Loss of histone H3.3 results in DNA replication defects and altered origin dynamics in C. elegans

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

Figure 1.
Figure 1.

Replication timing is unchanged in the absence of H3.3. (A) Schematic description of Repli-seq. Embryonic cells were dissociated, exposed to an EdU pulse for 5 min, and sorted according to their DNA content. EdU-labeled DNA was sequenced and mapped to the genome. (B) Representative genome browser views of Repli-seq and H3.3 ChIP-seq. Repli-seq signal is shown for wild-type (WT) and H3.3-null mutant (Δ H3.3) worms on regions of Chromosomes I and V. Early S phase is shown in black and late S phase in red. HIS-72 (H3.3) ChIP-seq signal is shown in green for the same regions. ChIP-seq data from Delaney et al. (2019). (C) Color-coded replication timing for each chromosome. Repli-seq signal from early (black), mid (orange), and late (red) S phase for WT and Δ H3.3. Data for each chromosome were sorted according to the signal of early S phase in WT.

This Article

  1. Genome Res. 30: 1740-1751

Preprint Server