Expression profiling by high throughput sequencing Genome binding/occupancy profiling by high throughput sequencing
Summary
Asymmetric cell divisions (ACDs) generate two daughter cells with identical genetic information but distinct cell fates. Epigenetic mechanisms are crucial for cell fate specification, and it remains unclear how epigenetic information is inherited. Here, we report asymmetric segregation of the nucleosome remodeling and deacetylase complex (NuRD) during ACDs in Caenorhabditis elegans. NuRD is enriched to chromosomes of the future surviving but not apoptotic daughter cell, whereas NuRD evenly distributes to two viable siblings. Disruption of ACDs causes symmetric NuRD inheritance, and an ectopic gain of NuRD in apoptotic daughters allows cell survival and differentiation. Lack of NuRD upregulates the expression of the vital cell death-inducing gene egl-1 by increasing H3K27 acetylation on the egl-1 locus, which activates the EGL-1-CED-9-CED-4-CED-3 pathway to promote apoptosis. We propose that biased NuRD segregation during ACDs provides a previously unrecognized yet common mechanism for asymmetrically partitioning epigenetic information that contributes to binary cell fate decisions.
Overall design
1.The embryonic SPLiT-seq of wild-type worms expressing Pegl-1::NLS::gfp;2.Embryonic mRNA profiles of wild type and hda-1/lin-53 RNAi worms;3. Examination of H3K27ac modifications in wild type and hda-1/lin-53 RNAi worms.
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