The conserved factor DE-ETIOLATED 1 cooperates with CUL4-DDB1^DDB2to maintain genome integrity upon UV stress

Abstract

Plants and many other eukaryotes can make use of two major pathways to cope with mutagenic effects of light, photoreactivation and nucleotide excision repair (NER). While photoreactivation allows direct repair by photolyase enzymes using light energy, NER requires a stepwise mechanism with several protein complexes acting at the levels of lesion detection, DNA incision and resynthesis. Here we investigated the involvement in NER of DE-ETIOLATED 1 (DET1), an evolutionarily conserved factor that associates with components of the ubiquitylation machinery in plants and mammals and acts as a negative repressor of light-driven photomorphogenic development in Arabidopsis. Evidence is provided that plant DET1 acts with CULLIN4-based ubiquitin E3 ligase, and that appropriate dosage of DET1 protein is necessary for efficient removal of UV photoproducts through the NER pathway. Moreover, DET1 is required for CULLIN4-dependent targeted degradation of the UV-lesion recognition factor DDB2. Finally, DET1 protein is degraded concomitantly with DDB2 upon UV irradiation in a CUL4-dependent mechanism. Altogether, these data suggest that DET1 and DDB2 cooperate during the excision repair process.

The tomato DDI2, a PCNA ortholog, associating with DDB1-CUL4 complex is required for UV-damaged DNA repair and plant tolerance to UV stress

“…The DDB1-CUL4-based E3 ubiquitin ligase (CRL4) in plant cells plays an indispensable role in many developmental processes [12] as well as in response to biotic [14] and abiotic stresses including UV irradiation [7,8,15]. Our previous work identified the DDB1-interacting protein 1 (DDI1) which is involved in response to abiotic stresses, including UV stress, high salinity and osmotic stress [15].…”

“…In plant, CRL4 ligase participates in various developmental processes such as photomorphorgenesis [12] and plastid division [13], and in the response to biotic [14] and abiotic stresses [15]. Also, plant CRL4 DDB2 E3 ligase is a key factor in DNA damage response and DNA repair [16] and in maintaining the genome integrity upon UV stress, as demonstrated by the facts that the genetic mutants of CUL4, DDB1a, and DDB2 in Arabidopsis exhibited hypersensitivity to UV-C stress [7,8].…”

“…This process is commonly termed as dark repair [6]. The NER mechanism is employed in two pathways called transcriptional coupled repair (TC-NER) and global genome repair (GG-NER) [7,8]. As the first step of GG-NER, the recognition of DNA lesions is mediated by DDB1-DDB2 complex.…”

UV Damaged DNA Repair & Tolerance in Plants

“…Polyubiquitinated DDB2 exhibits reduced affinity for damaged DNA and is subsequently displaced from the damaged foci, whereas polyubiquitinated XPC enhances its binding to DNA . In Arabidopsis, DDB2 turnover is abrogated in cul4, ddb1a, atr and det1 mutants suggesting that ATR and DET1 may co-operate with the CUL4-DDB1 E3 ligase complex in regulating NER (Castells et al, 2011;Molinier et al, 2008).…”

“…Recent papers show that det1 mutants exhibit enhanced UV tolerance through increased levels of secondary metabolites reflecting/absorbing UV irradiation as well as by upregulation of photolyase genes. Further it appears that DET1 protein dosage influences UV sensitivity of plants as DET1 overexpressing lines exhibit increased UV sensitivity (Castells et al, 2010(Castells et al, , 2011.…”