremely reduced or absent, whereas the opercular system is well developed. Our data, along with prior knowledge in other species of anurans, suggest that the species examined here probably perceived sound through extra-tympanic pathways. Given the limited knowledge about underwater calling in anurans, Telmatobius seems a logical candidate to study the functional and evolutionary bases of underwater hearing and tympanic middle-ear reduction in anurans.

Prx1 and Prx2 in skeletogenesis: roles in the craniofacial region, inner ear and limbs

Prx1 and Prx2 are closely related paired-class homeobox genes that are expressed in very similar patterns predominantly in mesenchyme. Prx1 loss-of-function mutants show skeletal defects in skull, limbs and vertebral column (Martin, J. F., Bradley, A. and Olson, E. N. (1995) Genes Dev. 9, 1237–1249). We report here that mice in which Prx2 is inactivated by a lacZ insertion had no skeletal defects, whereas Prx1/Prx2 double mutants showed many novel abnormalities in addition to an aggravation of the Prx1 single mutant phenotype. We found defects in external, middle and inner ear, reduction or loss of skull bones, a reduced and sometimes cleft mandible, and limb abnormalities including postaxial polydactyly and bent zeugopods. A single, or no incisor was present in the lower jaw, and ectopic expression of Fgf8 and Pax9 was found medially in the mandibular arch. A novel method to detect β-galactosidase activity in hydroxyethylmethacrylate sections allowed detailed analysis of Prx2 expression in affected structures. Our results suggest a role for Prx genes in mediating epitheliomesenchymal interactions in inner ear and lower jaw. In addition, Prx1 and Prx2 are involved in interactions between perichondrium and chondrocytes that regulate their proliferation or differentiation in the bones of the zeugopods.