Heather J Anderson

Publications (3)16.03 Total impact

• Article: Arabidopsis thaliana Y‐family DNA polymerase η catalyses translesion synthesis and interacts functionally with PCNA2

  Heather J. Anderson, Edward J. Vonarx, Landon Pastushok, Mayu Nakagawa, Atsushi Katafuchi, Petr Gruz, Antonio Di Rubbo, Desma M. Grice, Megan J. Osmond, Ayako N. Sakamoto, Takehiko Nohmi, Wei Xiao, Bernard A. Kunz
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  ABSTRACT: Upon blockage of chromosomal replication by DNA lesions, Y-family polymerases interact with monoubiquitylated proliferating cell nuclear antigen (PCNA) to catalyse translesion synthesis (TLS) and restore replication fork progression. Here, we assessed the roles of Arabidopsis thaliana POLH, which encodes a homologue of Y-family polymerase η (Polη), PCNA1 and PCNA2 in TLS-mediated UV resistance. A T-DNA insertion in POLH sensitized the growth of roots and whole plants to UV radiation, indicating that AtPolη contributes to UV resistance. POLH alone did not complement the UV sensitivity conferred by deletion of yeast RAD30, which encodes Polη, although AtPolη exhibited cyclobutane dimer bypass activity in vitro, and interacted with yeast PCNA, as well as with Arabidopsis PCNA1 and PCNA2. Co-expression of POLH and PCNA2, but not PCNA1, restored normal UV resistance and mutation kinetics in the rad30 mutant. A single residue difference at site 201, which lies adjacent to the residue (lysine 164) ubiquitylated in PCNA, appeared responsible for the inability of PCNA1 to function with AtPolη in UV-treated yeast. PCNA-interacting protein boxes and an ubiquitin-binding motif in AtPolη were found to be required for the restoration of UV resistance in the rad30 mutant by POLH and PCNA2. These observations indicate that AtPolη can catalyse TLS past UV-induced DNA damage, and links the biological activity of AtPolη in UV-irradiated cells to PCNA2 and PCNA- and ubiquitin-binding motifs in AtPolη.
  The Plant Journal 05/2008; 55(6):895 - 908. · 6.16 Impact Factor
• Article: Arabidopsis homologue of human transcription factor IIH/nucleotide excision repair factor p44 can function in transcription and DNA repair and interacts with AtXPD.

  Edward J Vonarx, Emma K Tabone, Megan J Osmond, Heather J Anderson, Bernard A Kunz
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  ABSTRACT: Eukaryotic general transcription factor (TF) IIH is composed of 10 proteins, seven of which are also required for nucleotide excision repair (NER) of UV radiation-induced DNA damage in human cells and yeast. Plant homologues of the human TFIIH subunits XPB and XPD that function in NER have been isolated but none has been shown to operate in transcription. Here we address the capabilities of Arabidopsis thaliana AtGTF2H2 and AtXPD, homologues of the essential interacting human/yeast TFIIH components p44/Ssl1 and XPD/Rad3, respectively. Expression of AtGTF2H2 or AtXPD cDNAs in yeast ssl1 or rad3 mutants temperature-sensitive for growth due to thermolabile transcription of mRNA restored growth and so transcription at the non-permissive temperature. AtGTF2H2 also complemented the NER deficiency of the corresponding yeast mutant, as measured by full recovery of UV resistance, whereas AtXPD did not despite being necessary for NER in Arabidopsis. UV treatment did not upregulate transcription of AtGTF2H2 or AtXPD in Arabidopsis. Suppression of a yeast translation initiation defect by the ssl1-1 mutation was prevented by expression of AtGTF2H2. Deletion of SSL1 in a yeast strain expressing AtGTF2H2 did not affect growth or confer UV sensitivity, demonstrating that AtGTF2H2 can perform all essential transcription functions and UV damage repair duties of Ssl1 in its absence. Furthermore, AtGTF2H2 interacted with AtXPD and yeast Rad3, and AtXPD also interacted with yeast Ssl1 in two-hybrid assays. Our results indicate that AtGTF2H2 can act in transcription and NER, and suggest that it participates in both processes in Arabidopsis as part of TFIIH.
  The Plant Journal 06/2006; 46(3):512-21. · 6.16 Impact Factor
• Article: Components of nucleotide excision repair and DNA damage tolerance in Arabidopsis thaliana.

  Bernard A Kunz, Heather J Anderson, Megan J Osmond, Edward J Vonarx
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  ABSTRACT: As obligate phototrophs, and despite shielding strategies, plants sustain DNA damage caused by UV radiation in sunlight. By inhibiting DNA replication and transcription, such damage may contribute to the detrimental effects of UV radiation on the growth, productivity, and genetic stability of higher plants. However, there is evidence that plants can reverse UV-induced DNA damage by photoreactivation or remove it via nucleotide excision repair. In addition, plants may have mechanisms for tolerating UV photoproducts as a means of avoiding replicative arrest. Recently, phenotypic characterization of plant mutants, functional complementation studies, and cDNA analysis have implicated genes isolated from the model plant Arabidopsis thaliana in nucleotide excision repair or tolerance of UV-induced DNA damage. Here, we briefly review features of these processes in human cells, collate information on Arabidopsis homologs of the relevant genes, and summarize the experimental findings that link certain of these plant genes to nucleotide excision repair or damage tolerance.
  Environmental and Molecular Mutagenesis 45(2-3):115-27. · 3.71 Impact Factor