UV Damaged DNA Repair &amp; Tolerance in Plants

Ganpudi, Ashwin; Schroeder, Dana F.

doi:10.5772/22138

Cited by 3 publications

(4 citation statements)

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“…NER is a well conserved repair process across both prokaryotes and eukaryotes. Defects in NER and failure to remove lesions from the genome cause xeroderma pigmentosa (UV-sensitivity with increased skin cancer risk) in humans [ 3 ], UV hypersensitivity ( uvh ) in Arabidopsis thaliana [ 4 ], and radiation sensitivity ( rad ) in the yeast Saccharomyces cerevisiae [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

“…This complex has E3 ubiquitin ligase activity that targets core histone proteins for chromatin modification, resulting in the recruitment and ubiquitination of Xeroderma Pigmentosa C (XPC) [ 13 , 14 ]. Then XPC, together with HR23B and Centrin2 (CEN2) proteins, form another complex that recruits the NER machinery [ 4 , 15 ]. S .…”

Section: Introductionmentioning

confidence: 99%

“…Nucleotide excision repair in plants has been studied in Arabidopsis thaliana , and the overall process appears to be well conserved [ 4 ]. Current understanding of this process is that it follows the mammalian model of GG-NER, given that mutations in the homologs of the core downstream NER components CEN2 and RAD23 result in UV sensitivity [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

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Arabidopsis RAD16 Homologues Are Involved in UV Tolerance and Growth

Alrayes,

Stout,

Schroeder

2023

Genes

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In plants, prolonged exposure to ultraviolet (UV) radiation causes harmful DNA lesions. Nucleotide excision repair (NER) is an important DNA repair mechanism that operates via two pathways: transcription coupled repair (TC-NER) and global genomic repair (GG-NER). In plants and mammals, TC-NER is initiated by the Cockayne Syndrome A and B (CSA/CSB) complex, whereas GG-NER is initiated by the Damaged DNA Binding protein 1/2 (DDB1/2) complex. In the yeast Saccharomyces cerevisiae (S. cerevisiae), GG-NER is initiated by the Radiation Sensitive 7 and 16, (RAD7/16) complex. Arabidopsis thaliana has two homologues of yeast RAD16, At1g05120 and At1g02670, which we named AtRAD16 and AtRAD16b, respectively. In this study, we characterized the roles of AtRAD16 and AtRAD16b. Arabidopsis rad16 and rad16b null mutants exhibited increased UV sensitivity. Moreover, AtRAD16 overexpression increased plant UV tolerance. Thus, AtRAD16 and AtRAD16b contribute to plant UV tolerance and growth. Additionally, we found physical interaction between AtRAD16 and AtRAD7. Thus, the Arabidopsis RAD7/16 complex is functional in plant NER. Furthermore, AtRAD16 makes a significant contribution to Arabidopsis UV tolerance compared to the DDB1/2 and the CSB pathways. This is the first time the role and interaction of DDB1/2, RAD7/16, and CSA/CSB components in a single system have been studied.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Arabidopsis RAD16 Homologues Are Involved in UV Tolerance and Growth

Alrayes,

Stout,

Schroeder

2023

Genes

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“…The primary function of this E3 ligase complex is facilitating UV damaged DNA repair. 16,17 In an example of CUL4-DDB1 complexes interacting with each other, examination of the effect of det1 on CUL4-DDB1/2 complexes showed that DET1 is required for DDB2 degradation. 18 In addition, while the Arabidopsis ddb2 single mutant has no significant developmental phenotypes, ddb2 modifies det1 phenotypes.…”

Section: Introductionmentioning

confidence: 99%

Arabidopsis DDB1-CUL4 E3 ligase complexes in det1 salt/osmotic stress resistant germination

Fernando

Schroeder

2016

Plant Signaling & Behavior

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A key regulatory mechanism in plant growth, development, and stress signaling utilizes E3 ubiquitin ligases, which target a variety of substrates for degradation. DE-ETIOLATED 1 (DET1) forms a complex with DDB1 (DAMAGED DNA BINDING protein 1) and CUL4 (CULLIN 4), and negatively regulates light signaling. Another DDB1-CUL4 complex containing DWA1 and DWA2 (DWD hypersensitive to ABA 1 and 2) has been shown to negatively regulate abscisic acid (ABA) signaling. Since distinct DDB1-CUL4 complexes have been shown to influence each other, we analyzed genetic interactions between DET1 and components of DDB1-CUL4 complexes during seed germination under salt and osmotic stress conditions. det1 germination was resistant to salt and osmotic stress and dwa1 and dwa2 enhanced this phenotype. In contrast, ddb1a partially suppressed the det1 germination phenotype on both salt and mannitol, while ddb1b had no effect. Mutations in DDB2, a DDB1-CUL4 complex component involved in DNA repair, also partially suppressed the det1 germination phenotype while mutants in COP1, another light signaling component, completely suppressed the det1 resistant germination phenotypes. Taken together these data suggest that components of E3 ubiquitin ligase complexes have variable but significant effects on det1 salt/osmotic stress responses.

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