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. 2019 Dec 16;2(6):406–416. doi: 10.1089/crispr.2019.0006

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© Emily Rayner et al. 2019; Published by Mary Ann Liebert, Inc.

This Open Access article is distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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FIG. 3. — CRIPSR clones exhibit chromosomal instability. (A) Mutation of SNP rs1800734 in the MLH1 promoter in COLO320 cells. Left panel: graphs showing the chromosome counts per cell of the parental and AA and GG sequenced clones. The parental cells show a variable number of chromosomes with the modal number of 52. The mutant clones show a wider distribution and no clear model number. Middle panel: graphs showing the number of double minutes per cell. The distribution is similar between the parental and AA clones but numbers are greatly increased in GG cells. Left panel: DAPI-stained metaphase spreads showing double minutes (red arrows). (B) Reversion of mutation in POLE exon 9 in HCC2998 cells. Graphs showing the chromosome counts per cell of the parental and clones 1, 2, and 3. The parental cells have a modal number of 47 chromosomes. Clones 2 and 3 also have a modal number of 47 and similar overall distribution. Clone 1 has more variable chromosome numbers. (C) Mutation of NFE2L2 gene in SW1463 cells. Graphs showing the chromosome counts per cell of the parental and sequenced clones 5 and 6. The parental cells show a variable number of chromosomes with the modal number of 49. The mutant clones show a wider distribution and no clear modal number.