Literature DB >> 28196404

A p57 conditional mutant allele that allows tracking of p57-expressing cells.

Despoina Mademtzoglou1,2, Sonia Alonso-Martin1,2, Ted Hung-Tse Chang1,2, Keren Bismuth3, Bernadette Drayton-Libotte1,2, Frédéric Aurade1,2,3, Frédéric Relaix1,2,4,5.   

Abstract

p57Kip2 (p57) is a maternally expressed imprinted gene regulating growth arrest which belongs to the CIP/KIP family of cyclin-dependent kinase inhibitors. While initially identified as a cell cycle arrest protein through inhibition of cyclin and cyclin-dependent kinase complexes, p57 activity has also been linked to differentiation, apoptosis, and senescence. In addition, p57 has recently been shown to be involved in tumorigenesis and cell fate decisions in stem cells. Yet, p57 function in adult tissues remains poorly characterized due to the perinatal lethality of p57 knock-out mice. To analyze p57 tissue-specific activity, we generated a conditional mouse line (p57FL-ILZ/+ ) by flanking the coding exons 2-3 by LoxP sites. To track p57-expressing or mutant cells, the p57FL-ILZ allele also contains an IRES-linked β-galactosidase reporter inserted in the 3' UTR of the gene. Here, we show that the β-galactosidase reporter expression pattern recapitulates p57 tissue specificity during development and in postnatal mice. Furthermore, we crossed the p57FL-ILZ/+ mice with PGK-Cre mice to generate p57cKO-ILZ/+ animals with ubiquitous loss of p57. p57cKO-ILZ/+ mice display developmental phenotypes analogous to previously described p57 knock-outs. Thus, p57FL-ILZ/+ is a new genetic tool allowing expression and functional conditional analyses of p57.
© 2017 Wiley Periodicals, Inc.

Entities:  

Keywords:  CDKIs; Cell cycle exit; Cre-inducible ablation; postnatal survival; β-galactosidase reporter

Mesh:

Substances:

Year:  2017        PMID: 28196404     DOI: 10.1002/dvg.23025

Source DB:  PubMed          Journal:  Genesis        ISSN: 1526-954X            Impact factor:   2.487


  4 in total

1.  CHD4 ensures stem cell lineage fidelity during skeletal muscle regeneration.

Authors:  Krishnamoorthy Sreenivasan; Alejandra Rodríguez-delaRosa; Johnny Kim; Diana Mesquita; Jessica Segalés; Pablo Gómez-Del Arco; Isabel Espejo; Alessandro Ianni; Luciano Di Croce; Frederic Relaix; Juan Miguel Redondo; Thomas Braun; Antonio L Serrano; Eusebio Perdiguero; Pura Muñoz-Cánoves
Journal:  Stem Cell Reports       Date:  2021-08-26       Impact factor: 7.765

2.  Cellular localization of the cell cycle inhibitor Cdkn1c controls growth arrest of adult skeletal muscle stem cells.

Authors:  Despoina Mademtzoglou; Yoko Asakura; Matthew J Borok; Sonia Alonso-Martin; Philippos Mourikis; Yusaku Kodaka; Amrudha Mohan; Atsushi Asakura; Frederic Relaix
Journal:  Elife       Date:  2018-10-04       Impact factor: 8.140

3.  Methylation of Cdkn1c may be involved in the regulation of tooth development through cell cycle inhibition.

Authors:  Qiulan Li; Yue Guo; Mianfeng Yao; Jun Li; Yingyi Chen; Qiong Liu; Yun Chen; Yuanyuan Zeng; Bin Ji; Yunzhi Feng
Journal:  J Mol Histol       Date:  2018-07-16       Impact factor: 2.611

Review 4.  The Role of CDKs and CDKIs in Murine Development.

Authors:  Grace Jean Campbell; Emma Langdale Hands; Mathew Van de Pette
Journal:  Int J Mol Sci       Date:  2020-07-28       Impact factor: 5.923

  4 in total

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