An essential role for the Ino80 chromatin remodeling complex in regulation of gene expression during cellular quiescence

Cellular quiescence is an important physiological state both in unicellular and multicellular eukaryotes. Quiescent cells are halted for proliferation and stop the cell cycle at the G0 stage. Using fission yeast as a model organism, we have previously found that several subunits of a conserved chromatin remodeling complex, Ino80C (INOsitol requiring nucleosome remodeling factor), are required for survival in quiescence. Here, we demonstrate that Ino80C has a key function in regulation of gene expression in G0 cells. We show that null mutants for two Ino80C subunits Arp42 and Iec1, a null mutant for histone variant H2A.Z, and a null mutant for the Inositol kinase Asp1 have very similar phenotypes in quiescence. These mutants show reduced transcription genome-wide, and specifically fail to activate 149 quiescence genes, of which many are localized to the subtelomeric regions. Based on these observations and previous findings, we propose a model in which Ino80C, modulated by Inositol kinase activity, is required to remove H2A.Z, especially in subtelomeric regions in order to reorganize the chromosome structure and activate genes required to survive in quiescence. There are in total 72 samples. There are wild type (smt0) and five different mutant (hht2, pht1, iec1, asp1, arp42) samples in triplicate at four time points (T0, T1D, T1W, T2W) of nitrogen starvation.