TY - JOUR
T1 - Tissue-specific disruption of rhythmic expression of Dec1 and Dec2 in clock mutant mice
AU - Noshiro, Mitsuhide
AU - Furukawa, Masae
AU - Honma, Sato
AU - Kawamoto, Takeshi
AU - Hamada, Taizo
AU - Honma, Ken Ichi
AU - Kato, Yukio
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2005/10
Y1 - 2005/10
N2 - DEC1 and DEC2-basic helix-loop-helix transcription factors-exhibit a arcadian expression in the suprachiasmatic nucleus and other peripheral tissues and seem to play roles in regulating the mammalian circadian rhythm by suppressing the CLOCK/BMAL1-activated promoters of Per1, Dec1, and Dec2. The authors present data on the expression patterns of mRNA for Dec1, Dec2, Per1, Dbp, and Npas2 in various tissues of wild-type and homozygous Clock mutant mice (Clock/Clock). The Clock mutation resulted in extreme reduction of Dec1 expression in kidney, heart, and skeletal muscle but not in liver, whereas it strongly repressed Dec2 expression in liver, kidney, and heart, while Dec2 expression in skeletal muscle remained rhythmic. Per1 also showed the tissue-dependent disruption of the rhythmicity by Clock mutation, whereas rhythmic expression of Dbp in Clock mutant mice disappeared in all tissues examined. Npas2, a structurally and functionally related gene to Clock, showed significant levels of expression in the liver and kidney with a robust rhythmicity, which was also affected by Clock mutation. These marked changes in the Dec1 and Dec2 expression, as well as in the Per1, Dbp, and Npas2 expression in the periphery by Clock mutation, indicated that CLOCK plays a major role in the expression of these genes in most tissues. However, circadian expression of Dec1 in liver and kidney and that of Dec2 in skeletal muscle of Clock mutant mice suggested that CLOCK-independent circadian regulation operates in some tissues.
AB - DEC1 and DEC2-basic helix-loop-helix transcription factors-exhibit a arcadian expression in the suprachiasmatic nucleus and other peripheral tissues and seem to play roles in regulating the mammalian circadian rhythm by suppressing the CLOCK/BMAL1-activated promoters of Per1, Dec1, and Dec2. The authors present data on the expression patterns of mRNA for Dec1, Dec2, Per1, Dbp, and Npas2 in various tissues of wild-type and homozygous Clock mutant mice (Clock/Clock). The Clock mutation resulted in extreme reduction of Dec1 expression in kidney, heart, and skeletal muscle but not in liver, whereas it strongly repressed Dec2 expression in liver, kidney, and heart, while Dec2 expression in skeletal muscle remained rhythmic. Per1 also showed the tissue-dependent disruption of the rhythmicity by Clock mutation, whereas rhythmic expression of Dbp in Clock mutant mice disappeared in all tissues examined. Npas2, a structurally and functionally related gene to Clock, showed significant levels of expression in the liver and kidney with a robust rhythmicity, which was also affected by Clock mutation. These marked changes in the Dec1 and Dec2 expression, as well as in the Per1, Dbp, and Npas2 expression in the periphery by Clock mutation, indicated that CLOCK plays a major role in the expression of these genes in most tissues. However, circadian expression of Dec1 in liver and kidney and that of Dec2 in skeletal muscle of Clock mutant mice suggested that CLOCK-independent circadian regulation operates in some tissues.
KW - Circadian rhythm
KW - Clock mutant mice
KW - Dbp
KW - Dec1
KW - Dec2
KW - Npas2
KW - Per2
KW - bHLH transcription factor
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U2 - 10.1177/0748730405280195
DO - 10.1177/0748730405280195
M3 - Article
C2 - 16267380
AN - SCOPUS:24944497666
VL - 20
SP - 404
EP - 418
JO - Journal of Biological Rhythms
JF - Journal of Biological Rhythms
SN - 0748-7304
IS - 5
ER -