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Fig. 4 | BMC Genomics

Fig. 4

From: A prototypical non-malignant epithelial model to study genome dynamics and concurrently monitor micro-RNAs and proteins in situ during oncogene-induced senescence

Fig. 4

Cytogenetic analysis revealed an altered karyotype in the “escaped” cells, displaying novel clonal numerical and structural chromosome aberrations coinciding with common fragile sites (CFS). a Multi-Color FISH spectral karyotyping (M-FISH/SKY) of the non-induced and the “escaped” HBECs combined with inverted DAPI banding, as described in [143], revealed a near diploid numerical constitution of 48 chromosomes. Yellow arrows indicate unique clonal rearrangements for each population whereas the blue arrows depict the common structural anomaly der(16)t(5;16). b Partial karyotypes in Inverted DAPI Banding demonstrate the breakpoints of clonal structural chromosome rearrangements in the two populations, OFF (upper panel) and “escaped” (lower panel). nl: normal copy. Several clonal structural rearrangements characteristic of the control cells (OFF), were lost in the cytogenetically examined “escaped” cells; these included the products of the translocation t(7;18), der(7)t(7;18)(q11.2;q22.2)(found in two copies) and der(18)t(7;18)(q11.2;q22.2). Lost in the “escaped” cells were also the der(19)t(17;19)(p13.3;q23.1) and the extra copy of chromosome 20 bearing a duplication of the long arm. Despite the clonal chromosome losses, the “escaped” cells displayed at least 6 novel clonal structural chromosome anomalies and their cytogenetic constitution was shaped by non-disjunctions of chromosomes 1, 5, 7, 12 16, 18 and 19. The karyotype of the "escaped" cells was characterized by the clonal gain of genomic material from 1q and most of chromosome 12, introduced by the emergence of the novel unbalanced translocation involving chromosomes 1 and 12, der(12)t(1;12)(p11;q24.1), as well as deletions of 8p23.1. In addition to these novel anomalies, the “escaped” cells presented an unbalanced translocation involving chromosomes 6 and 9, an extra copy of a rearranged derivative of chromosome 9, a translocation between 16 and 20 and two copies of isochromosome 5p. c Breakpoints of all the novel structural chromosome rearrangements identified in the “escaped” HBECs coincide with common aphidicolin induced fragile sites [78]

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