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Mettl14-mediated m6A modification is essential for visual function and retinal photoreceptor survival
Yeming Yang1,2,3, Ping Shuai1,2, Xiao Li1,2
1Health Management Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 61007, Sichuan, China.
BMC Biology
|June 13, 2022
Summary
N6-methyladenosine (m6A) modification, regulated by Mettl14, is crucial for retinal photoreceptor function. Loss of Mettl14 impairs phototransduction and ciliogenesis, leading to vision loss and photoreceptor degeneration.
Area of Science:
- Molecular Biology
- Epigenetics
- Neuroscience
Background:
- N6-methyladenosine (m6A) is the most abundant mRNA modification in eukaryotes.
- m6A regulates mRNA synthesis and degradation in the nervous system.
- The role of m6A in retinal photoreceptors is currently unknown.
Purpose of the Study:
- To investigate the function of Mettl14, an m6A writer, in retinal rod and cone photoreceptors.
- To elucidate the role of m6A modification in visual function.
Main Methods:
- Generated retina-specific Mettl14-knockout mouse models (Rho-Cre and HRGP-Cre).
- Analyzed photoreceptor function using electroretinography.
- Investigated protein localization and gene expression via transcriptomics and MeRIP-seq.
Main Results:
- Mettl14 deficiency in rods caused weakened scotopic photoresponse and degeneration, with protein mislocalization.
- Mettl14 deficiency in cones led to opsin mislocalization and cell death.
- Mettl14 depletion reduced m6A levels and expression of phototransduction and ciliogenesis genes, impairing protein transport.
Conclusions:
- Mettl14 is essential for photoreceptor function and survival by regulating phototransduction and ciliogenesis.
- m6A modification plays a critical role in maintaining visual function.
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