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METTL5 regulates cranial suture fusion via Wnt signaling

Fundamental Research 2023年第3期3卷 369-376页

作者： Kexin Lei Ruoshi Xu Qian Wang Qiuchan Xiong Xinyi Zhou Qiwen Li Dutmanee Seriwatanachai Shuibin Lin Chenchen Zhou Quan Yuan State Key Laboratory of Oral Diseases National Clinical Research Center for Oral DiseasesWest China Hospital of StomatologySichuan UniversityChengdu 610041China Department of Oral Biology Faculty of DentistryMahidol UniversityBangkok 73170Thailand Center for Translational Medicine Precision Medicine InstituteThe First Affiliated Hospital of Sun Yat-sen UniversityGuangzhou 510080China

METTL5 is a methyltransferase that mediates eukaryotic 18S ribosomal RNA m^(6)A modification,and its mutations lead to intellectual disability,microcephaly,and facial dysmorphism in patients.However,the role of METTL5 in craniofacial development remains poorly understood.This study demonstrates that Mettl5 knockout mice exhibit poor ossification,widened cranial sutures,and a cleidocranial dysplasia-like phenotype.Deletion of Mettl5 leads to increased proliferation and decreased osteogenic differentiation of suture mesenchymal stem cells.Mechanistically,we find that Wnt signaling is significantly downregulated after Mettl5 knockout.Overall,we reveal an essential role of METTL5 in craniofacial development and osteogenic differentiation of suture mesenchymal stem cells,making METTL5 a potential diagnostic and therapeutic target for craniofacial developmental diseases.

关键词： METTL5 N6-methyladenosine Cranial suture Osteogenic differentiation Mesenchymal stem cells

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METTL3-mediated m^(6)A RNA methylation regulates dorsal lingual epithelium homeostasis

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International Journal of Oral Science 2022年第3期14卷 287-296页

作者： Qiuchan Xiong Caojie Liu Xin Zheng Xinyi Zhou Kexin Lei Xiaohan Zhang Qian Wang Weimin Lin Ruizhan Tong Ruoshi Xu Quan Yuan State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&West China Hospital of Stomatology Sichuan UniversityChengduChina Department of Thoracic Oncology Cancer Centerand Laboratory of Clinical Cell TherapyWest China HospitalSichuan UniversityChengduChina

The dorsal lingual epithelium,which is composed of taste buds and keratinocytes differentiated from K14^(+)basal cells,discriminates taste compounds and maintains the epithelial barrier.N6-methyladenosine(m^(6)A)is the most abundant mRNA modification in eukaryotic cells.How METTL3-mediated m^(6)A modification regulates K14^(+)basal cell fate during dorsal lingual epithelium formation and regeneration remains unclear.Here we show knockout of Mettl3 in K14^(+)cells reduced the taste buds and enhanced keratinocytes.Deletion of Mettl3 led to increased basal cell proliferation and decreased cell division in taste buds.Conditional Mettl3 knock-in mice showed little impact on taste buds or keratinization,but displayed increased proliferation of cells around taste buds in a protective manner during post-irradiation recovery.Mechanically,we revealed that the most frequent m^(6)A modifications were enriched in Hippo and Wnt signaling,and specific peaks were observed near the stop codons of Lats1 and FZD7.Our study elucidates that METTL3 is essential for taste bud formation and could promote the quantity recovery of taste bud after radiation.

关键词： METTL3-mediated m^(6)A RNA methylation regulates dorsal lingual epithelium homeostasis RNA

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Mettl5 mediated 18S rRNA N6-methyladenosine(m^(6)A)modification controls stem cell fate determination and neural function

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Genes & Diseases 2022年第1期9卷 268-274页

作者： Lu Wang Yu Liang Rongzhi Lin Qiuchan Xiong Peng Yu Jieyi Ma Maosheng Cheng Hui Han Xiaochen Wang Ganping Wang Fengyin Liang Zhong Pei Demeng Chen Quan Yuan Yi-Zhou Jiang Shuibin Lin Center for Translational Medicine Precision Medicine InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong 510080PR China Institute for Advanced Study Shenzhen UniversityShenzhenGuangdong 518060PR China Department of Otorhinolaryngology The Second Affiliated Hospital of Fujian Medical UniversityQuanzhouFujian 362000PR China State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases West China Hospital of StomatologySichuan UniversityChengduSichuan 610041PR China Department of Neurology The First Affiliated HospitalSun Yat-sen UniversityGuangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological DiseasesNational Key Clinical Department and Key Discipline of NeurologyGuangzhouGuangdong 510080PR China

Ribosome RNA(rRNA)accounts for more than 80%of the cell's total RNA,while the physiological functions of rRNA modifications are poorly understood.Mutations of 18S rRNA m6A methyltransferase METTL5 cause intellectual disability,microcephaly,and facial dysmorphisms in patients,however,little is known about the underlying mechanisms.In this study,we identified METTL5 protein complex and revealed that METTL5 mainly interacts with RNA binding proteins and ribosome proteins.Functionally,we found that Mettl5 knockout in mESCs leads to the abnormal craniofacial and nervous development.Moreover,using Mettl5 knockout mouse model,we further demonstrated that Mettl5 knockout mice exhibit intellectual disability,recapitulating the human phenotype.Mechanistically,we found that Mettl5 maintains brain function and intelligence by regulating the myelination process.Our study uncovered the causal correlation between mis-regulated 18S rRNA m6A modification and neural function defects,supporting the important physiological functions of rRNA modifications in human diseases.

关键词： 18S rRNA Intellectual disability METTL5 N6-methyladenosine(m^(6)A) Neural development

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