The eukaryotic nucleosome prevents access to the genome. Convergently evolving histone isoforms, also called histone variants, form diverse families that are enriched over distinct features of plant genomes. Among the diverse families of plant histone variants, H2A.Z exclusively marks genes. Here we review recent research progress on the genome-wide distribution patterns and deposition of H2A.Z in plants as well as its association with histone modifications and roles in plant chromatin regulation. We also discuss some hypotheses that explain the different findings about the roles of H2A.Z in plants.

Highlights d Selection of the motif KSPK marks evolution of H2A.W in vascular plants d Synthetic addition of the KSPK motif to yeast H2A affects only heterochromatin d Histone variants can be selected prior to their segregation to chromatin domains

BackgroundDNA damage response (DDR) plays pivotal roles in maintaining genome integrity and stability. An effective DDR requires the involvement of hundreds of genes that compose a complicated network. Because DDR is highly conserved in evolution, studies in lower eukaryotes can provide valuable information to elucidate the mechanism in higher organisms. Fission yeast (Schizosaccharomyces pombe) has emerged as an excellent model for DDR research in recent years. To identify novel genes involved in DDR, we screened a genome-wide S. pombe haploid deletion library against six different DNA damage reagents. The library covered 90.5% of the nonessential genes of S. pombe.ResultsWe have identified 52 genes that were actively involved in DDR. Among the 52 genes, 20 genes were linked to DDR for the first time. Flow cytometry analysis of the repair defective mutants revealed that most of them exhibited a defect in cell cycle progression, and some caused genome instability. Microarray analysis and genetic complementation assays were carried out to characterize 6 of the novel DDR genes in more detail. Data suggested that SPBC2A9.02 and SPAC27D7.08c were required for efficient DNA replication initiation because they interacted genetically with DNA replication initiation proteins Abp1 and Abp2. In addition, deletion of sgf73+, meu29+, sec65+ or pab1+ caused improper cytokinesis and DNA re-replication, which contributed to the diploidization in the mutants.ConclusionsA genome-wide screen of genes involved in DDR emphasized the key role of cell cycle control in the DDR network. Characterization of novel genes identified in the screen helps to elucidate the mechanism of the DDR network and provides valuable clues for understanding genome stability in higher eukaryotes.