Fig. 6
From: KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development

Knockout of Kif20a causes a subtle increase in apoptosis without obvious defect in cytokinesis. a TUNEL staining for visualizing cells in apoptosis. An increase of numbers of apoptotic cells in the Kif20a germline knockout mutant cortices was seen at E12.5. Apoptosis status in the mutant and wild-type cortices appeared comparable at E15.5. Scale bar represents 100 μm. TUNEL-positive cells in the entire cortical region were counted. **P < 0.01. b Anti-activated caspase 3 staining for detecting cells in apoptosis. Staining of activated caspase 3 showed a similar trend of apoptosis status in the germline knockout mutant and wild-type cortices to TUNEL staining. Scale bar represents 100 μm. Caspase 3-positive cells in the entire cortical region were counted. **P < 0.01. c No obvious bi- or multinucleated cells were seen in the wild-type or Kif20a germline knockout mutant cortices. ConA (cyan) and propidium iodide (red) were used for visualizing cell peripherals and nuclei, respectively. Scale bar represents 100 μm. d Cell cycle analysis of wild-type and mutant cortical cells. Tamoxifen was administered to Kif20a inducible knockout mice at E9.5 and E10.5 consecutively. Littermates of Nestin-CreERT2; KIF20Afl/fl and control KIF20Afl/fl embryos were collected at E15.5. Cortical cells were examined for their DNA contents by FACS analysis. PI propidium iodide, 2N cells in G1/S phase, 4N cells in G2/M phase or bi-nucleated cells. No obvious difference in DNA content of cortical cells was observed (P = 0.73 and 0.93 for 2N and 4N, respectively)