PMID- 10652231
OWN - NLM
STAT- MEDLINE
DCOM- 20000301
LR  - 20091119
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 268
IP  - 1
DP  - 2000 Feb 5
TI  - Rhythmic expression of BMAL1 mRNA is altered in Clock mutant mice: differential
      regulation in the suprachiasmatic nucleus and peripheral tissues.
PG  - 164-71
AB  - BMAL1 is a putative clock gene which encodes a basic helix-loop-helix (bHLH)-PAS 
      transcription factor. To examine whether the CLOCK protein is required for the
      circadian expression of BMAL1 mRNA, in situ hybridization and Northern blot
      analysis were performed in the suprachiasmatic nucleus (SCN) and peripheral
      tissues of homozygous Clock mutant mice. In the SCN of Clock mutants, BMAL1 mRNA 
      did not oscillate significantly but apparently expressed with low levels, while
      in wild-type mice the mRNA was robustly oscillated in a circadian manner. The
      peak-trough amplitudes of BMAL1 mRNA levels were 6.5-, 8.6-, and 6.7-fold in
      liver, heart, and kidney of wild-type mice, respectively. In Clock mutants, the
      amplitudes were extremely damped to 1.2-, 2.1-, and 1.4-fold, respectively.
      Furthermore, expressions of BMAL1 mRNA in the peripheral of Clock mutant mice
      were close to the peak level in wild-type mice, whereas mPer2 mRNA levels were
      severely blunted at trough values. Daily expression of albumin site D-binding
      protein (DBP), a clock controlled output gene (CCG), was also abolished at trough
      values by the Clock mutation in all tissues examined. These observations suggest 
      that the circadian expression of BMAL1 mRNA is affected by the CLOCK-induced
      transcriptional feedback loop in the SCN and peripheral tissues in a different
      way and that the regulation mechanism appeared to be different from those in
      mPer2 and DBP expressions in vivo.
CI  - Copyright 2000 Academic Press.
FAU - Oishi, K
AU  - Oishi K
AD  - Ishida Group of Clock Gene, National Institute of Bioscience and Human
      Technology, Agency of Industrial Science and Technology, MITI, Higashi 1-1,
      Tsukuba, Ibaraki, 305-8566, Japan.
FAU - Fukui, H
AU  - Fukui H
FAU - Ishida, N
AU  - Ishida N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (ARNTL Transcription Factors)
RN  - 0 (ARNTL protein, human)
RN  - 0 (Arntl protein, mouse)
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Dbp protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - ARNTL Transcription Factors
MH  - Animals
MH  - Basic Helix-Loop-Helix Transcription Factors
MH  - Brain/metabolism
MH  - Circadian Rhythm/*genetics/*physiology
MH  - *DNA-Binding Proteins
MH  - Gene Expression
MH  - Gene Expression Regulation
MH  - Helix-Loop-Helix Motifs/genetics
MH  - Kidney/metabolism
MH  - Liver/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Mutant Strains
MH  - Myocardium/metabolism
MH  - RNA, Messenger/*genetics/*metabolism
MH  - Suprachiasmatic Nucleus/*metabolism
MH  - Tissue Distribution
MH  - Transcription Factors/*genetics
EDAT- 2000/02/01 09:00
MHDA- 2000/03/04 09:00
CRDT- 2000/02/01 09:00
PHST- 2000/02/01 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/02/01 09:00 [entrez]
AID - 10.1006/bbrc.1999.2054 [doi]
AID - S0006-291X(99)92054-5 [pii]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2000 Feb 5;268(1):164-71. doi:
      10.1006/bbrc.1999.2054.