DTL facilitates the Fanconi anemia pathway for ultraviolet-induced DNA repair in retinal pigment epithelial cells

Biocell

article

JIUCHUN GUO¹  JIE PAN²  QIANQIAN GUO² 

[1] Binzhou Second People’s Hospital;Department of Ophthalmology, Zibo Central Hospital

关键词: DTL;    Fanconi anemia pathway;    Retinal pigment epithelial;    p53;   

DOI  :  10.32604/biocell.2021.015785

学科分类：仪器

来源: Biocell

【 摘 要 】

The excessive energy of light, especially the invisible rays with lower wavelength, is basically absorbed by retinalpigment epithelium (RPE) and usually causes DNA damage. The molecular mechanism behind DNA damage repairresponse to this frequent stress in RPE is not clearly understood. In this study, we determined that the Fanconianemia (FA) pathway was activated in human RPE ARPE-19 cells after ultraviolet (UV) B and C treatment.Moreover, immunoprecipitation (IP) of FANCD2 indicated that denticleless E3 ubiquitin protein ligase homolog(DTL) closely interacted with FANCD2. Knockdown of DTL weakened the activity of the FA pathway in ARPE-19cells responding to UV treatment. Finally, the DTL promoter was incubated with a biotin-labeled probe and pulleddown by streptavidin beads followed by the genomic DNA sonication. p53 was indicated by mass spectrum andfurther determined by chromatin IP assay. Taken together, our results demonstrated that DTL regulated by p53 couldactivate the FA pathway for UV-induced DNA damage repair in retinal pigment epithelial cells.

【 授权许可】

CC BY