Until recently protein O-Mannosylation in yeast and metazoans was thought to be directed by a single family of conserved orthologous protein O-Mannosyltransferases (pmts/POMTs). The family of pmts is essential in yeast, and in humans the orthologous POMTs underlie a subgroup of congenital muscular dystrophies designated α-dystroglycanopathies that are caused by loss of O-Mannosylation of a-dystroglycan. Recently, novel types of O-mannosylation in yeast and in metazoans were discovered using gene engineering and lectin-enriched O-Mannose glycoproteomics, and it appears there may be more to come. Analysis of the yeast O-Mannose glycoproteome pointed to a novel nucleocytoplasmic type of O-mannosylation resembling the nucleocytoplasmic O-GlcNAcylation found in eukaryotic cells except yeast1, 2, although the yeast enzyme(s) responsible for the O-mannosylation is still unknown. In higher eukaryotes O-mannosylation of cadherins was found to be independent of the POMTs3, 4, and using a CRISPR/Cas9 genetic dissection strategy combined with sensitive and quantitative O-Man glycoproteomics, we identified a novel family of TMTCs encoded O-Mannosyltransferases5. Congenital deficiency in the TMTC3 gene was shown to underlie Cobblestone Lissencephaly with brain malformation. The TMTC1-4 genes were imperative for cadherin and protocadherin O-Man glycosylation, and using combinatorial knockout of TMTC1-4 distinct roles of the individual isoenzymes for specific b-strands of the cadherin EC domains were identified. In addition, O-Man glycosylation of IPT/TIG domains of Plexins and hepatocyte growth factor receptor (HGFR) was not affected in TMTC KO cells, suggesting the existence of yet another O-Man glycosylation machinery. Our study demonstrates that regulation of O-mannosylation in higher eukaryotes is much more complex than envisioned.