Depletion of Maternal Cyclin B3 Contributes to Zygotic Genome Activation in the Ciona Embryo

Nicholas Treen, Tyler Heist, Wei Wang, Michael Levine

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


Most animal embryos display a delay in the activation of zygotic transcription during early embryogenesis [1]. This process is thought to help coordinate rapid increases in cell number during early development [2]. The timing of zygotic genome activation (ZGA) during the maternal-to-zygotic transition (MZT) remains uncertain despite extensive efforts. We explore ZGA in the simple protovertebrate, Ciona intestinalis. Single-cell RNA sequencing (RNA-seq) assays identified Cyclin B3 (Ccnb3) as a putative mediator of ZGA. Maternal Ccnb3 transcripts rapidly diminish in abundance during the onset of zygotic transcription at the 8-cell and 16-cell stages. Disruption of Ccnb3 activity results in precocious activation of zygotic transcription, while overexpression abolishes normal activation. These observations suggest that the depletion of maternal Cyclin B3 products is a critical component of the MZT and ZGA. We discuss evidence that this mechanism might play a conserved role in the MZT of other metazoans, including mice and humans. Using a single-cell RNA-seq approach, Treen et al. investigate zygotic genome activation in Ciona, and they demonstrate that a maternal mRNA encoding Cyclin B3 is a key mediator of the process. This study provides new insights into how the timing of zygotic genome activation can be coordinated with the depletion of maternal mRNAs.

Original languageEnglish (US)
Pages (from-to)1150-1156.e4
JournalCurrent Biology
Issue number7
StatePublished - Apr 2 2018

All Science Journal Classification (ASJC) codes

  • General Biochemistry, Genetics and Molecular Biology
  • General Agricultural and Biological Sciences


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