Recruitment of HP1 beta to UVA-induced DNA lesions is independent of radiation-induced changes in A-type lamins
Abstract
Background InformationThe optimal repair of DNA lesions is fundamental for physiological processes. We asked whether the recruitment of HP1, 53BP1 and BMI1 proteins to ultraviolet (UVA)-induced DNA lesions requires functional A-type lamins.
ResultsWe found that UVA irradiation of nuclear lamina abolished the fluorescence of mCherry-tagged A-type lamins and destroyed the nuclear lamina as also observed by electron microscopy studies. Similarly, an absence of endogenous A- and B-type lamins was found in irradiated regions by UVA.
However, irradiation did not affect the recruitment of HP1, 53BP1 and BMI1 to DNA lesions. The UVA-induced shrinkage of the nuclear lamina, which anchors chromatin, explains why UVA-micro-irradiated chromatin is relaxed.
Conversely, additional experiments with -irradiation showed that the nuclear lamina remained intact and the genome-wide level of HP1 was stable. Fluorescence intensity of HP1 and BMI1 in UVA-induced DNA lesions and level of HP1 after -irradiation were unaffected by deficiency in A-type lamins, whereas those parameters of 53BP1 were changed.
ConclusionsWe conclude that only the 53BP1 status in DNA lesions, induced by UVA or -rays, is affected by A-type lamin deficiency, which was not observed for heterochromatin-related proteins HP1 and BMI1.