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Letter
Nature 454, 771-775 (7 August 2008) | doi:10.1038/nature07090; Received 4 February 2008; Accepted 15 May 2008; Published online 29 June 2008
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Research Fellows in Pluripotent Stem Cell Technology
- The University of Nottingham
- Nottingham, UK
Faculty Position in Biochemistry
- University of Tuebingen
- Tuebingen 72076 Germany
cAMP signalling in mushroom bodies modulates temperature preference behaviour in Drosophila
Sung-Tae Hong1, Sunhoe Bang1, Seogang Hyun1, Jongkyun Kang1, Kyunghwa Jeong1, Donggi Paik1, Jongkyeong Chung1 & Jaeseob Kim1
- Department of Biological Sciences, Korea Advanced Institute of Science & Technology, Guseong-Dong, Yusong-Gu, Daejeon, 305-701, Korea
Correspondence to: Jaeseob Kim1 Correspondence and requests for materials should be addressed to J.K. (Email: kjaeseob@kaist.ac.kr).
Abstract
Homoiotherms, for example mammals, regulate their body temperature with physiological responses such as a change of metabolic rate and sweating. In contrast, the body temperature of poikilotherms, for example Drosophila, is the result of heat exchange with the surrounding environment as a result of the large ratio of surface area to volume of their bodies1, 2. Accordingly, these animals must instinctively move to places with an environmental temperature as close as possible to their genetically determined desired temperature. The temperature that Drosophila instinctively prefers has a function equivalent to the 'set point' temperature in mammals. Although various temperature-gated TRP channels have been discovered3, 4, molecular and cellular components in Drosophila brain responsible for determining the desired temperature remain unknown. We identified these components by performing a large-scale genetic screen of temperature preference behaviour (TPB) in Drosophila5, 6. In parallel, we mapped areas of the Drosophila brain controlling TPB by targeted inactivation of neurons with tetanus toxin7 and a potassium channel (Kir2.1)8 driven with various brain-specific GAL4s. Here we show that mushroom bodies (MBs) and the cyclic AMP–cAMP-dependent protein kinase A (cAMP–PKA) pathway are essential for controlling TPB. Furthermore, targeted expression of cAMP–PKA pathway components in only the MB was sufficient to rescue abnormal TPB of the corresponding mutants. Preferred temperatures were affected by the level of cAMP and PKA activity in the MBs in various PKA pathway mutants.
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