PT  - JOURNAL ARTICLE
AU  - Jia-Da Li
AU  - Wang-Ping Hu
AU  - Lisa Boehmer
AU  - Michelle Y. Cheng
AU  - Alex G. Lee
AU  - Alexander Jilek
AU  - Jerome M. Siegel
AU  - Qun-Yong Zhou
TI  - Attenuated Circadian Rhythms in Mice Lacking the <em>Prokineticin 2</em> Gene
AID  - 10.1523/JNEUROSCI.3679-06.2006
DP  - 2006 Nov 08
TA  - The Journal of Neuroscience
PG  - 11615--11623
VI  - 26
IP  - 45
4099  - http://www.jneurosci.org/content/26/45/11615.short
4100  - http://www.jneurosci.org/content/26/45/11615.full
SO  - J. Neurosci.2006 Nov 08; 26
AB  - Circadian clocks drive daily rhythms in virtually all organisms. In mammals, the suprachiasmatic nucleus (SCN) is recognized as the master clock that synchronizes central and peripheral oscillators to evoke circadian rhythms of diverse physiology and behavior. How the timing information is transmitted from the SCN clock to generate overt circadian rhythms is essentially unknown. Prokineticin 2 (PK2), a clock-controlled gene that encodes a secreted protein, has been indicated as a candidate SCN clock output signal that regulates circadian locomotor rhythm. Here we report the generation and analysis of PK2-null mice. The reduction of locomotor rhythms in PK2-null mice was apparent in both hybrid and inbred genetic backgrounds. PK2-null mice also displayed significantly reduced rhythmicity for a variety of other physiological and behavioral parameters, including sleep–wake cycle, body temperature, circulating glucocorticoid and glucose levels, as well as the expression of peripheral clock genes. In addition, PK2-null mice showed accelerated acquisition of food anticipatory activity during a daytime food restriction. We conclude that PK2, acting as a SCN output factor, is important for the maintenance of robust circadian rhythms.