Histone H4 LRS mutations can attenuate UV mutagenesis without affecting PCNA ubiquitination or sumoylation

DNA Repair ◽  
2020 ◽  
Vol 95 ◽  
pp. 102959
Author(s):  
Kathiresan Selvam ◽  
Sheikh Arafatur Rahman ◽  
Derek Forrester ◽  
Adam Bao ◽  
Michael Lieu ◽  
...  
Keyword(s):  
2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Bo Qin ◽  
Jia Yu ◽  
Somaira Nowsheen ◽  
Minghui Wang ◽  
Xinyi Tu ◽  
...  
Keyword(s):  

Genetics ◽  
1990 ◽  
Vol 124 (4) ◽  
pp. 817-831 ◽  
Author(s):  
R H Schiestl ◽  
S Prakash ◽  
L Prakash

Abstract rad6 mutants of Saccharomyces cerevisiae are defective in the repair of damaged DNA, DNA damage induced mutagenesis, and sporulation. In order to identify genes that can substitute for RAD6 function, we have isolated genomic suppressors of the UV sensitivity of rad6 deletion (rad6 delta) mutations and show that they also suppress the gamma-ray sensitivity but not the UV mutagenesis or sporulation defects of rad6. The suppressors show semidominance for suppression of UV sensitivity and dominance for suppression of gamma-ray sensitivity. The six suppressor mutations we isolated are all alleles of the same locus and are also allelic to a previously described suppressor of the rad6-1 nonsense mutation, SRS2. We show that suppression of rad6 delta is dependent on the RAD52 recombinational repair pathway since suppression is not observed in the rad6 delta SRS2 strain containing an additional mutation in either the RAD51, RAD52, RAD54, RAD55 or RAD57 genes. Possible mechanisms by which SRS2 may channel unrepaired DNA lesions into the RAD52 DNA repair pathway are discussed.


Genetics ◽  
2002 ◽  
Vol 162 (2) ◽  
pp. 973-976 ◽  
Author(s):  
Mirela Matecic ◽  
Shelagh Stuart ◽  
Scott G Holmes

Abstract We have identified histone H4 as a high-expression suppressor of Sir2-induced inviability in yeast cells. Overexpression of histone H3 does not suppress Sir2-induced lethality, nor does overexpression of histone H4 alleles associated with silencing defects. These results suggest a direct and specific interaction between Sir2 and H4 in the silencing mechanism.


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