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Taste function in mice with a targeted mutation of the pkd1l3 gene
Theodore M Nelson1, Nelson D Lopezjimenez, Lino Tessarollo
1Monell Chemical Senses Center, PA 19104, USA. tnelson@monell.org
Abstract:
Recent studies, both in vitro and in vivo, have suggested the involvement of the polycystic kidney disease-1 and -2 like genes, Pkd1l3 and Pkd2l1, in acid taste transduction. In mice, disruption of taste cells expressing PKD2L1 eliminates gustatory neural responses to acids. However, no previous data exist on taste responses in the absence of PKD1L3 or on behavioral responses in mice lacking either of these proteins. In order to assess the function of PKD1L3, we genetically engineered mice with a targeted mutation of the Pkd1l3 gene. We then examined taste responsiveness of mutant and wild-type mice using several different approaches. In separate groups of mice, we measured preference scores in 48-h 2-bottle tests, determined NaCl or citric acid taste thresholds using a conditioned taste aversion technique, and conducted electrophysiological recordings of activity in the chorda tympani and glossopharyngeal nerves. Multiple taste compounds representing all major taste qualities were used in the preference tests and nerve-recording experiments. We found no significant reduction in taste responsiveness in Pkd1l3 mutant mice in behavioral or electrophysiological tests when compared with wild-type controls. Therefore, further studies are needed to elucidate the function of PKD1L3 in taste bud cells.
Insights
Polycystic kidney disease-1 like 3 (PKD1L3) is not essential for acid taste transduction in mice. Genetic disruption of PKD1L3 did not alter taste responses in behavioral or electrophysiological studies.
Area of Science:
- Genetics
- Neuroscience
- Sensory Biology
Background:
- Recent research implicates polycystic kidney disease-1 like genes (PKD1L3, PKD2L1) in acid taste transduction.
- While PKD2L1's role is supported by studies showing loss of acid taste response upon its disruption, PKD1L3's function remains unclear.
- No prior data existed on taste responses or behaviors in mice lacking PKD1L3.
Purpose of the Study:
- To investigate the function of PKD1L3 in taste transduction.
- To assess the role of PKD1L3 in behavioral and neural taste responses to acids and other taste qualities.
Main Methods:
- Genetically engineered Pkd1l3 mutant mice.
- Assessed taste responsiveness using 48-hour two-bottle preference tests.
- Determined taste thresholds for NaCl and citric acid via conditioned taste aversion.
- Performed electrophysiological recordings of chorda tympani and glossopharyngeal nerves.
Main Results:
- Pgd1l3 mutant mice showed no significant reduction in taste responsiveness compared to wild-type controls.
- Behavioral tests (preference, aversion) did not reveal altered taste perception in mutants.
- Electrophysiological recordings confirmed normal gustatory nerve activity in the absence of PKD1L3.
Conclusions:
- PKD1L3 is not essential for acid taste transduction in mice.
- The function of PKD1L3 in taste bud cells requires further investigation.
- Other genes or mechanisms may play a more significant role in PKD1L3-mediated taste signaling.
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