A genetic screen identifies Etl4-deficiency capable of stabilizing the haploidy in embryonic stem cells

We performed a genome-wild loss-of-function screening and revealed several gene mutations could significantly reduce the rate of self-diploidization in haESCs. We further demonstrated that CRISPR/Cas9 mediated Etl4 knockout stabilizes the haploid state in different haploid cell lines. More interestingly, Etl4 deficiency could increase the mitochondrial oxidative phosphorylation (OXPHOS) capacity and decrease glycolysis in haESCs. Collectively, our study identifies Etl4 as a novel haploidy-related factor and suggests that the changes of energy metabolism is associated with self-diploidization. Overall design: mRNA profiles of Etl4 knockout haploid ESCs and wild type haploid ESCs