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. 2012 Apr 12;5(6):914–920. doi: 10.1242/dmm.008995

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© 2012. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 1. — Validation and characterization of the Tp53^R270H/+Nkx3.1-Cre mouse. (A) Schematic representation of the targeting vector and the floxed allele following excision of the STOP cassette by Nkx3.1 Cre recombinase. The R270H mutation is located in exon 8 (marked as a star). (B) Congenic backcross onto FVB/NJ was performed to ensure a uniform strain background. Speed congenics (N3 through N5) produced a close to 100% FVB/NJ congenic mouse. (C) RT-PCR and sequencing analysis of laser capture microdissected PIN lesions confirmed that Nkx3.1-Cre-mediated deletion of the floxed STOP cassette resulted in prostate-specific expression of the p53 R270H mutation. (D) Well-developed PIN lesions were observed in Tp53^R270H^/+ Nkx3.1-Cre mice as early as 4 months and more than 60% of mice examined between 5 and 60 weeks developed grade 2 or higher PIN (n=16). Nkx3.1 haploinsufficient littermate mice (Nkx3.1-Cre; n=6), which did not express the Tp53 mutation, did not develop PIN even at 60 weeks (see Fig. 2).