In mammals,
circadian genes, Clock, Arntl (also known as Bmal1), Cry1, Cry2, Per1, Per2, and Per3, are rhythmically transcribed every 24 h in almost all
organs and tissues to tick the
circadian clock. However, their expression and function in
oocytes and preimplantation
embryos have not been investigated. In this study we found that the
circadian clock may stop in
mouse oocytes and preimplantation
embryos.
Real-time PCR analysis revealed the presence of transcripts of these genes in both
oocytes and preimplantation
embryos; however, their amounts did not oscillate every 24 h in one- to four-cell and blastocyst-stage
embryos. Moreover,
immunofluorescence analyses revealed that
CLOCK,
ARNTL, and
CRY1 were localized similarly in the nuclei of
germinal vesicle (GV)
oocytes and one-cell- to four-cell-stage
embryos. Because
CRY1 is known to interact with the CLOCK-ARNTL complex to suppress transcription-promoting activity of the complex for genes such as
Wee1, Cry2, Per1, Per2, and Per3 in cells having the ticking
circadian clock, we hypothesized that if the
circadian clock functions in GV
oocytes and one-cell- to four-cell-stage
embryos,
CLOCK,
ARNTL, and
CRY1 might suppress the transcription of these genes in GV
oocytes and one-cell- to 4-cell-stage
embryos as well. As a result,
knockdown of
CRY1 in GV
oocytes by
RNA interference did not affect the transcription levels of
Wee1, Cry2, Per1, Per2, and Per3, but it reduced maturation ability. Thus, it seems that
circadian genes are not involved in
circadian clock regulation in
mouse oocytes and preimplantation
embryos but are involved in physiologies, such as
meiosis.
