Fig. 3: Mechanism underlying Trp53 LOH in AKTP+/M cells. | Nature Communications

Fig. 3: Mechanism underlying Trp53 LOH in AKTP+/M cells.

From: Loss of wild-type p53 promotes mutant p53-driven metastasis through acquisition of survival and tumor-initiating properties

Fig. 3

a Direct sequencing of genomic DNA fragments including codon 270 (under line) of Trp53 in CMT93 cells, AKTP+/M, and AKTPM/LOH cells. WT, wild-type Trp53; and MT, mutant Trp53 (R270H). b A whole-genome CGH analysis of the indicated AKTPM/LOH subclones (1C9, 2A6, and 3F9) and parental AKTP+/M cells. Chr indicates chromosome number. c TaqMan SNP genotyping results of AKTPM/LOH 2A6 cells (open diamonds with red line), AKTPM/LOH 1C9 cells (red diamonds with black line), AKTPM/LOH 3F9 cells (magenta diamonds), AKTP+/M cells (green squares), AKTP+/+ cells (blue squares), and no template control (NTC) (yellow triangles) are shown as a scatter plot. The Trp53 allelic discrimination data are shown as a scatter plot of Trp53 wild-type codon 270 (CGT) (HEX dye) versus Trp53 mutant codon R270H (CAT) (FAM dye). Note that two AKTPM/LOH subclones (2A6 and 1C9) carry two copies of mutant Trp53 R270H, while one AKTPM/LOH subclone 3F9 carries one copy or Trp53 R270H. Source data are provided as a Source data file.

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