Mettl14 and Mettl3 work cooperatively to regulate retinal development
N6-methylenadenosine (m6A) modification, the most abundant epitranscriptomic modification in eukaryotic mRNAs, has been shown to play crucial roles in regulating various aspects of mRNA metabolism and functions. In this study, we applied the Cre-Loxp conditional knockout system to investigate the role of core component of the m6A methyltransferase complex, METTL14 and METTL3, in retinal development. Our results showed that double absence of Mettl14 and Mettl3 caused structural disturbance in the retina and prolonged proliferation activity of retinal progenitor cells. Interestingly, this did not affect the generation of various retinal cells, but this severely disrupted their distribution. In addition, double deletion of Mettl14 together with Mettl3 caused a stronger phenotype than the Mettl14 single deletion. In conclusion, our study demonstrated that Mettl14 and Mettl3 work cooperatively to regulate retinal development, and that this basis of regulation is mainly dependent on m6A modification. Overall design: retinas of postnatal day 7 pups of different genotype were collected and processed for RNA-Seq sequencing and analyses.