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Cell numbers contribute to cell fate during Ciona cardiopharyngeal mesoderm specification

Emily Singer1, Haram Kim1, Michael S Levine1,2

  • 1Department of Molecular Biology, Princeton University, Princeton, NJ 08544.

Proceedings of the National Academy of Sciences of the United States of America
|January 8, 2026
PubMed

Insights

In Ciona, cell cycle regulation of the B7.5 lineage by Cdkn1.b controls cell numbers. Altering cell division timing unexpectedly shifted cell fate to tail muscle, revealing a link between cell number control and developmental fate.

Area of Science:

  • Developmental biology
  • Cellular and molecular biology

Background:

  • The Ciona heart cell lineage originates from B7.5 blastomeres.
  • B7.5 cells contribute to heart, tail muscle, and siphon muscles.
  • Developmental specification of B7.5 derivatives is understood, but cell number regulation is less clear.

Purpose of the Study:

  • Investigate Ciona embryo's precise cell number regulation in the B7.5 lineage.
  • Determine the effects of altered cell numbers on B7.5 lineage development.
  • Explore the connection between cell number control and cell fate.

Main Methods:

  • Analysis of cell cycle inhibitor Cdkn1.b transcription.
  • Investigating repression by Prdm1-r.a and Prdm1-r.b paralogs.
  • Studying effects of precocious cell division arrest in B7.5 lineage.

Main Results:

  • Cell numbers in the B7.5 lineage are controlled by Cdkn1.b transcription pulses.
  • Prdm1-r.a and Prdm1-r.b repress Cdkn1.b exclusively in B7.5 cells at the 112-cell stage.
  • Precocious cell division arrest in B7.5 lineage led to tail muscle fate reversion.

Conclusions:

  • Cdkn1.b acts as a key regulator of cell numbers in the Ciona B7.5 lineage.
  • Prdm1-r paralogs modulate Cdkn1.b to control cell proliferation.
  • Cell number regulation is unexpectedly linked to cell fate determination in Ciona development.

Keywords:
developmentgene expressionheart development

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