To evaluate the effects of calling site on call degradation, we broadcast synthetic advertisement calls of male gray treefrogs through forest, over open terrain, and across pond water. Calls were recorded at distances of 1, 2, 4, 8, 16, and 32 m. We varied speaker and microphone heights for a total of five elevation combinations ranging from surface level to a height of 1.5 m. We quantified structural degradation in recorded calls using BΔV,^a measure of relative sound energy in call pulses and interpulse intervals. A subset of recorded calls was used in two-speaker discrimination tests with females. Finally, we examined male selection of perch height by recording locations of calling males on ladder-like trellises positioned around the periphery of a breeding pond. We found the greatest degradation for calls broadcast through forest followed by calls transmitted across open terrain and then pond water. At relatively small source-receiver separations, elevation had only small effects on degradation. However, for separations greater than 4 m (especially through forest), elevation had a significant impact on ΔV-with calls broadcast and recorded near the substrate particularly vulnerable to degradation. Choice tests demonstrated that such levels of degradation could significantly reduce a male's attractiveness. This may, in part, explain why males only seldom called from low rungs of trellises.
SUMMARYResearch has demonstrated that certain midbrain neurons of anurans 'count' interpulse intervals (IPIs). Some neurons fire after exposure to fewer intervals than do others. Counting can be reset to zero if an IPI falls outside the cell's tolerance range. We tested female gray treefrogs for behavioral correlates of these neural response patterns using phonotaxis tests in order to gain a better understanding of the mechanistic bases of female responses to calls. For example, previous work demonstrated females often prefer longer to shorter pulsed advertisement calls, even when the former occur at lower rates. Call attractiveness can also be reduced when pulse duration and timing have been manipulated experimentally or disrupted by acoustic interference. In this study, female responses were consistent with neural data, emphasizing the importance of IPIs. Females discriminated in favor of calls with normal interpulse timing relative to those in which a single IPI was too long or too short. Our data suggest that neural resetting of interval counting by inappropriate intervals may more strongly influence females than reduced firing in response to such intervals on an individual basis. Data also suggest a transition point between 125ms and 175ms at which an interval between pulse strings is treated as an interval between calls.
The Retinoblastoma protein (Rb) is important in the control of cell proliferation and apoptosis. Its activity is controlled by reversible phosphorylation on several serine and threonine residues. When Rb is hypophosphorylated, it inhibits proliferation by preventing passage through the G1- S phase transition. Hyperphosphorylated Rb promotes cell cycle progression. The role of Rb phosphorylation in the control of apoptosis is largely unknown, although several apoptotic stimuli result in dephosphorylation of Rb. It may be the case that dephosphorylation of specific amino acids may signal apoptosis versus cell cycle arrest. Using glutamic acid mutagenesis, we have generated 15 single phosphorylation site mutants from serine/threonine to glutamic acid, to mimic the phosphorylated state. By calcium phosphate transfection mutant plasmids were introduced into C33A Rb-null cells and apoptosis was induced using UV. Apoptosis was measured by ELISA detection of degraded DNA and by immunoblotting to assess proteolytic cleavage of PARP. We found that only threonine-821 when mutated to glutamic acid blocked apoptosis by 50% whereas other sites tested had little effect. In addition, endogenous Rb is dephosphorylated on threonine-821 when cells are undergoing apoptosis. Experiments to determine the effect of this mutation in response to additional apoptotic stimuli are underway. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1193. doi:1538-7445.AM2012-1193
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.