TY  - GEN
T1  - Loss of nucleosome remodelers CHRAC/ACF does not sensitize early Drosophila embryos to X-rays
AU  - Scacchetti, Alessandro
AU  - Becker, Peter B.
DO  - 10.17912/micropub.biology.000287
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000287/
AB  - The ‘Chromatin Accessibility Complex’ (CHRAC) and ‘ATP-utilizing chromatin assembly and remodeling factor’ (ACF) of Drosophila melanogaster are chromatin remodeling complexes that slide nucleosomes (Becker and Horz, 2002). Both originate from the association of the ATPase ISWI and a large subunit ACF1. CHRAC contains two additional histone-fold subunits, CHRAC-14 and CHRAC-16 (Corona et al., 2000), but its nucleosome sliding activity is essentially similar to ACF in vitro (Hartlepp et al., 2005). CHRAC/ACF are implicated in several developmental processes. Mutations of ACF1, which disrupt both complexes, mildly perturb embryogenesis and oogenesis (Boerner et al., 2016; Chioda et al., 2010), and compromise Polycomb silencing and heterochromatin formation (Fyodorov et al., 2004). Through their nucleosome sliding activity CHRAC/ACF contribute to the genome-wide formation of regular nucleosome arrays. Altered nucleosome spacing and regularity in their absence correlates with leakiness of the repressive ground state of chromatin in early embryos (Baldi et al., 2018; Scacchetti et al., 2018). CHRAC/ACF complexes are also conserved in yeast (Iida and Araki, 2004) and mammals (LeRoy et al., 2000; Poot et al., 2000).
PY  - 2020
JO  - microPublication Biology
ER  -