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The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis.
Curr Biol. 2001 Oct 30; 11(21):1722-7.CB

Abstract

In mammals, one of the key regulators necessary for responding to genotoxic stress is the p53 transcription factor. p53 is the single most commonly mutated tumor suppressor gene in human cancers. Here we report the identification of a C. elegans homolog of mammalian p53. Using RNAi and DNA cosuppression technology, we show that C. elegans p53 (cep-1) is required for DNA damage-induced apoptosis in the C. elegans germline. However,cep-1 RNAi does not affect programmed cell death occurring during worm development and physiological (radiation-independent) germ cell death. The DNA binding domain of CEP-1 is related to vertebrate p53 members and possesses the conserved residues most frequently mutated in human tumors. Consistent with this, CEP-1 acts as a transcription factor and is able to activate a transcriptional reporter containing consensus human p53 binding sites. Our data support the notion that p53-mediated transcriptional regulation is part of an ancestral pathway mediating DNA damage-induced apoptosis and reveals C. elegans as a genetically tractable model organism for studying the p53 apoptotic pathway.

Links

Publisher Full Text
linkinghub.elsevier.com
linkinghub.elsevier.com

Authors+Show Affiliations

Schumacher B
Max Planck Institut für Biochemie, Department of Cell Biology, Am Klopferspitz 18A, 82152 Martinsried, Germany.
Hofmann K
No affiliation info available
Boulton S
No affiliation info available
Gartner A
No affiliation info available

MeSH

Amino Acid SequenceAnimalsApoptosisCaenorhabditis elegansCaenorhabditis elegans ProteinsConserved SequenceDNA DamageMolecular Sequence DataSequence Homology, Amino AcidTranscription FactorsTumor Suppressor Protein p53

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11696333

Citation

Schumacher, B, et al. "The C. Elegans Homolog of the P53 Tumor Suppressor Is Required for DNA Damage-induced Apoptosis." Current Biology : CB, vol. 11, no. 21, 2001, pp. 1722-7.
Schumacher B, Hofmann K, Boulton S, et al. The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis. Curr Biol. 2001;11(21):1722-7.
Schumacher, B., Hofmann, K., Boulton, S., & Gartner, A. (2001). The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis. Current Biology : CB, 11(21), 1722-7.
Schumacher B, et al. The C. Elegans Homolog of the P53 Tumor Suppressor Is Required for DNA Damage-induced Apoptosis. Curr Biol. 2001 Oct 30;11(21):1722-7. PubMed PMID: 11696333.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis. AU - Schumacher,B, AU - Hofmann,K, AU - Boulton,S, AU - Gartner,A, PY - 2001/11/7/pubmed PY - 2002/1/23/medline PY - 2001/11/7/entrez SP - 1722 EP - 7 JF - Current biology : CB JO - Curr Biol VL - 11 IS - 21 N2 - In mammals, one of the key regulators necessary for responding to genotoxic stress is the p53 transcription factor. p53 is the single most commonly mutated tumor suppressor gene in human cancers. Here we report the identification of a C. elegans homolog of mammalian p53. Using RNAi and DNA cosuppression technology, we show that C. elegans p53 (cep-1) is required for DNA damage-induced apoptosis in the C. elegans germline. However,cep-1 RNAi does not affect programmed cell death occurring during worm development and physiological (radiation-independent) germ cell death. The DNA binding domain of CEP-1 is related to vertebrate p53 members and possesses the conserved residues most frequently mutated in human tumors. Consistent with this, CEP-1 acts as a transcription factor and is able to activate a transcriptional reporter containing consensus human p53 binding sites. Our data support the notion that p53-mediated transcriptional regulation is part of an ancestral pathway mediating DNA damage-induced apoptosis and reveals C. elegans as a genetically tractable model organism for studying the p53 apoptotic pathway. SN - 0960-9822 UR - https://www.unboundmedicine.com/medline/citation/11696333/The_C__elegans_homolog_of_the_p53_tumor_suppressor_is_required_for_DNA_damage_induced_apoptosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0960-9822(01)00534-6 DB - PRIME DP - Unbound Medicine ER -