In response to Liet al.: Linker histones function inDrosophilaembryogenesis

In an earlier paper (Pérez-Montero et al., 2013), we reported that the embryonic linker histone ofDrosophiladBigH1 was essential for earlyDrosophilaembryogenesis since embryos homozygous for thebigH1¹⁰⁰mutation showed strong defects and did not survive beyond zygotic genome activation (ZGA) at cellularization. Recent results challenge these observations since nullbigH1mutations generated by CRISPR/Cas9 methodology turn out to be homozygous viable, as reported in Liet al. (2019) and here. In this regard, Liet al. 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 inbigH1¹⁰⁰embryos.