QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, March 7, 2007, 27(10):2539-2547; doi:10.1523/JNEUROSCI.4870-06.2007

This Article Full Text Full Text (PDF) Supplemental Data Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Benito, J. Articles by Hardin, P. E. Search for Related Content PubMed PubMed Citation Articles by Benito, J. Articles by Hardin, P. E.

 Previous Article  |  Next Article 

Cellular/Molecular
PDP1 Functions Downstream of the Circadian Oscillator to Mediate Behavioral Rhythms

Juliana Benito,^1 * Hao Zheng,^1,2 * and Paul E. Hardin²

¹Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204, and ²Center for Research on Biological Clocks, Department of Biology, Texas A&M University, College Station, Texas 77843

Correspondence should be addressed to Dr. Paul E. Hardin, Center for Research on Biological Clocks, Department of Biology, Texas A&M University, College Station, TX 77843. Email: phardin{at}mail.bio.tamu.edu

The Drosophila circadian oscillator is composed of autoregulatory period/timeless (per/tim) and Clock (Clk) feedback loops that control rhythmic transcription. In the Clk loop, CLOCK-CYCLE heterodimers activate vrille (vri) and PAR domain protein 1 (Pdp1) transcription, then sequential repression by VRI and activation by PDP1 mediate rhythms in Clk transcription. Because VRI and PDP1 bind the same regulatory element, the VRI/PDP1 ratio is thought to control the level of Clk transcription. Thus, constant high or low PDP1 levels in clock cells should eliminate Clk mRNA cycling and disrupt circadian oscillator function. Here we show that reducing PDP1 levels in clock cells by 70% via RNA interference or increasing PDP1 levels by 10-fold in clock cells does not alter Clk mRNA cycling or circadian oscillator function. However, constant low or high PDP1 levels in clock cells disrupt locomotor activity rhythms despite persistent circadian oscillator function in brain pacemaker neurons that extend morphologically normal projections into the dorsal brain. These results demonstrate that the VRI/PDP1 ratio neither controls Clk mRNA cycling nor circadian oscillator function and argue that PDP1 is not essential for Clk activation. PDP1 is nevertheless required for behavioral rhythmicity, which suggests that it functions to regulate oscillator output.

Key words: circadian rhythms; transcription regulation; feedback; Drosophila; behavior; biological clocks

---

Received June 23, 2006; revised Jan. 19, 2006; accepted Feb. 1, 2007.

Correspondence should be addressed to Dr. Paul E. Hardin, Center for Research on Biological Clocks, Department of Biology, Texas A&M University, College Station, TX 77843. Email: phardin{at}mail.bio.tamu.edu

This article has been cited by other articles:

				B. Richier, C. Michard-Vanhee, A. Lamouroux, C. Papin, and F. Rouyer The Clockwork Orange Drosophila Protein Functions as Both an Activator and a Repressor of Clock Gene Expression J Biol Rhythms, April 1, 2008; 23(2): 103 - 116. [Abstract] [PDF]

				X. Zheng and A. Sehgal Probing the Relative Importance of Molecular Oscillations in the Circadian Clock Genetics, March 1, 2008; 178(3): 1147 - 1155. [Abstract] [Full Text] [PDF]

				V. Codd, D. Dolezel, J. Stehlik, A. Piccin, K. J. Garner, S. N. Racey, K. R. Straatman, E. J. Louis, R. Costa, I. Sauman, et al. Circadian Rhythm Gene Regulation in the Housefly Musca domestica Genetics, November 1, 2007; 177(3): 1539 - 1551. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help