Skip to main content


Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Figure 4 | Cell Division

Figure 4

From: Merotelic attachments and non-homologous end joining are the basis of chromosomal instability

Figure 4

Model for amplification of chromosomal instability by DNA damage. Initial merotelic attachments activate DNA damage signaling and inhibit cell proliferation through anaphase delay and induction of apoptosis or senescence. To overcome the block, the downstream spindle checkpoint is suppressed in CIN tumors, increasing the frequency of spindle attachment errors. As a side effect of this continuous breakage, DNA repair mechanisms remain activated, leading ultimately to adaptation through suppression of apoptosis and senescence and through spindle checkpoint relaxation (dashed lines).

Back to article page