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p53 deficiency rescues apoptosis and differentiation of multiple cell types in zebrafish flathead mutants defcient for zygotic DNA polymerase δ1

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Sonntag,  C.
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Busse,  C. E.
Max-Planck Research Group Molecular Immunology, Max Planck Institute for Infection Biology, Max Planck Society;

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Hammerschmidt,  M.
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Plaster, N., Sonntag, C., Busse, C. E., & Hammerschmidt, M. (2006). p53 deficiency rescues apoptosis and differentiation of multiple cell types in zebrafish flathead mutants defcient for zygotic DNA polymerase δ1. Cell Death and Differentiation, 13, 223-235.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-92A2-B
Abstract
Cell culture work has identified the tumor suppressor p53 as a component of the S-phase checkpoint control system, while in vivo studies of this role of p53 in whole-vertebrate systems were limited. Here, we describe zebrafish mutants in the DNA polymerase delta catalytic subunit 1, based on the positional cloning of the flathead (fla) gene. fla mutants display specific defects in late proliferative zones, such as eyes, brain and cartilaginous elements of the visceral head skeleton, where cells display compromised DNA replication, followed by apoptosis, and partial or complete loss of affected tissues. Antisense-mediated knockdown of p53 in fla mutants leads to a striking rescue of all phenotypic traits, including completion of replication, survival of cells, and normal differentiation and tissue formation. This indicates that under replication-compromised conditions, the p53 branch of the S-phase checkpoint is responsible for eliminating stalled cells that, given more time, would have otherwise finished their normal developmental program.