Mar 24, 2020

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

BioRxiv : the Preprint Server for Biology
A. CarbonellFernando Azorín


In an earlier paper (Perez-Montero et al., 2013), we reported that the embryonic linker histone of Drosophila dBigH1 was essential for early Drosophila embryogenesis since embryos homozygous for the bigH1100 mutation showed strong defects and did not survive beyond zygotic genome activation (ZGA) at cellularization. Recent results challenge these observations since null bigH1 mutations generated by CRISPR/Cas9 methodology turn out to be homozygous viable, as reported in Li et al. (2019) and here. In this regard, Li et 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 in bigH1100 embryos.

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Mentioned in this Paper

Disease Transmission
Laboratory Culture
Migration, Cell
Population Group
Biological Evolution

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