Abstract
Organisms are continuously exposed to DNA damaging agents, consequently, cells have developed an intricate system known as the DNA damage response (DDR) in order to detect and repair DNA lesions. This response has to be rapid and accurate in order to keep genome integrity. It has been observed that the condensation state of chromatin hinders a proper DDR. However, the condensation state of chromatin is not the only barrier to DDR. In this review, we have collected data regarding the presence of DDR factors on micronuclear DNA lesions that indicate that micronuclei are almost incapable of generating an effective DDR because of defects in their nuclear envelope. Finally, considering the recent observations about the reincorporation of micronuclei to the main bulk of chromosomes, we suggest that, under certain circumstances, micronuclei carrying DNA damage might be a source of chromosome instability.
Highlights
To answer to the diversity of DNA lesions, cells have developed a complex defense system in order to detect them, signal their presence and promote their repair
This breakage may result in the formation of acentric fragments that, at the end of mitosis, arise as micronuclei [5] or as nuclear blebs, which are micronucleus-like bodies physically connected to the nucleus by a chromatinic filament [6,7]
Even if our results indicate that some DNA damage response (DDR) factors are capable to get into micronuclei after their formation, the low frequency of 53BP1 and γH2AX colocalization and the low number of XPC positive micronuclei suggests the presence of a general impediment to the import of repair factors into the micronucleus
Summary
To answer to the diversity of DNA lesions, cells have developed a complex defense system in order to detect them, signal their presence and promote their repair. This system, known as the DNA damage response (DDR), is a hierarchical cascade of proteins composed of sensors, mediators, transducers and effectors. Transducers activate the effectors that coordinate the temporary delay of cell cycle progression, which is needed for DNA damage repair, and, sometimes, the activation of apoptosis or senescence. We review different studies that analyze the presence of factors involved in the response to DNA double strand breaks (DSBs) and of those involved in the repair of helix-distorting base lesions in micronuclei
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