Abstract
Autophagy and DNA repair are two essential biological mechanisms that maintain cellular homeostasis. Impairment of these mechanisms was associated with several pathologies such as premature aging, neurodegenerative diseases, and cancer. Intrinsic or extrinsic stress stimuli (e.g., reactive oxygen species or ionizing radiation) cause DNA damage. As a biological stress response, autophagy is activated following insults that threaten DNA integrity. Hence, in collaboration with DNA damage repair and response mechanisms, autophagy contributes to the maintenance of genomic stability and integrity. Yet, connections and interactions between these two systems are not fully understood. In this review article, current status of the associations and crosstalk between autophagy and DNA repair systems is documented and discussed.
Highlights
Maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions
We briefly describe autophagy and DNA repair pathways and dissect molecular and cellular outcomes of interactions and crosstalk between these pathways
Cdmediated DNA damage-induced autophagy through the inhibition of mTOR by AMPK which activated upon the increased level of Ataxia-telangiectasia mutated (ATM) (Li et al, 2017)
Summary
Maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Autophosphorylation of ULK1 further promotes its activity and induces phosphorylation of several autophagy proteins, including ATG13 and FIP200 (Hosokawa et al, 2009); mTOR complexes are found to be associated with lysosomes where autophagic cargos are degraded. DDR is a complex cellular mechanism which involves the activation of several molecules that are stimulated in response to DNA damages (Matt and Hofmann, 2016).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have