The role of RAD16 and elongin A/C homologs in Arabidopsis UV tolerance and growth

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dc.contributor.authorAlrayes, Linda NH
dc.contributor.examiningcommitteeStout Jake, Biological Sciencesen_US
dc.contributor.examiningcommitteeRenault Sylvie, Biological Sciencesen_US
dc.contributor.examiningcommitteeAyele Belay, Plant Scienceen_US
dc.contributor.examiningcommitteeStone Sophia, Biologyen_US
dc.contributor.supervisorStout, Jake
dc.date.accessioned2022-11-29T21:50:12Z
dc.date.available2022-11-29T21:50:12Z
dc.date.copyright2022-11-29
dc.date.issued2022-11-29
dc.date.submitted2022-11-29T20:06:25Zen_US
dc.degree.disciplineBiological Sciencesen_US
dc.degree.levelDoctor of Philosophy (Ph.D.)en_US
dc.description.abstractUV-B and UV-C can damage DNA by generating DNA photoproducts such as cyclobutane pyrimidine dimers (CPDs), pyrimidine 6-4 pyrimidone (6-4 PPs) and its Dewar isomers (Dewar PP). These DNA photoproducts inhibit DNA transcription and replication, and cause mutations. Thus, DNA photoproducts must be repaired. Plants use two different mechanisms to repair these DNA photoproducts: light-dependent repair via photolyase and light-independent repair via nucleotide excision repair (NER). The NER mechanism in plants is similar to that elucidated in yeast and mammalian models. In yeast systems, the global genomic NER (GG-NER) damage recognition complex RAD7/RAD16/ELOC/ CUL3 recognizes the damaged DNA in the non-transcribed regions of the genome. The mammalian Elongin A/B/C/CUL5 /RBX2 and the yeast Elongin A/C/CUL3/RBX1 complexes target the large subunit of the lesion stalled RNAPII on the transcribed strand for ubiqitination and degradation. Arabidopsis has two RAD16 homologs: AtRAD16 and AtRAD16b. In this thesis, I characterized the role of AtRAD16 and AtRAD16b in plant UV tolerance and growth using loss of function and gain of function analysis. Atrad16 and Atrad16b null mutants exhibited increased UV sensitivity, early flowering time and short silique length. AtRAD16 overexpression increased UV resistance, and YFP-tagged RAD16 is localized in the nucleus. In addition, AtRAD16 physically interacts with AtRAD7, all these results indicate that the role of AtRAD16 in GG-NER is conserved with its yeast counterpart. I also identified Arabidopsis ELOA homolog, ELOA, and characterized the role of both Arabidopsis ELOA and ELOC homologs in plant UV tolerance and growth. Ateloa and Ateloc null mutants exhibited increased UV sensitivity in seedlings and adult plants. AtELOA was found to physically and genetically interact with AtELOC. AtELOA is nuclear localized, whereas AtELOC localized in the nuclei and the cytosol. ELOA overexpression increases hypocotyl UV resistance and ELOA/ELOC overexpression increases the silique length and seed number. Thus, Arabidopsis RAD16, ELOA, and ELOC are implicated in UV tolerance and development.en_US
dc.description.noteFebruary 2023en_US
dc.identifier.urihttp://hdl.handle.net/1993/36977
dc.language.isoengen_US
dc.rightsopen accessen_US
dc.subjectAbiotic stressen_US
dc.subjectPlant growth and developmenten_US
dc.titleThe role of RAD16 and elongin A/C homologs in Arabidopsis UV tolerance and growthen_US
dc.typedoctoral thesisen_US
local.subject.manitobanoen_US
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