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. 2015 Oct 6;6:8450. doi: 10.1038/ncomms9450

Figure 1. KLF14 KO mice develop spontaneous tumours.

Figure 1

(a–d) Generation of KLF14 KO mice using TALENs. (a) Schematic drawing of TALENs and the recognition sequences of KLF14 (in blue). (b) KLF14 DNA and amino acid sequences from live WT (+/+) and KLF14-KO (−/−) mice. ‘− − −' denotes the eight nucleotides deleted. (c) PCR genotyping of WT and KLF14-KO mice. One upper band, WT (+/+); two bands, heterozygous (+/−); one lower band, KO (−/−). (d) MEFs from WT and KLF14-KO mice were analysed for KLF14 and actin (as protein loading control) expression levels by western blotting. (e,f) Loss of KLF14 induces spontaneous tumorigenesis. (e) Macroscopic view of tumour-bearing organs (left panel) and microscopic view of haematoxylin and eosin staining of tumour tissue sections (middle and right panels) in 13- to 14-month-old KLF14-KO mice. Right panel shows enlargements of boxed areas. Dotted line denotes border between normal (N) and tumour (T) tissue. Pathologic analysis revealed that KLF14-KO mice developed pulmonary adenomas and lymphomas in the spleen and lymph node. Splenomegaly was observed in mice with spleen tumours. Lymphoma of the spleen exhibits the effacement of lymphoid follicle and the appearance of typical neoplastic Reed/Sternberg cells (arrow). Lymphoma developed in lymph node exhibits the hallmark cells with horse-shoe-shaped nucleus (arrow). (f) Spontaneous tumour incidences in KLF14-WT (+/+) and -KO (−/−) mice. The frequency of spontaneous tumours in KO mice (9 of 27 in total) versus WT mice (0 of 27 in total) was statistically significant (P<0.01).