Abstract
Reparative chromatin assembly is an important step in maintaining the stability of the genome. Proper chromatin assembly is provided by histone chaperones. Violation of the function of these proteins can lead to the development of various forms of cancer and to a number of hereditary diseases in humans. One of the key processes in the reparative assembly of chromatin is acetylation and deacetylation of histones, complexes NuB4 and RPD3. Results presented in this work demonstrate that inactivation of Rpd3 and Sin3 subunits of the RPD3 complex blocks super activation of RNR3 gene. The phenotypes of rpd3Δ and sin3Δ mutants differ due to different activation of Rad53 kinase in these mutants, which may be due to deacetylation of Rad53 by Rpd3 deacetylase. Our findings revealed that the contribution of deacetylation of Rad53 kinase makes a significant contribution to the regulation hyperactivation RNR complex after UV irradiation. In addition, this work provides indirect evidence that the Him1 protein may participate as a histone chaperone in chromatin repair assembly.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
