The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

RAD30  -  Rad30p

Saccharomyces cerevisiae S288c

Synonyms: DBH1, DNA polymerase eta, Radiation-sensitive protein 30, YDR419W
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of RAD30


High impact information on RAD30

  • Here, RAD30 is shown to encode a DNA polymerase that can replicate efficiently past a thymine-thymine cis-syn cyclobutane dimer, a lesion that normally blocks DNA polymerases [3].
  • Some discontinuities accumulate in the absence of RAD30-encoded DNA polymerase eta (Poleta) but not in the absence of REV3-encoded DNA Polzeta [4].
  • Mutation of Glu156 in motif III to alanine confers a large reduction in the efficiency of nucleotide incorporation, whereas the remaining five Rad30 mutant proteins retain wild-type levels of DNA polymerase and T-T dimer bypass activities [5].
  • To identify the active-site residues of Rad30 important for catalysis, we generated mutations of nine acidic residues that are invariant or highly conserved among Rad30 proteins from different eukaryotic species [5].
  • The formation of MNNG-induced mutations is almost abolished in the rad30Delta pol32Delta double mutant of yeast, which lacks the RAD30 gene that encodes Poleta and the Pol32 subunit of DNA polymerase delta (Poldelta) [6].

Biological context of RAD30

  • Like many S. cerevisiae genes involved in error-prone DNA repair, epistasis analysis clearly places RAD30 in the RAD6 group and rad30 mutants display moderate UV sensitivity reminiscent of rev mutants [7].
  • Deletion of RAD30 did not affect spontaneous mutagenesis [8].
  • While the sensitivity of a rev3 Delta mutant indicates Pol zeta is needed for optimal ICL repair, isogenic cells deficient in Pol eta (rad30 Delta cells) were not significantly more sensitive to ICL agents than wild-type cells, and have no S-phase delay [9].
  • The rad30 rev3 double mutant exhibited a similar phenotype as the single rev3 mutant with respect to translesion synthesis and mutagenesis [10].
  • To address this possibility, Saccharomyces cerevisiae strains lacking either pol zeta (rev7), pol eta (rad30), or both were tested for trinucleotide repeat (TNR) contractions using three separate, sensitive genetic assays [11].

Associations of RAD30 with chemical compounds

  • To determine whether the DNA polymerase activity of Rad30 was essential for its biological function, we made a mutation in the highly conserved SIDE sequence in Rad30, in which the aspartate and glutamate residues have each been changed to alanine [12].

Other interactions of RAD30

  • Employing the same two conditions, we now examined the effect of deletions of the genes coding for polymerase eta (Pol eta) (RAD30) and Rev1p (REV1) [13].
  • Moreover, while excess wild-type Pol eta primarily induced base substitutions in the msh6 and pms1 strains, excess inactive Rad30p induced both base substitutions and frameshifts [8].


  1. Efficient and accurate replication in the presence of 7,8-dihydro-8-oxoguanine by DNA polymerase eta. Haracska, L., Yu, S.L., Johnson, R.E., Prakash, L., Prakash, S. Nat. Genet. (2000) [Pubmed]
  2. Deletion of the Saccharomyces cerevisiae gene RAD30 encoding an Escherichia coli DinB homolog confers UV radiation sensitivity and altered mutability. Roush, A.A., Suarez, M., Friedberg, E.C., Radman, M., Siede, W. Mol. Gen. Genet. (1998) [Pubmed]
  3. Efficient bypass of a thymine-thymine dimer by yeast DNA polymerase, Poleta. Johnson, R.E., Prakash, S., Prakash, L. Science (1999) [Pubmed]
  4. Requirement of RAD5 and MMS2 for postreplication repair of UV-damaged DNA in Saccharomyces cerevisiae. Torres-Ramos, C.A., Prakash, S., Prakash, L. Mol. Cell. Biol. (2002) [Pubmed]
  5. Acidic residues critical for the activity and biological function of yeast DNA polymerase eta. Kondratick, C.M., Washington, M.T., Prakash, S., Prakash, L. Mol. Cell. Biol. (2001) [Pubmed]
  6. Replication past O(6)-methylguanine by yeast and human DNA polymerase eta. Haracska, L., Prakash, S., Prakash, L. Mol. Cell. Biol. (2000) [Pubmed]
  7. The Saccharomyces cerevisiae RAD30 gene, a homologue of Escherichia coli dinB and umuC, is DNA damage inducible and functions in a novel error-free postreplication repair mechanism. McDonald, J.P., Levine, A.S., Woodgate, R. Genetics (1997) [Pubmed]
  8. Mutator effects of overproducing DNA polymerase eta (Rad30) and its catalytically inactive variant in yeast. Pavlov, Y.I., Nguyen, D., Kunkel, T.A. Mutat. Res. (2001) [Pubmed]
  9. S. cerevisiae has three pathways for DNA interstrand crosslink repair. Grossmann, K.F., Ward, A.M., Matkovic, M.E., Folias, A.E., Moses, R.E. Mutat. Res. (2001) [Pubmed]
  10. Poleta, Polzeta and Rev1 together are required for G to T transversion mutations induced by the (+)- and (-)-trans-anti-BPDE-N2-dG DNA adducts in yeast cells. Zhao, B., Wang, J., Geacintov, N.E., Wang, Z. Nucleic Acids Res. (2006) [Pubmed]
  11. Examining the potential role of DNA polymerases eta and zeta in triplet repeat instability in yeast. Dixon, M.J., Lahue, R.S. DNA Repair (Amst.) (2002) [Pubmed]
  12. Requirement of DNA polymerase activity of yeast Rad30 protein for its biological function. Johnson, R.E., Prakash, S., Prakash, L. J. Biol. Chem. (1999) [Pubmed]
  13. Epistatic participation of REV1 and REV3 in the formation of UV-induced frameshift mutations in cell cycle-arrested yeast cells. Heidenreich, E., Eisler, H., Steinboeck, F. Mutat. Res. (2006) [Pubmed]
WikiGenes - Universities