Involvement of posttranscriptional regulation of Clock in the emergence of circadian clock oscillation during mouse development

Aug 23, 2017Proceedings of the National Academy of Sciences of the United States of America

How gene regulation after transcription helps the body clock start working during mouse development

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Abstract

Circadian clock oscillation is absent in mouse fetal hearts around E10 but becomes evident by E18.

Circadian clock development is linked to cellular differentiation in mammalian embryos.
Temporal RNA-sequencing indicates a significant increase in rhythmic genes from 63 at E10-12 to 483 at E17-19.
Functional circadian feedback loops of core circadian genes are not present in E10 mouse fetal hearts.
CLOCK protein, necessary for molecular oscillation in differentiated cells, is absent in E10 embryos despite mRNA expression.
Posttranscriptional regulation plays a crucial role in the timing of circadian clock emergence during development.

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Circadian clock oscillation emerges in mouse embryo in the later developmental stages. Although circadian clock development is closely correlated with cellular differentiation, the mechanisms of its emergence during mammalian development are not well understood. Here, we demonstrate an essential role of the posttranscriptional regulation ofsubsequent to the cellular differentiation for the emergence of circadian clock oscillation in mouse fetal hearts and mouse embryonic stem cells (ESCs). In mouse fetal hearts, no apparent oscillation of cell-autonomous molecular clock was detectable around E10, whereas oscillation was clearly visible in E18 hearts. Temporal RNA-sequencing analysis using mouse fetal hearts reveals many fewer rhythmic genes in E10-12 hearts (63, no core circadian genes) than in E17-19 hearts (483 genes), suggesting the lack of functional circadian transcriptional/translational feedback loops (TTFLs) of core circadian genes in E10 mouse fetal hearts. In both ESCs and E10 embryos, CLOCK protein was absent despite the expression ofmRNA, which we showed was due to-dependent translational suppression of CLOCK. The CLOCK protein is required for the discernible molecular oscillation in differentiated cells, and the posttranscriptional regulation ofplays a role in setting the timing for the emergence of the circadian clock oscillation during mammalian development. Clock Clock Dicer/Dgcr8Clock

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Involvement of posttranscriptional regulation of Clock in the emergence of circadian clock oscillation during mouse development

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