Regulators specifying cell fate activate cell cycle regulator genes to determine cell numbers in ascidian larval tissues
Author(s) -
Kenji Kobayashi,
Miki Tokuoka,
Hiroaki Sato,
Manami Ariyoshi,
Shiori Kawahara,
Shigeki Fujiwara,
Takeo Kishimoto,
Yutaka Satou
Publication year - 2022
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.201218
Subject(s) - biology , notochord , cell fate determination , microbiology and biotechnology , endoderm , cell cycle , mesenchyme , transcription factor , mesoderm , embryonic stem cell , cellular differentiation , cell , genetics , embryo , gene , embryogenesis
In animal development, most cell types stop dividing before terminal differentiation; thus, cell cycle control is tightly linked to cell differentiation programmes. In ascidian embryos, cell lineages do not vary among individuals, and rounds of the cell cycle are determined according to cell lineages. Notochord and muscle cells stop dividing after eight or nine rounds of cell division depending on their lineages. In the present study, we showed that a Cdk inhibitor, Cdkn1.b, is responsible for stopping cell cycle progression in these lineages. Cdkn1.b is also necessary for epidermal cells to stop dividing. In contrast, mesenchymal and endodermal cells continue to divide even after hatching, and Myc is responsible for maintaining cell cycle progression in these tissues. Expression of Cdkn1.b in notochord and muscle is controlled by transcription factors that specify the developmental fate of notochord and muscle. Likewise, expression of Myc in mesenchyme and endoderm is under control of transcription factors that specify the developmental fate of mesenchyme and endoderm. Thus, cell fate specification and cell cycle control are linked by these transcription factors.
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