Chromatin mobility upon DNA damage: state of the art and remaining questions

Abstract

Chromosome organization and chromatin mobility are central to DNA metabolism. In particular, it has been recently shown by several labs that double strand breaks (DSBs) in yeast induce a change in chromatin mobility at the site of the damage. Intriguingly, DSB also induces a global mobility of the genome, at others, potentially undamaged positions. How mobility is regulated and what are the functional outcomes of these global changes in chromatin dynamics are, however, not yet fully understood. We present the current state of knowledge in light of the recent literature and discuss some perspectives opened by these discoveries towards genome stability.

Keep moving and stay in a good shape to find your homologous recombination partner

“…Indeed, the broken site mobility was shown to increase four- to fivefold and mobility of other sites in the genome also elevates, albeit to a lesser extent (Dion et al 2012 ; Miné-Hattab and Rothstein 2012 ). Both global and local increase in motion depend on checkpoint activation and diverse, non-exclusive, mechanisms have been proposed (for a Review Smith and Rothstein 2017 ; Zimmer and Fabre 2018 ). First, a checkpoint-mediated disruption of centromeres anchoring has recently been proposed to participate in this DSB- induced chromatin mobility (Strecker et al 2016 ).…”

Copper Tolerance Mediated by FgAceA and FgCrpA in Fusarium graminearum

“…Fungal biomass was compared by collecting mycelia from 3-day-old liquid FMM culture incubated at 25°C in a shaker (180 rpm). For conidiation, five 5 mm mycelial plugs of the wild type strain PH-1 and its mutants taken from the edge of a 3-day-old colony were inoculated in a 150 ml triangular flask containing 50 ml of CMC (carboxymethyl cellulose) medium and incubated at 25°C, 180 rpm for 3 days in a shaker with light ( Iida et al, 2008 ; Chen et al, 2018 ). The number of conidia in CMC medium was counted using a hemacytometer.…”

Quantitative mechanisms of DNA damage sensing and signaling

“…H2A is an integral component of chromatin and as such immediately available as substrate for phosphorylation. Therefore, and despite the fact that histones were shown to display plasticity at DSBs (Hauer et al 2017;Hauer and Gasser 2017;Adam et al 2016;Tsabar et al 2016), encounters between Mec1 and H2A over the broad γH2A domain will rather be defined by chromatin architecture and mobility than recruitment (Caron et al 2015;Aymard and Legube 2016;Lee et al 2013;Renkawitz et al 2013;Zimmer and Fabre 2019). Taken together, we therefore propose that Mec1 targets are phosphorylated dependent on the frequency of kinase-substrate encounters, which in the global signaling circuit is determined by recruitment and in the local signaling circuit depends on chromatin architecture (Fig.…”