In response to Li et al. : Linker histones function in Drosophila embryogenesis

In an earlier paper (), we reported that the embryonic linker histone of dBigH1 was essential for early embryogenesis since embryos homozygous for the mutation showed strong defects and did not survive beyond zygotic genome activation (ZGA) at cellularization. Recent results challenge these observations since null mutations generated by CRISPR/Cas9 methodology turn out to be homozygous viable, as reported in and here. In this regard, Li . described a novel mechanism by which lack of dBigH1 is compensated by the early expression of maternal dH1. Here, we confirm this observation and show that such compensatory mechanism is not activated in embryos.