Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Mar 11;5(3):140156. doi: 10.1098/rsob.140156

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2015 The Authors. Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

PMC Copyright notice

Figure 1. — The period of mitotic arrest controls subsequent DNA damage signalling, cell cycle progression and apoptosis. (a) Experimental protocol. (b) DNA damage signalling in response to a prolonged mitotic arrest. Samples were analysed by immunoblotting using the antibodies indicated. Asterisk denotes a non-specific signal on pS15-p53 blot. (c,d) DNA damage signalling in G1 following mitotic arrest. Samples were analysed by immunoblotting using specified antibodies (c), and cell cycle profiles were characterized by flow cytometry using propidium iodide as a marker of DNA content and phosphorylated Ser10 histone H3 as a marker of mitosis (d). (e) Induction of apoptosis during a mitotic arrest. Cells were incubated with a FAM-DEVD-fmk probe and analysed by flow cytometry. Percentages represent the amount of active cleaved caspase-3/7 positive cells. (f) γH2AX induction in cells arrested in mitosis is caspase-dependent. Cells were synchronized for 10 h in mitosis in the presence of z-VAD-fmk where indicated, cytospun and immunostained using an anti-γH2AX antibody. Representative microscopic fields are shown; Ap, apoptotic cells; scale bar, 50 µm.